kir4 1 ab  (Alomone Labs)


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    Structured Review

    Alomone Labs kir4 1 ab
    In vivo intravitreal application of <t>Kir4.1-Ab:carrier</t> reduces STR and PhNR electronegative ERG potentials in RCS rat. ( A ) STR and PhNR were diminished in the eye of a 15-wk-old rat injected with Kir4.1-Ab:carrier (red) relative to the contralateral IgG:carrier control eye (black). ( B ) Light-adapted ERG responses (stimulus intensity 0.6 log cd-s/m 2 ) before (black) and 2 h after injection in a representative RCS rat at 14 wk of age. One eye was injected with Kir4.1-Ab:carrier (red) and the contralateral control eye with rabbit IgG:carrier (gray). PhNR amplitudes were decreased by 29 ± 5% ( n = 3) compared with the same eye baseline, whereas no change in PhNR amplitude was seen in the contralateral control eyes.
    Kir4 1 Ab, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 1 article reviews
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    kir4 1 ab - by Bioz Stars, 2022-05
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    Images

    1) Product Images from "Probing potassium channel function in vivo by intracellular delivery of antibodies in a rat model of retinal neurodegeneration"

    Article Title: Probing potassium channel function in vivo by intracellular delivery of antibodies in a rat model of retinal neurodegeneration

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi: 10.1073/pnas.0913472107

    In vivo intravitreal application of Kir4.1-Ab:carrier reduces STR and PhNR electronegative ERG potentials in RCS rat. ( A ) STR and PhNR were diminished in the eye of a 15-wk-old rat injected with Kir4.1-Ab:carrier (red) relative to the contralateral IgG:carrier control eye (black). ( B ) Light-adapted ERG responses (stimulus intensity 0.6 log cd-s/m 2 ) before (black) and 2 h after injection in a representative RCS rat at 14 wk of age. One eye was injected with Kir4.1-Ab:carrier (red) and the contralateral control eye with rabbit IgG:carrier (gray). PhNR amplitudes were decreased by 29 ± 5% ( n = 3) compared with the same eye baseline, whereas no change in PhNR amplitude was seen in the contralateral control eyes.
    Figure Legend Snippet: In vivo intravitreal application of Kir4.1-Ab:carrier reduces STR and PhNR electronegative ERG potentials in RCS rat. ( A ) STR and PhNR were diminished in the eye of a 15-wk-old rat injected with Kir4.1-Ab:carrier (red) relative to the contralateral IgG:carrier control eye (black). ( B ) Light-adapted ERG responses (stimulus intensity 0.6 log cd-s/m 2 ) before (black) and 2 h after injection in a representative RCS rat at 14 wk of age. One eye was injected with Kir4.1-Ab:carrier (red) and the contralateral control eye with rabbit IgG:carrier (gray). PhNR amplitudes were decreased by 29 ± 5% ( n = 3) compared with the same eye baseline, whereas no change in PhNR amplitude was seen in the contralateral control eyes.

    Techniques Used: In Vivo, Injection

    IHC of rat retina shows Kir4.1 colocalization with Müller cell GFAP marker. ( A ) Conventional postmortem double labeling with Kir4.1-Ab (red) and GFAP-Ab (green) shows colocalization with Müller cells in a dystrophic 14 wk-old RCS retina. ( B ) In vivo intravitreal application of Kir4.1-Ab:carrier complex gives prominent labeling of Müller cell endfeet with extensions along Müller cell processes in the IPL (red) in a 15-wk-old dystrophic RCS rat and colocalizes with GFAP (green). GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; ONL, outer nuclear layer.
    Figure Legend Snippet: IHC of rat retina shows Kir4.1 colocalization with Müller cell GFAP marker. ( A ) Conventional postmortem double labeling with Kir4.1-Ab (red) and GFAP-Ab (green) shows colocalization with Müller cells in a dystrophic 14 wk-old RCS retina. ( B ) In vivo intravitreal application of Kir4.1-Ab:carrier complex gives prominent labeling of Müller cell endfeet with extensions along Müller cell processes in the IPL (red) in a 15-wk-old dystrophic RCS rat and colocalizes with GFAP (green). GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; ONL, outer nuclear layer.

    Techniques Used: Immunohistochemistry, Marker, Labeling, In Vivo

    2) Product Images from "Expressional analysis of the astrocytic Kir4.1 channel in a pilocarpine-induced temporal lobe epilepsy model"

    Article Title: Expressional analysis of the astrocytic Kir4.1 channel in a pilocarpine-induced temporal lobe epilepsy model

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2013.00104

    Immunohistochemical analysis of Kir4.1- and GFAP-immunoreactivity (IR)-positive cells in pilocarpine-inducedTLE rats. (A) Schematic illustrations of the brain sections selected for quantitative analysis of Kir4.1- and GFAP-IR-positive cells. Squares in each section indicate the area analyzed for counting of Kir4.1- and GFAP-IR-positive cells. The distance from the Bregma is shown on the bottom of each section. MC, motor cortex; SC, sensory cortex; AID, agranular insular cortex; Pir, piriform cortex; dmST, vmST, dlST and vlST, dorsomedial, ventromedial, dorsolateral, and ventrolateral striatum, respectively; AcbC and AcbSh, core and shell regions of nucleus accumbens, respectively; Ect-PRh, ectorhinal–perirhinal cortex; MePV and MePD, medial amygdaloid nucleus, posteroventral and posterodorsal part; BLP, basolateral amygdaloid nucleus, posterior part; BMP, basomedial amygdaloid nucleus, posterior part; PMCo, posteromedial cortical amygdaloid nucleus; CA1, CA3, and DG: CA1, CA3, and dentate gyrus of the hippocampus. (B) Representative photographs illustrating the Kir4.1 (upper panels)- and GFAP (lower panels)-positive cells in the sensory cortex (SC) and the medial amygdaloid nucleus, posterodorsal part (MePD). Scale bar: 50 μ m.
    Figure Legend Snippet: Immunohistochemical analysis of Kir4.1- and GFAP-immunoreactivity (IR)-positive cells in pilocarpine-inducedTLE rats. (A) Schematic illustrations of the brain sections selected for quantitative analysis of Kir4.1- and GFAP-IR-positive cells. Squares in each section indicate the area analyzed for counting of Kir4.1- and GFAP-IR-positive cells. The distance from the Bregma is shown on the bottom of each section. MC, motor cortex; SC, sensory cortex; AID, agranular insular cortex; Pir, piriform cortex; dmST, vmST, dlST and vlST, dorsomedial, ventromedial, dorsolateral, and ventrolateral striatum, respectively; AcbC and AcbSh, core and shell regions of nucleus accumbens, respectively; Ect-PRh, ectorhinal–perirhinal cortex; MePV and MePD, medial amygdaloid nucleus, posteroventral and posterodorsal part; BLP, basolateral amygdaloid nucleus, posterior part; BMP, basomedial amygdaloid nucleus, posterior part; PMCo, posteromedial cortical amygdaloid nucleus; CA1, CA3, and DG: CA1, CA3, and dentate gyrus of the hippocampus. (B) Representative photographs illustrating the Kir4.1 (upper panels)- and GFAP (lower panels)-positive cells in the sensory cortex (SC) and the medial amygdaloid nucleus, posterodorsal part (MePD). Scale bar: 50 μ m.

    Techniques Used: Immunohistochemistry

    Western blot analysis for Kir4.1, Kir5.1 and Kir2.1 expression in pilocarpine-inducedTLE rats. (A) Representative Western blots visualizing Kir4.1, Kir5.1, and Kir2.1 expression in the frontal cortex (fCx), occipito-temporal cortex (otCx), striatum (St), and hypothalamus (Ht). (B–D) Regional expression of Kir4.1 (B) , Kir5.1 (C) , and Kir2.1 (D) in pilocarpine-induced TLE rats. Kir expression was expressed as relative optical density (ROD) to β-actin. fCx, frontal cortex; ptCx, parieto-temporal cortex; otCx, occipito-temporal cortex; St, striatum; Hpc, hippocampus; Th, thalamus; Ht, hypothalamus; Mid, midbrain; P/MO, pons/medulla oblongata; Cer, cerebellum. Each column represents the mean ± SEM of four animals. * P
    Figure Legend Snippet: Western blot analysis for Kir4.1, Kir5.1 and Kir2.1 expression in pilocarpine-inducedTLE rats. (A) Representative Western blots visualizing Kir4.1, Kir5.1, and Kir2.1 expression in the frontal cortex (fCx), occipito-temporal cortex (otCx), striatum (St), and hypothalamus (Ht). (B–D) Regional expression of Kir4.1 (B) , Kir5.1 (C) , and Kir2.1 (D) in pilocarpine-induced TLE rats. Kir expression was expressed as relative optical density (ROD) to β-actin. fCx, frontal cortex; ptCx, parieto-temporal cortex; otCx, occipito-temporal cortex; St, striatum; Hpc, hippocampus; Th, thalamus; Ht, hypothalamus; Mid, midbrain; P/MO, pons/medulla oblongata; Cer, cerebellum. Each column represents the mean ± SEM of four animals. * P

    Techniques Used: Western Blot, Expressing

    Topographical expression of Kir4.1 and GFAP in the cortical regions of pilocarpine-inducedTLE rats. (A,B) Number of Kir4.1 (A) - or GFAP (B) -immunoreactivity (IR)-positive cells. (C) Relative Kir4.1 expression ratios in astrocytes. A pair of successive slices in each region from the same animal was stained with anti-Kir4.1 or anti-GFAP antibody. The Kir4.1 expression ratios were calculated as the ratios of Kir4.1-positive astrocytes relative to the total number of astrocytes (Kir4.1-positive cells/GFAP-positive cells) in each animal. MC, motor cortex; SC, sensory cortex; AID, agranular insular cortex, dorsal part; Ect-PRh, ectorhinal-perirhinal cortex; Pir, piriform cortex. Each column represents the mean ± S.E.M. of seven animals. * P
    Figure Legend Snippet: Topographical expression of Kir4.1 and GFAP in the cortical regions of pilocarpine-inducedTLE rats. (A,B) Number of Kir4.1 (A) - or GFAP (B) -immunoreactivity (IR)-positive cells. (C) Relative Kir4.1 expression ratios in astrocytes. A pair of successive slices in each region from the same animal was stained with anti-Kir4.1 or anti-GFAP antibody. The Kir4.1 expression ratios were calculated as the ratios of Kir4.1-positive astrocytes relative to the total number of astrocytes (Kir4.1-positive cells/GFAP-positive cells) in each animal. MC, motor cortex; SC, sensory cortex; AID, agranular insular cortex, dorsal part; Ect-PRh, ectorhinal-perirhinal cortex; Pir, piriform cortex. Each column represents the mean ± S.E.M. of seven animals. * P

    Techniques Used: Expressing, Staining

    Topographical expression of Kir4.1 and GFAP in the basal ganglia and limbic regions of pilocarpine-inducedTLE rats. (A,B) Number of Kir4.1 (A) - or GFAP (B) -immunoreactivity (IR)-positive cells. (C) Relative Kir4.1 expression ratios in astrocytes. A pair of successive slices in each region from the same animal was stained with anti-Kir4.1 or anti-GFAP antibody. The Kir4.1 expression ratios were calculated as the ratios of Kir4.1-positive astrocytes relative to the total number of astrocytes (Kir4.1Kir4.1-positive cells/GFAP-positive cells) in each animal. dmST, vmST, dlST, and vlST, dorsomedial, ventromedial, dorsolateral, and ventrolateral striatum, respectively; AcbC and AcbSh, core and shell regions of the nucleus accumbens, respectively; MePV and MePD, medial amygdaloid nucleus, posteroventral and posterodorsal part; BLP, basolateral amygdaloid nucleus, posterior part; BMP, basomedial amygdaloid nucleus, posterior part; PMCo, posteromedial cortical amygdaloid nucleus; CA1, CA3, and DG, CA1, CA3, and dentate gyrus of the hippocampus. Each column represents the mean ± SEM of seven animals. * P
    Figure Legend Snippet: Topographical expression of Kir4.1 and GFAP in the basal ganglia and limbic regions of pilocarpine-inducedTLE rats. (A,B) Number of Kir4.1 (A) - or GFAP (B) -immunoreactivity (IR)-positive cells. (C) Relative Kir4.1 expression ratios in astrocytes. A pair of successive slices in each region from the same animal was stained with anti-Kir4.1 or anti-GFAP antibody. The Kir4.1 expression ratios were calculated as the ratios of Kir4.1-positive astrocytes relative to the total number of astrocytes (Kir4.1Kir4.1-positive cells/GFAP-positive cells) in each animal. dmST, vmST, dlST, and vlST, dorsomedial, ventromedial, dorsolateral, and ventrolateral striatum, respectively; AcbC and AcbSh, core and shell regions of the nucleus accumbens, respectively; MePV and MePD, medial amygdaloid nucleus, posteroventral and posterodorsal part; BLP, basolateral amygdaloid nucleus, posterior part; BMP, basomedial amygdaloid nucleus, posterior part; PMCo, posteromedial cortical amygdaloid nucleus; CA1, CA3, and DG, CA1, CA3, and dentate gyrus of the hippocampus. Each column represents the mean ± SEM of seven animals. * P

    Techniques Used: Expressing, Staining

    3) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    4) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    5) Product Images from "Renal Tubule Nedd4-2 Deficiency Stimulates Kir4.1/Kir5.1 and Thiazide-Sensitive NaCl Cotransporter in Distal Convoluted Tubule"

    Article Title: Renal Tubule Nedd4-2 Deficiency Stimulates Kir4.1/Kir5.1 and Thiazide-Sensitive NaCl Cotransporter in Distal Convoluted Tubule

    Journal: Journal of the American Society of Nephrology : JASN

    doi: 10.1681/ASN.2019090923

    NCC expression is suppressed in Ks-Nedd4-2/Kir4.1 KO mice. Images show tNCC immunostaining in (A–C) WT ( Nedd4l flox/flox /Kcnj10 flox/flox ), (D–F) Ks-Nedd4-2/Kir4.1 KO, (G–I) Ks-Nedd4-2 KO, and (J–L) Ks-Kir4.1 KO mice. The images in red squares in (A, D, G, and J) are magnified with intermediate (B, E, H, and K) and large resolution (C, F, I, and L). Original magnification, ×4 in A, D, G, and J; ×20 in B, E, H, and K; ×60 in C, F, I, and L.
    Figure Legend Snippet: NCC expression is suppressed in Ks-Nedd4-2/Kir4.1 KO mice. Images show tNCC immunostaining in (A–C) WT ( Nedd4l flox/flox /Kcnj10 flox/flox ), (D–F) Ks-Nedd4-2/Kir4.1 KO, (G–I) Ks-Nedd4-2 KO, and (J–L) Ks-Kir4.1 KO mice. The images in red squares in (A, D, G, and J) are magnified with intermediate (B, E, H, and K) and large resolution (C, F, I, and L). Original magnification, ×4 in A, D, G, and J; ×20 in B, E, H, and K; ×60 in C, F, I, and L.

    Techniques Used: Expressing, Mouse Assay, Immunostaining

    Double deletion of Kir4.1 and Nedd4-2 impairs NCC function. (A) A scatter plot showing the Δ values of HCTZ-induced net E Na in WT ( Nedd4l flox/flox /Kcnj10 flox/flox ), Ks-Nedd4-2/Kir4.1 KO, and Ks-Kir4.1 KO mice. (B) A scatter line graph showing the results of each experiment in which the effect of single-dose HCTZ (30 mg/kg body wt [BW]) on urinary Na + excretion ( E Na ) within 120 minutes was measured with the renal clearance method in WT ( Nedd4l flox/flox /Kcnj10 flox/flox ) and Ks-Nedd4-2/Kir4.1 KO mice. The significance is determined by t test. (C) A scatter line graph showing the results of each experiment in which the effect of single-dose HCTZ (30 mg/kg BW) on urinary K + excretion ( E K ) within 120 minutes was measured with the renal clearance method in WT ( Nedd4l flox/flox /Kcnj10 flox/flox ) and Ks-Nedd4-2/Kir4.1 KO mice. (D) A scatter plot shows the plasma K + concentrations in WT ( Nedd4l flox/flox and Nedd4l flox/flox /Kcnj10 flox/flox ), Ks-Nedd4-2 KO, Ks-Nedd4-2/Kir4.1 KO, and Ks-Kir4.1 KO mice. The experiments were performed in the mice treated with doxycycline followed by a 14-day recovery period.
    Figure Legend Snippet: Double deletion of Kir4.1 and Nedd4-2 impairs NCC function. (A) A scatter plot showing the Δ values of HCTZ-induced net E Na in WT ( Nedd4l flox/flox /Kcnj10 flox/flox ), Ks-Nedd4-2/Kir4.1 KO, and Ks-Kir4.1 KO mice. (B) A scatter line graph showing the results of each experiment in which the effect of single-dose HCTZ (30 mg/kg body wt [BW]) on urinary Na + excretion ( E Na ) within 120 minutes was measured with the renal clearance method in WT ( Nedd4l flox/flox /Kcnj10 flox/flox ) and Ks-Nedd4-2/Kir4.1 KO mice. The significance is determined by t test. (C) A scatter line graph showing the results of each experiment in which the effect of single-dose HCTZ (30 mg/kg BW) on urinary K + excretion ( E K ) within 120 minutes was measured with the renal clearance method in WT ( Nedd4l flox/flox /Kcnj10 flox/flox ) and Ks-Nedd4-2/Kir4.1 KO mice. (D) A scatter plot shows the plasma K + concentrations in WT ( Nedd4l flox/flox and Nedd4l flox/flox /Kcnj10 flox/flox ), Ks-Nedd4-2 KO, Ks-Nedd4-2/Kir4.1 KO, and Ks-Kir4.1 KO mice. The experiments were performed in the mice treated with doxycycline followed by a 14-day recovery period.

    Techniques Used: Mouse Assay

    Nedd4-2 deletion delays Kir4.1 deletion-induced inhibition of NCC. (A) An immunoblot showing the expression of pNCC, tNCC, Kir4.1, and Nedd4-2 in WT ( Kcnj10 flox/flox and Kcnj10 flox/flox /Nedd4l flox/flox ), Ks-Kir4.1 KO, and Ks-Nedd4-2/Kir4.1 KO mice. The experiments was conducted in the mice immediately after treatment of doxycycline without a 14-day transition period. Gapdh, glyceraldehyde-3-phosphate dehydrogenase. (B) A scatter graph summarizes the normalized band intensity of the pNCC (left panel) and tNCC (right panel) in WT ( Kcnj10 flox/flox and Kcnj10 flox/flox /Nedd4l flox/flox ), Ks-Kir4.1 KO, and Ks-Nedd4-2/Kir4.1 KO mice. The mean value and SEM are shown on the left of each row. Male mice were used for the western blot. (C) A scatter plot shows the HCTZ-induced net renal Na + excretion in WT, Ks-Nedd4-2/Kir4.1 KO, and Ks-Kir4.1 KO mice. The mice were used immediately after either doxycycline or vehicle treatment. BW, body weight.
    Figure Legend Snippet: Nedd4-2 deletion delays Kir4.1 deletion-induced inhibition of NCC. (A) An immunoblot showing the expression of pNCC, tNCC, Kir4.1, and Nedd4-2 in WT ( Kcnj10 flox/flox and Kcnj10 flox/flox /Nedd4l flox/flox ), Ks-Kir4.1 KO, and Ks-Nedd4-2/Kir4.1 KO mice. The experiments was conducted in the mice immediately after treatment of doxycycline without a 14-day transition period. Gapdh, glyceraldehyde-3-phosphate dehydrogenase. (B) A scatter graph summarizes the normalized band intensity of the pNCC (left panel) and tNCC (right panel) in WT ( Kcnj10 flox/flox and Kcnj10 flox/flox /Nedd4l flox/flox ), Ks-Kir4.1 KO, and Ks-Nedd4-2/Kir4.1 KO mice. The mean value and SEM are shown on the left of each row. Male mice were used for the western blot. (C) A scatter plot shows the HCTZ-induced net renal Na + excretion in WT, Ks-Nedd4-2/Kir4.1 KO, and Ks-Kir4.1 KO mice. The mice were used immediately after either doxycycline or vehicle treatment. BW, body weight.

    Techniques Used: Inhibition, Expressing, Mouse Assay, Western Blot

    Deletion of Nedd4-2 increases the expression of ENaC α . (A) An immunoblot showing the expression of full-length (f) ENaC α and cleaved (c) ENaC α in WT ( Kcnj10 flox/flox , Nedd4l flox/flox , and Nedd4l flox/flox -Kcnj10 flox/flox ), Ks-Kir4.1 KO, Ks-Nedd4-2 KO, and Ks-Nedd4-2/Kir4.1 KO mice. Gapdh, glyceraldehyde-3-phosphate dehydrogenase; IB, immunoblot. A scatter graph summarizes the normalized band intensity of the above experiments for (B) f-ENaC α and (C) c-ENaC α . The mean value and SEM are shown on the left of each row. *Difference is significant at P =0.05; **difference is significant at P =0.01.
    Figure Legend Snippet: Deletion of Nedd4-2 increases the expression of ENaC α . (A) An immunoblot showing the expression of full-length (f) ENaC α and cleaved (c) ENaC α in WT ( Kcnj10 flox/flox , Nedd4l flox/flox , and Nedd4l flox/flox -Kcnj10 flox/flox ), Ks-Kir4.1 KO, Ks-Nedd4-2 KO, and Ks-Nedd4-2/Kir4.1 KO mice. Gapdh, glyceraldehyde-3-phosphate dehydrogenase; IB, immunoblot. A scatter graph summarizes the normalized band intensity of the above experiments for (B) f-ENaC α and (C) c-ENaC α . The mean value and SEM are shown on the left of each row. *Difference is significant at P =0.05; **difference is significant at P =0.01.

    Techniques Used: Expressing, Mouse Assay

    Deletion of Nedd4-2 stimulates Kir4.1/Kir5.1 in the DCT. (A) Representative single-channel recordings showing the basolateral K + channel activity in the DCT of WT and Ks-Nedd4-2 KO mice. The experiments were performed in cell-attached patches with bath solution containing 140 mM NaCl and 5 mM KCl and pipette solution containing 140 mM KCl. The channel closed level is indicated by “C,” and the holding potential was 0 mV. (B) Probability of finding basolateral K + channel activity, mean NP o , and P o in the DCT of WT and Ks-Nedd4-2 KO mice. *Significant difference between WT and Ks-Nedd4-2 KO mice. (C) An immunoblot showing the expression of Kir4.1 and Nedd4-2 in WT and Ks-Nedd4-2 KO mice. The sample from Ks-Kir4.1 KO mice serves as a negative control for Kir4.1. IB, immunoblot.
    Figure Legend Snippet: Deletion of Nedd4-2 stimulates Kir4.1/Kir5.1 in the DCT. (A) Representative single-channel recordings showing the basolateral K + channel activity in the DCT of WT and Ks-Nedd4-2 KO mice. The experiments were performed in cell-attached patches with bath solution containing 140 mM NaCl and 5 mM KCl and pipette solution containing 140 mM KCl. The channel closed level is indicated by “C,” and the holding potential was 0 mV. (B) Probability of finding basolateral K + channel activity, mean NP o , and P o in the DCT of WT and Ks-Nedd4-2 KO mice. *Significant difference between WT and Ks-Nedd4-2 KO mice. (C) An immunoblot showing the expression of Kir4.1 and Nedd4-2 in WT and Ks-Nedd4-2 KO mice. The sample from Ks-Kir4.1 KO mice serves as a negative control for Kir4.1. IB, immunoblot.

    Techniques Used: Activity Assay, Mouse Assay, Transferring, Expressing, Negative Control

    A cell scheme illustrates the role of Kir4.1/Kir5.1 in mediating the effect of Nedd4-2 on thiazide-sensitive NCC. The inhibition of Kir4.1/Kir5.1 activity by Nedd4-2 should depolarize the DCT membrane voltage (V). A decrease in the cell negativity reduces the driving force for Cl − exit by basolateral Cl − channels, thereby increasing intracellular Cl − (Cl − i ), which inhibits WNK and SPAK. This leads to inhibition of NCC phosphorylation and activity. Nedd4-2 is expected to facilitate the degradation of non-pNCC. In addition, Nedd4-2 also regulates NCC retrieval from the apical membrane of the DCT by Kir4.1-indipendent mechanism (blue arrow). The dotted line indicates the inhibition.
    Figure Legend Snippet: A cell scheme illustrates the role of Kir4.1/Kir5.1 in mediating the effect of Nedd4-2 on thiazide-sensitive NCC. The inhibition of Kir4.1/Kir5.1 activity by Nedd4-2 should depolarize the DCT membrane voltage (V). A decrease in the cell negativity reduces the driving force for Cl − exit by basolateral Cl − channels, thereby increasing intracellular Cl − (Cl − i ), which inhibits WNK and SPAK. This leads to inhibition of NCC phosphorylation and activity. Nedd4-2 is expected to facilitate the degradation of non-pNCC. In addition, Nedd4-2 also regulates NCC retrieval from the apical membrane of the DCT by Kir4.1-indipendent mechanism (blue arrow). The dotted line indicates the inhibition.

    Techniques Used: Inhibition, Activity Assay

    NCC expression is not increased in the double-KO mice. (A) An immunoblot showing the expression of pNCC, tNCC, Kir4.1, and Nedd4-2 in WT ( Kcnj10 flox/flox , Nedd4l flox/flox , and Kcnj10 flox/flox /Nedd4l flox/flox ), Ks-Kir4.1 KO, Ks-Nedd4-2 KO, and Ks-Nedd4-2/Kir4.1 KO mice. Gapdh, glyceraldehyde-3-phosphate dehydrogenase; IB, immunoblot. A scatter graph summarizes the normalized band intensity of the (B) pNCC and (C) tNCC in WT ( Kcnj10 flox/flox , Nedd4l flox/flox , and Kcnj10 flox/flox /Nedd4l flox/flox ), Ks-Kir4.1 KO, Ks-Nedd4-2 KO, and Ks-Nedd4-2/Kir4.1 KO mice, respectively. The mean value and SEM are shown on the left of each row. Both male and female mice were used for the western blot, and the data obtained from male/female mice were normalized with corresponding male/female WT mice. *Significant difference ( P =0.05) determined by t test; # value is significantly different between Ks-Kir4.1 KO and Ks-Nedd4-2/Kir4.1 KO mice.
    Figure Legend Snippet: NCC expression is not increased in the double-KO mice. (A) An immunoblot showing the expression of pNCC, tNCC, Kir4.1, and Nedd4-2 in WT ( Kcnj10 flox/flox , Nedd4l flox/flox , and Kcnj10 flox/flox /Nedd4l flox/flox ), Ks-Kir4.1 KO, Ks-Nedd4-2 KO, and Ks-Nedd4-2/Kir4.1 KO mice. Gapdh, glyceraldehyde-3-phosphate dehydrogenase; IB, immunoblot. A scatter graph summarizes the normalized band intensity of the (B) pNCC and (C) tNCC in WT ( Kcnj10 flox/flox , Nedd4l flox/flox , and Kcnj10 flox/flox /Nedd4l flox/flox ), Ks-Kir4.1 KO, Ks-Nedd4-2 KO, and Ks-Nedd4-2/Kir4.1 KO mice, respectively. The mean value and SEM are shown on the left of each row. Both male and female mice were used for the western blot, and the data obtained from male/female mice were normalized with corresponding male/female WT mice. *Significant difference ( P =0.05) determined by t test; # value is significantly different between Ks-Kir4.1 KO and Ks-Nedd4-2/Kir4.1 KO mice.

    Techniques Used: Expressing, Mouse Assay, Western Blot

    6) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    7) Product Images from "Down-Regulation of Astrocytic Kir4.1 Channels during the Audiogenic Epileptogenesis in Leucine-Rich Glioma-Inactivated 1 (Lgi1) Mutant Rats"

    Article Title: Down-Regulation of Astrocytic Kir4.1 Channels during the Audiogenic Epileptogenesis in Leucine-Rich Glioma-Inactivated 1 (Lgi1) Mutant Rats

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms20051013

    Changes in astrocytic Kir4.1 expression after the development of audiogenic epilepsy. The Kir4.1 expression rate in each group of wild-type rats (A–D) and Lgi1 mutant rats are shown in each region of the cortex ( A ), hippocampus ( B ), and amygdala ( C ). The Kir4.1 expression rate was expressed as the ration of Kir4.1-immunoreactivity (IR)-positive cells to GFAP-IR-positive cells in each region by staining a pair of successive brain sections with anti-Kir4.1 or anti-GFAP antibodies. Each point represents the mean ± S.E.M. of six to eight animals. * p
    Figure Legend Snippet: Changes in astrocytic Kir4.1 expression after the development of audiogenic epilepsy. The Kir4.1 expression rate in each group of wild-type rats (A–D) and Lgi1 mutant rats are shown in each region of the cortex ( A ), hippocampus ( B ), and amygdala ( C ). The Kir4.1 expression rate was expressed as the ration of Kir4.1-immunoreactivity (IR)-positive cells to GFAP-IR-positive cells in each region by staining a pair of successive brain sections with anti-Kir4.1 or anti-GFAP antibodies. Each point represents the mean ± S.E.M. of six to eight animals. * p

    Techniques Used: Expressing, Mutagenesis, Staining

    Expression changes in astrocytic Kir4.1 with treatment of valproic acid (VPA). Kir4.1 expression ratios of wild-type rats treated with saline and Lgi1 mutant rats treated with saline or VPA (30 mg/kg or 200 mg/kg) are shown in each region of the cortex ( A ), hippocampus, and amygdala ( B ). The Kir4.1 expression rate was expressed as the ratio of Kir4.1-IR-positive cells to GFAP-IR-positive cells in each region. Each point represents the mean ± S.E.M. of four to six animals. * p
    Figure Legend Snippet: Expression changes in astrocytic Kir4.1 with treatment of valproic acid (VPA). Kir4.1 expression ratios of wild-type rats treated with saline and Lgi1 mutant rats treated with saline or VPA (30 mg/kg or 200 mg/kg) are shown in each region of the cortex ( A ), hippocampus, and amygdala ( B ). The Kir4.1 expression rate was expressed as the ratio of Kir4.1-IR-positive cells to GFAP-IR-positive cells in each region. Each point represents the mean ± S.E.M. of four to six animals. * p

    Techniques Used: Expressing, Mutagenesis

    Changes in the number of Kir4.1-immunoreactivity (IR)-positive cells after development of audiogenic epilepsy. Kir4.1-IR-positive cells in each group of wild-type rats (A–D) and Lgi1 mutant rats are shown in each region of the cortex ( A ), hippocampus ( B ), and amygdala ( C ). Each point represents the mean ± S.E.M. of six to eight animals. * p
    Figure Legend Snippet: Changes in the number of Kir4.1-immunoreactivity (IR)-positive cells after development of audiogenic epilepsy. Kir4.1-IR-positive cells in each group of wild-type rats (A–D) and Lgi1 mutant rats are shown in each region of the cortex ( A ), hippocampus ( B ), and amygdala ( C ). Each point represents the mean ± S.E.M. of six to eight animals. * p

    Techniques Used: Mutagenesis

    Kir4.1 expression in astrocytes. ( A ) Representative images of immunofluorescence double staining for glial fibrillary acidic protein (GFAP) and Kir4.1 in the hippocampal CA1 region in wild-type F344 rats (top panels) and Lgi1 mutant rats (bottom panels). Scale bar: 100 μm. ( B ) Schematic illustration of a brain section (Bregma −3.48 mm level) selected for quantitative analysis of immunoreactivity (IR) of Kir4.1 or GFAP. Squares in each brain region indicate the areas analyzed for counting of Kir4.1-IR-positive or GFAP-IR-positive cells. Medial parietal association cortex (MPtA), primary somatosensory cortex barrel field (S1BF), primary auditory cortex (Au1), perirhinal cortex (PRh), piriform cortex (Pir), hippocampal CA1, CA2, CA3, and dentate gyrus (DG), medial amygdaloid nucleus posteroventral part (MePV), medial amygdaloid nucleus posterodorsal part (MePD), posteromedial cortical amygdaloid nucleus (PMCo), basomedial amygdaloid nucleus posterior part (BMP), basolateral amygdaloid nucleus posterior part (BLP), lateral amygdaloid nucleus ventromedial part (LaVM), lateral habenula (LHb), ventromedial thalamus (VM), posterior hypothalamus (PH), dorsomedial hypothalamic nucleus, and dorsal part (DMD). ( C ) Representative images of immunohistochemical staining for GFAP and Kir4.1 in the hippocampal CA1 regions of non-primed wild type rats (upper left panels), primed wild type rats (lower left panels), non-primed Lgi1 mutant rats (upper right panels), and primed Lgi1 mutant rats (lower right panels) after audiogenic seizure induction. Scale bar: 100 μm.
    Figure Legend Snippet: Kir4.1 expression in astrocytes. ( A ) Representative images of immunofluorescence double staining for glial fibrillary acidic protein (GFAP) and Kir4.1 in the hippocampal CA1 region in wild-type F344 rats (top panels) and Lgi1 mutant rats (bottom panels). Scale bar: 100 μm. ( B ) Schematic illustration of a brain section (Bregma −3.48 mm level) selected for quantitative analysis of immunoreactivity (IR) of Kir4.1 or GFAP. Squares in each brain region indicate the areas analyzed for counting of Kir4.1-IR-positive or GFAP-IR-positive cells. Medial parietal association cortex (MPtA), primary somatosensory cortex barrel field (S1BF), primary auditory cortex (Au1), perirhinal cortex (PRh), piriform cortex (Pir), hippocampal CA1, CA2, CA3, and dentate gyrus (DG), medial amygdaloid nucleus posteroventral part (MePV), medial amygdaloid nucleus posterodorsal part (MePD), posteromedial cortical amygdaloid nucleus (PMCo), basomedial amygdaloid nucleus posterior part (BMP), basolateral amygdaloid nucleus posterior part (BLP), lateral amygdaloid nucleus ventromedial part (LaVM), lateral habenula (LHb), ventromedial thalamus (VM), posterior hypothalamus (PH), dorsomedial hypothalamic nucleus, and dorsal part (DMD). ( C ) Representative images of immunohistochemical staining for GFAP and Kir4.1 in the hippocampal CA1 regions of non-primed wild type rats (upper left panels), primed wild type rats (lower left panels), non-primed Lgi1 mutant rats (upper right panels), and primed Lgi1 mutant rats (lower right panels) after audiogenic seizure induction. Scale bar: 100 μm.

    Techniques Used: Expressing, Immunofluorescence, Double Staining, Mutagenesis, Immunohistochemistry, Staining

    8) Product Images from "Spatial and temporal correlation in progressive degeneration of neurons and astrocytes in contusion-induced spinal cord injury"

    Article Title: Spatial and temporal correlation in progressive degeneration of neurons and astrocytes in contusion-induced spinal cord injury

    Journal: Journal of Neuroinflammation

    doi: 10.1186/1742-2094-9-100

    Loss of astrocytes and reduced expression of GLT-1 and Kir4.1 in injured spinal cords. (A, D) Sections from intact and P1 areas at the indicated times after injury were stained with NeuN/GFAP (A), and GLT-1 or Kir4.1 ( D ) antibodies. Right panels in ( A ) and lower panels in ( D ) are higher magnification images of indicated regions in the left and upper panels, respectively. (B, C) Spinal cord tissues (2 mm in length around the contusion center) were obtained at the indicated times after SCI, and total RNA was prepared and analyzed by RT-PCR ( B ) or q-PCR ( C ) as described in Materials and Methods. Values in ( C ) are means ± SEMs of five animals. ( D ) The white arrow represents neuronal cell body-like morphology. Data shown are representative of three independent experiments. Scale bars: 200 μm (left panels in A and upper panels in D), 10 μm (right panels in A), and 50 μm (lower panels in D).
    Figure Legend Snippet: Loss of astrocytes and reduced expression of GLT-1 and Kir4.1 in injured spinal cords. (A, D) Sections from intact and P1 areas at the indicated times after injury were stained with NeuN/GFAP (A), and GLT-1 or Kir4.1 ( D ) antibodies. Right panels in ( A ) and lower panels in ( D ) are higher magnification images of indicated regions in the left and upper panels, respectively. (B, C) Spinal cord tissues (2 mm in length around the contusion center) were obtained at the indicated times after SCI, and total RNA was prepared and analyzed by RT-PCR ( B ) or q-PCR ( C ) as described in Materials and Methods. Values in ( C ) are means ± SEMs of five animals. ( D ) The white arrow represents neuronal cell body-like morphology. Data shown are representative of three independent experiments. Scale bars: 200 μm (left panels in A and upper panels in D), 10 μm (right panels in A), and 50 μm (lower panels in D).

    Techniques Used: Expressing, Staining, Reverse Transcription Polymerase Chain Reaction, Polymerase Chain Reaction

    9) Product Images from "Hearing Loss Controlled by Optogenetic Stimulation of Nonexcitable Nonglial Cells in the Cochlea of the Inner Ear"

    Article Title: Hearing Loss Controlled by Optogenetic Stimulation of Nonexcitable Nonglial Cells in the Cochlea of the Inner Ear

    Journal: Frontiers in Molecular Neuroscience

    doi: 10.3389/fnmol.2017.00300

    The mechanism underlying photoreduction in the EP. (A) Cellular components of the lateral cochlear wall. The lateral wall consists of the StV and spiral ligament. MC in the StV constitute a monolayer. IC and BC in the stria and fibrocytes (FC) in the ligament form an electrochemical syncytium through gap junctions. Therefore, the lateral wall is composed of two functional layers, the inner MC layer and the outer syncytial layer. In this arrangement, the apical (api) and basolateral (baso) surface of the syncytial layer are formed by the membranes of IC and FC, respectively. Between the two layers lies the 15-nm intrastrial space (IS) and capillaries. In bigenic mice, ChR2(C128S) is expressed in the IC membranes (i.e., syncytial apical surface). Ion channels and transporters involved in formation of the EP are shown. Note that the apical surfaces of the syncytial and MC layers are dominated by K + channels Kir4.1 and KCNQ1/KCNE1, respectively. Legend: NKCC1, Na + ,K + ,2Cl − -cotransporter type 1; K V , voltage-dependent K + channel; ClC-K, ClC-Ka/Kb Cl − channel; TJ, tight junction; PL, perilymph; EL, endolymph. (B) Electrochemical properties of the lateral wall. Values of the potential ( red ) and [K + ] ( pale blue ) within the lateral wall are displayed as predicted by our electrophysiological measurements of guinea pig cochleae under physiological conditions (Nin et al., 2008 ; Yoshida et al., 2016 ). v SB , v SA , v MB , and v MA indicate the membrane potentials across the basolateral and apical surfaces of the syncytial layer and across the basolateral and apical surfaces of the MC layer, respectively. During in vivo recordings, the potential of PL is defined as 0 mV. IS potential (ISP) is highly positive. A large difference in potentials across the apical surface of the syncytial layer forms a major fraction of the ISP and corresponds to the IC membrane potential that is deeply hyperpolarized relative to the neighboring extracellular space: IS. Optical stimulation of ChR2(C128S) depolarizes the IC (see Figure 4 ) and therefore likely reduces the ISP. This change seems to result in the decline of the EP (see Figure 5 ). Because the values of light-evoked changes of the IC membrane potential are similar to those of the EP (see Figures 4 , 5 ), differences in potentials across the MC layer and the basolateral surface of the syncytial layer are expected to be altered only minimally.
    Figure Legend Snippet: The mechanism underlying photoreduction in the EP. (A) Cellular components of the lateral cochlear wall. The lateral wall consists of the StV and spiral ligament. MC in the StV constitute a monolayer. IC and BC in the stria and fibrocytes (FC) in the ligament form an electrochemical syncytium through gap junctions. Therefore, the lateral wall is composed of two functional layers, the inner MC layer and the outer syncytial layer. In this arrangement, the apical (api) and basolateral (baso) surface of the syncytial layer are formed by the membranes of IC and FC, respectively. Between the two layers lies the 15-nm intrastrial space (IS) and capillaries. In bigenic mice, ChR2(C128S) is expressed in the IC membranes (i.e., syncytial apical surface). Ion channels and transporters involved in formation of the EP are shown. Note that the apical surfaces of the syncytial and MC layers are dominated by K + channels Kir4.1 and KCNQ1/KCNE1, respectively. Legend: NKCC1, Na + ,K + ,2Cl − -cotransporter type 1; K V , voltage-dependent K + channel; ClC-K, ClC-Ka/Kb Cl − channel; TJ, tight junction; PL, perilymph; EL, endolymph. (B) Electrochemical properties of the lateral wall. Values of the potential ( red ) and [K + ] ( pale blue ) within the lateral wall are displayed as predicted by our electrophysiological measurements of guinea pig cochleae under physiological conditions (Nin et al., 2008 ; Yoshida et al., 2016 ). v SB , v SA , v MB , and v MA indicate the membrane potentials across the basolateral and apical surfaces of the syncytial layer and across the basolateral and apical surfaces of the MC layer, respectively. During in vivo recordings, the potential of PL is defined as 0 mV. IS potential (ISP) is highly positive. A large difference in potentials across the apical surface of the syncytial layer forms a major fraction of the ISP and corresponds to the IC membrane potential that is deeply hyperpolarized relative to the neighboring extracellular space: IS. Optical stimulation of ChR2(C128S) depolarizes the IC (see Figure 4 ) and therefore likely reduces the ISP. This change seems to result in the decline of the EP (see Figure 5 ). Because the values of light-evoked changes of the IC membrane potential are similar to those of the EP (see Figures 4 , 5 ), differences in potentials across the MC layer and the basolateral surface of the syncytial layer are expected to be altered only minimally.

    Techniques Used: Functional Assay, Mouse Assay, In Vivo

    Distribution and cellular localization of ChR2(C128S) in the cochlea. (A) Immunohistochemical analysis of a cochlear cross-section from a bigenic mouse. Overall, morphology of the cells and tissues was similar to that in the cochlea of WT mouse, as shown in Supplementary Figures S2, S3. Here, the tissue slices were incubated with an anti-GFP antibody that reacts with EYFP fused to ChR2(C128S). The lateral walls of all turns, modiolus and area of auditory nerve (AN) were stained as depicted in the left panel . Higher magnification of the region outlined by the dashed box is displayed in the right panel . In this image, the positive signal was detected in the stria vascularis (StV), cell body of the spiral ganglion (SG; arrowhead ), and peripheral and central processes of the pSG. The organ of Corti (OC) did not show staining. Localization of the YFP in the AN, SG and pSG was further precisely determined by confocal microscopic examination (see Supplementary Figure S4). SM, scala media; ST, scala tympani. (B,C) Immunolabeling of strial cells. Intermediate cells (IC) and marginal cells (MC) were dissociated from the StV of the bigenic mice and were immunolabeled with antibodies against Kir4.1 (B) or barttin (C) TRITC ( red ). Expression of ChR2(C128S) was visualized simultaneously with the YFP signal ( green ). Nuclei were stained with DAPI ( blue ). In (B,C) areas outlined by dashed boxes in the top panels are enlarged in middle and bottom panels . Using a cochlear cross-section, the YFP signal was compared with immunoreactivity of each of Kir4.1, barttin, and glucose transporter 1 (GLUT1), a marker for basal cells (BC), in the StV (see Supplementary Figure S5). Of note, YFP-positive cells in the StV and SG were counted in the assay of Supplementary Figure S6.
    Figure Legend Snippet: Distribution and cellular localization of ChR2(C128S) in the cochlea. (A) Immunohistochemical analysis of a cochlear cross-section from a bigenic mouse. Overall, morphology of the cells and tissues was similar to that in the cochlea of WT mouse, as shown in Supplementary Figures S2, S3. Here, the tissue slices were incubated with an anti-GFP antibody that reacts with EYFP fused to ChR2(C128S). The lateral walls of all turns, modiolus and area of auditory nerve (AN) were stained as depicted in the left panel . Higher magnification of the region outlined by the dashed box is displayed in the right panel . In this image, the positive signal was detected in the stria vascularis (StV), cell body of the spiral ganglion (SG; arrowhead ), and peripheral and central processes of the pSG. The organ of Corti (OC) did not show staining. Localization of the YFP in the AN, SG and pSG was further precisely determined by confocal microscopic examination (see Supplementary Figure S4). SM, scala media; ST, scala tympani. (B,C) Immunolabeling of strial cells. Intermediate cells (IC) and marginal cells (MC) were dissociated from the StV of the bigenic mice and were immunolabeled with antibodies against Kir4.1 (B) or barttin (C) TRITC ( red ). Expression of ChR2(C128S) was visualized simultaneously with the YFP signal ( green ). Nuclei were stained with DAPI ( blue ). In (B,C) areas outlined by dashed boxes in the top panels are enlarged in middle and bottom panels . Using a cochlear cross-section, the YFP signal was compared with immunoreactivity of each of Kir4.1, barttin, and glucose transporter 1 (GLUT1), a marker for basal cells (BC), in the StV (see Supplementary Figure S5). Of note, YFP-positive cells in the StV and SG were counted in the assay of Supplementary Figure S6.

    Techniques Used: Immunohistochemistry, Incubation, Staining, Immunolabeling, Mouse Assay, Expressing, Marker

    10) Product Images from "Dietary grape seed polyphenols repress neuron and glia activation in trigeminal ganglion and trigeminal nucleus caudalis"

    Article Title: Dietary grape seed polyphenols repress neuron and glia activation in trigeminal ganglion and trigeminal nucleus caudalis

    Journal: Molecular Pain

    doi: 10.1186/1744-8069-6-91

    Basal MPK-1 expression is increased in both neurons and satellite glia cells after GSE treatment . (A) An image from a longitudinal section of trigeminal ganglia costained with the neuronal cell marker NeuN, the glial cell marker Kir4.1, or the nuclear dye DAPI is shown. The bottom right image shows a merged image of NeuN, Kir 4.1 and DAPI staining. Thick horizontal arrows identify the cell bodies of neurons while thin vertical arrows indicate satellite glia cells. (B) Sections of the posterolateral portion of the ganglion (V3) were obtained from untreated animals (CON) or animals treated with GSE for 14 days (GSE). Images of neuron-satellite glial cell enriched regions stained for MKP-1 are shown in the top panels. The bottom panels represent the same section costained for MKP-1 and DAPI. (C) The average fold change ± SEM of MKP-1 staining intensity from control values, which were made equal to one, is reported (n = 3 independent experiments) *  P
    Figure Legend Snippet: Basal MPK-1 expression is increased in both neurons and satellite glia cells after GSE treatment . (A) An image from a longitudinal section of trigeminal ganglia costained with the neuronal cell marker NeuN, the glial cell marker Kir4.1, or the nuclear dye DAPI is shown. The bottom right image shows a merged image of NeuN, Kir 4.1 and DAPI staining. Thick horizontal arrows identify the cell bodies of neurons while thin vertical arrows indicate satellite glia cells. (B) Sections of the posterolateral portion of the ganglion (V3) were obtained from untreated animals (CON) or animals treated with GSE for 14 days (GSE). Images of neuron-satellite glial cell enriched regions stained for MKP-1 are shown in the top panels. The bottom panels represent the same section costained for MKP-1 and DAPI. (C) The average fold change ± SEM of MKP-1 staining intensity from control values, which were made equal to one, is reported (n = 3 independent experiments) * P

    Techniques Used: Expressing, Marker, Staining

    11) Product Images from "Differential expression of Kir4.1 and aquaporin 4 in the retina from endotoxin-induced uveitis rat"

    Article Title: Differential expression of Kir4.1 and aquaporin 4 in the retina from endotoxin-induced uveitis rat

    Journal: Molecular Vision

    doi:

    Immunohistochemical detection of Kir4.1, aquaporin-4, and anti-glial fibrillary acidic protein in the retina. In the normal eyes, Kir4.1 ( A ) and aquaporin-4 (AQP4; I ) were enriched in the endfoot membranes facing the vitreous body (arrowheads) and retinal blood vessels (arrows). Staining for AQP4 ( K - P ) maintained the same pattern during the different stages of endotoxin-induced uveitis (EIU), and only a slight reduction in immunostaining was seen in the inner plexiform at 1-7 day after lipopolysaccharide (LPS) injection. Kir4.1 ( C - H ) immunoreactivity decreased significantly from one day after LPS injection, had almost disappeared at 3-7 day after injection, and had partially recovered by 14 days. Anti-glial fibrillary acidic protein (GFAP; Q - X ) was predominantly found in astrocytes in the retinas of the untreated controls. Seven days and 14 days after intravitreal LPS injection, GFAP ( W - X ) immunoreactivity was significantly increased in Müller cells. In the retinas of sham-treated eyes, the immunostaining for Kir4.1 ( A - H ) was unchanged at 3 day after phosphate-buffered saline (PBS) treatment ( B ). AQP4 immunoreactivity was unchanged at one day after PBS treatment ( J ). GFAP immunoreactivity was mildly increased at 7 day after PBS treatment ( R ). GCL indicates ganglion cell layer; INL indicates inner nuclear layer; IPL indicates inner plexiform layer; ONL indicates outer nuclear layer; OPL indicates outer plexiform layer. Scale bar represents 20 μm.
    Figure Legend Snippet: Immunohistochemical detection of Kir4.1, aquaporin-4, and anti-glial fibrillary acidic protein in the retina. In the normal eyes, Kir4.1 ( A ) and aquaporin-4 (AQP4; I ) were enriched in the endfoot membranes facing the vitreous body (arrowheads) and retinal blood vessels (arrows). Staining for AQP4 ( K - P ) maintained the same pattern during the different stages of endotoxin-induced uveitis (EIU), and only a slight reduction in immunostaining was seen in the inner plexiform at 1-7 day after lipopolysaccharide (LPS) injection. Kir4.1 ( C - H ) immunoreactivity decreased significantly from one day after LPS injection, had almost disappeared at 3-7 day after injection, and had partially recovered by 14 days. Anti-glial fibrillary acidic protein (GFAP; Q - X ) was predominantly found in astrocytes in the retinas of the untreated controls. Seven days and 14 days after intravitreal LPS injection, GFAP ( W - X ) immunoreactivity was significantly increased in Müller cells. In the retinas of sham-treated eyes, the immunostaining for Kir4.1 ( A - H ) was unchanged at 3 day after phosphate-buffered saline (PBS) treatment ( B ). AQP4 immunoreactivity was unchanged at one day after PBS treatment ( J ). GFAP immunoreactivity was mildly increased at 7 day after PBS treatment ( R ). GCL indicates ganglion cell layer; INL indicates inner nuclear layer; IPL indicates inner plexiform layer; ONL indicates outer nuclear layer; OPL indicates outer plexiform layer. Scale bar represents 20 μm.

    Techniques Used: Immunohistochemistry, Staining, Immunostaining, Injection

    Time course of Kir4.1 and aquaporin-4 mRNA expression in lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Total RNA (1 μg) was used for reverse transcriptase polymerase chain reaction (RT-PCR). A 330-bp product for aquaporin-4 (AQP4), a 225-bp product for Kir4.1, and a 240-bp product for β-actin were separated on a 2.0% agarose gel. B , C : The relative levels of Kir4.1 and AQP4 mRNA expression were quantified. Compared with the control, there was a significant decline in Kir4.1 in lipopolysaccharide (LPS)-treated animals, whereas there was no change in AQP4 after LPS injection (means±SEM, n=4; asterisk (*) indicates p
    Figure Legend Snippet: Time course of Kir4.1 and aquaporin-4 mRNA expression in lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Total RNA (1 μg) was used for reverse transcriptase polymerase chain reaction (RT-PCR). A 330-bp product for aquaporin-4 (AQP4), a 225-bp product for Kir4.1, and a 240-bp product for β-actin were separated on a 2.0% agarose gel. B , C : The relative levels of Kir4.1 and AQP4 mRNA expression were quantified. Compared with the control, there was a significant decline in Kir4.1 in lipopolysaccharide (LPS)-treated animals, whereas there was no change in AQP4 after LPS injection (means±SEM, n=4; asterisk (*) indicates p

    Techniques Used: Expressing, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Agarose Gel Electrophoresis, Injection

    Time courses of Kir4.1 and aquaporin-4 protein expression in retinas from lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Equal amounts of protein (30 μg) were subjected to immunoblotting analysis. A band at about 200 kDa represents Kir4.1 in its tetrameric form; aquaporin-4 (AQP4) consists of two bands, representing its M1 and M23 forms. B , C : The relative levels of Kir4.1 and AQP4 protein expression were quantified. Compared with that of the control, the expression of Kir4.1 was significantly reduced after LPS injection. In contrast, there was only a slight, statistically insignificant decline in AQP4 expression from 1 day to 7 day after LPS injection. (means±SEM, n=5; double asterisks (**) p
    Figure Legend Snippet: Time courses of Kir4.1 and aquaporin-4 protein expression in retinas from lipopolysaccharide- or phosphate-buffered saline-treated rats. A : Equal amounts of protein (30 μg) were subjected to immunoblotting analysis. A band at about 200 kDa represents Kir4.1 in its tetrameric form; aquaporin-4 (AQP4) consists of two bands, representing its M1 and M23 forms. B , C : The relative levels of Kir4.1 and AQP4 protein expression were quantified. Compared with that of the control, the expression of Kir4.1 was significantly reduced after LPS injection. In contrast, there was only a slight, statistically insignificant decline in AQP4 expression from 1 day to 7 day after LPS injection. (means±SEM, n=5; double asterisks (**) p

    Techniques Used: Expressing, Injection

    12) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    13) Product Images from "Phenotypical peculiarities and species‐specific differences of canine and murine satellite glial cells of spinal ganglia. Phenotypical peculiarities and species‐specific differences of canine and murine satellite glial cells of spinal ganglia"

    Article Title: Phenotypical peculiarities and species‐specific differences of canine and murine satellite glial cells of spinal ganglia. Phenotypical peculiarities and species‐specific differences of canine and murine satellite glial cells of spinal ganglia

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.16701

    3D‐reconstructed confocal laser images of formalin‐fixed paraffin‐embedded canine spinal ganglia (A‐D): Double labelling with glutamine synthetase (GS; green; A, B) or inwardly rectifying potassium channel Kir 4.1 (green; C, D), respectively, and the neuronal marker NeuN (magenta). Nuclei are counterstained with bisbenzimide (blue). The zoomed in pictures (B, D) show that GS‐, respectively, Kir4.1‐positive satellite glial cells (SGCs) tightly envelop NeuN‐positive neurons. For GS/NeuN staining (A‐B), 32 z‐stack frames (5.2 µm total size; approx. 0.16 µm steps) and for Kir4.1/NeuN staining (C‐D), 31 z‐stack frames (5.0 µm total size; approx. 0.16 µm steps) were collected. Scale bars: 20 µm. A movie of 3D confocal reconstructions is provided in Video   [Link] ,   [Link]  and Video   [Link] ,   [Link]
    Figure Legend Snippet: 3D‐reconstructed confocal laser images of formalin‐fixed paraffin‐embedded canine spinal ganglia (A‐D): Double labelling with glutamine synthetase (GS; green; A, B) or inwardly rectifying potassium channel Kir 4.1 (green; C, D), respectively, and the neuronal marker NeuN (magenta). Nuclei are counterstained with bisbenzimide (blue). The zoomed in pictures (B, D) show that GS‐, respectively, Kir4.1‐positive satellite glial cells (SGCs) tightly envelop NeuN‐positive neurons. For GS/NeuN staining (A‐B), 32 z‐stack frames (5.2 µm total size; approx. 0.16 µm steps) and for Kir4.1/NeuN staining (C‐D), 31 z‐stack frames (5.0 µm total size; approx. 0.16 µm steps) were collected. Scale bars: 20 µm. A movie of 3D confocal reconstructions is provided in Video [Link] , [Link] and Video [Link] , [Link]

    Techniques Used: Formalin-fixed Paraffin-Embedded, Marker, Staining

    3D‐reconstructed confocal laser images of formalin‐fixed paraffin‐embedded murine spinal ganglia (A‐D): Double labelling with glutamine synthetase (GS; green; A, B) or inwardly rectifying potassium channel Kir 4.1 (green; C, D), respectively, and the neuronal marker NeuN (magenta). Nuclei are counterstained with Bisbenzimide (blue). GS‐ / Kir4.1‐positive satellite glial cells (SGCs) form a tight sheath around the neuronal bodies. The zoomed in images (B, D) clearly illustrate the close contact between SGCs and neurons. For GS/NeuN staining (A‐B), 39 z‐stack frames (6.4 µm total size; approx. 0.16 µm steps) and for Kir4.1/NeuN staining (C‐D), 39 z‐stack frames (4.7 µm total size; approx. 0.12 µm steps) were obtained. Scale bars: 20 µm (A, B, C); 10 µm (D). A movie of 3D confocal reconstructions is provided in Video   [Link] ,   [Link]  and Video   [Link] ,   [Link]
    Figure Legend Snippet: 3D‐reconstructed confocal laser images of formalin‐fixed paraffin‐embedded murine spinal ganglia (A‐D): Double labelling with glutamine synthetase (GS; green; A, B) or inwardly rectifying potassium channel Kir 4.1 (green; C, D), respectively, and the neuronal marker NeuN (magenta). Nuclei are counterstained with Bisbenzimide (blue). GS‐ / Kir4.1‐positive satellite glial cells (SGCs) form a tight sheath around the neuronal bodies. The zoomed in images (B, D) clearly illustrate the close contact between SGCs and neurons. For GS/NeuN staining (A‐B), 39 z‐stack frames (6.4 µm total size; approx. 0.16 µm steps) and for Kir4.1/NeuN staining (C‐D), 39 z‐stack frames (4.7 µm total size; approx. 0.12 µm steps) were obtained. Scale bars: 20 µm (A, B, C); 10 µm (D). A movie of 3D confocal reconstructions is provided in Video [Link] , [Link] and Video [Link] , [Link]

    Techniques Used: Formalin-fixed Paraffin-Embedded, Marker, Staining

    14) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    15) Product Images from "Molecular Basis of Decreased Kir4.1 Function in SeSAME/EAST Syndrome"

    Article Title: Molecular Basis of Decreased Kir4.1 Function in SeSAME/EAST Syndrome

    Journal: Journal of the American Society of Nephrology : JASN

    doi: 10.1681/ASN.2009121227

    Mutant Kir4.1 channels show markedly decreased function. (A) Structure of Kir4.1 with SeSAME/EAST mutations indicated. (B) I-V curves for Kir4.1 expressed in Xenopus oocytes as bath [K + ] was lowered from 110 to 4 mM followed by the addition of 5 mM Ba 2+ . Steady-state currents at each stage were measured in response to a series of voltage steps from −140 to + 80 mV from a holding potential of −80 mV. I-V curves for each batch of oocytes were normalized by the mean current at +40 mV with 110 mM K + in the bath. The error bars represent SEM for at least 12 oocytes from at least two batches. (C) In the upper panel, representative current traces for WT and SeSAME/EAST syndrome mutants expressed in oocytes. The two compound heterozygotes, R65P/R199X and A167V/R297C, were formed by 1:1 coexpression of the component mutant subunits. The currents were measured as in B with 4 mM K + in the bath. In the lower panel, normalized I-V curves were generated from the current traces above. The currents were leak-subtracted and normalized by the WT current at +40 mV for that day. R65P, R65P/R199X, and A167V/R297C had residual currents of 23, 17, and 13%, respectively, of WT current (at +40 mV), whereas the other mutants had currents similar to H 2 O-injected oocytes. The error bars indicate SEM for at least 14 oocytes from at least two batches. (D) Representative immunoblot (upper panel) of oocyte lysates probed with a polyclonal Kir4.1 antibody showing a doublet/triplet band at approximately 42 kD as well as a higher molecular mass singlet doublet band at approximately 200 kD, neither of which are seen in water-injected oocytes. Densitometric quantification (lower panel) of immunoblots, as above, showing the contribution to the total from both lower and higher molecular mass bands. The error bars represent SEM for lysates from three oocyte batches. (E) Representative current traces (upper panel) and normalized currents measured at +40 mV (lower panel) for compound heterozygotes showing component mutations individually and then together. The data were obtained as in C. The error bars indicate SEM for at least 14 oocytes from at least two batches. (F) Representative immunoblot (upper panel) and densitometric quantification (lower panel) of compound heterozygous mutants shown in E, analyzed as in D.
    Figure Legend Snippet: Mutant Kir4.1 channels show markedly decreased function. (A) Structure of Kir4.1 with SeSAME/EAST mutations indicated. (B) I-V curves for Kir4.1 expressed in Xenopus oocytes as bath [K + ] was lowered from 110 to 4 mM followed by the addition of 5 mM Ba 2+ . Steady-state currents at each stage were measured in response to a series of voltage steps from −140 to + 80 mV from a holding potential of −80 mV. I-V curves for each batch of oocytes were normalized by the mean current at +40 mV with 110 mM K + in the bath. The error bars represent SEM for at least 12 oocytes from at least two batches. (C) In the upper panel, representative current traces for WT and SeSAME/EAST syndrome mutants expressed in oocytes. The two compound heterozygotes, R65P/R199X and A167V/R297C, were formed by 1:1 coexpression of the component mutant subunits. The currents were measured as in B with 4 mM K + in the bath. In the lower panel, normalized I-V curves were generated from the current traces above. The currents were leak-subtracted and normalized by the WT current at +40 mV for that day. R65P, R65P/R199X, and A167V/R297C had residual currents of 23, 17, and 13%, respectively, of WT current (at +40 mV), whereas the other mutants had currents similar to H 2 O-injected oocytes. The error bars indicate SEM for at least 14 oocytes from at least two batches. (D) Representative immunoblot (upper panel) of oocyte lysates probed with a polyclonal Kir4.1 antibody showing a doublet/triplet band at approximately 42 kD as well as a higher molecular mass singlet doublet band at approximately 200 kD, neither of which are seen in water-injected oocytes. Densitometric quantification (lower panel) of immunoblots, as above, showing the contribution to the total from both lower and higher molecular mass bands. The error bars represent SEM for lysates from three oocyte batches. (E) Representative current traces (upper panel) and normalized currents measured at +40 mV (lower panel) for compound heterozygotes showing component mutations individually and then together. The data were obtained as in C. The error bars indicate SEM for at least 14 oocytes from at least two batches. (F) Representative immunoblot (upper panel) and densitometric quantification (lower panel) of compound heterozygous mutants shown in E, analyzed as in D.

    Techniques Used: Mutagenesis, Generated, Injection, Western Blot

    16) Product Images from "Inhibition of Inwardly Rectifying Potassium (Kir) 4.1 Channels Facilitates Brain-Derived Neurotrophic Factor (BDNF) Expression in Astrocytes"

    Article Title: Inhibition of Inwardly Rectifying Potassium (Kir) 4.1 Channels Facilitates Brain-Derived Neurotrophic Factor (BDNF) Expression in Astrocytes

    Journal: Frontiers in Molecular Neuroscience

    doi: 10.3389/fnmol.2017.00408

    Relationship between potencies of antidepressants for the blockade of Kir4.1 channels and for the astrocytic BDNF induction. (A) Inhibition percentage (I Drug /I Control ) of Kir4.1-conducted currents by sertraline (30 μM), fluoxetine (30 μM), imipramine (100 μM), fluvoxamine (100 μM), or mianserin (100 μM) in HEK293T cells. (B) Enhancement of BDNF mRNA expression by sertraline, fluoxetine, imipramine, fluvoxamine, or mianserin in astrocytes. Astrocytes were treated with each antidepressant (30 μM) for 8 h and the BDNF mRNA expression was analyzed by RT-PCR. The BDNF mRNA levels are expressed as the ratio to GAPDH mRNA. Each point represents the mean ± SEM of six separate experiments. ∗ P
    Figure Legend Snippet: Relationship between potencies of antidepressants for the blockade of Kir4.1 channels and for the astrocytic BDNF induction. (A) Inhibition percentage (I Drug /I Control ) of Kir4.1-conducted currents by sertraline (30 μM), fluoxetine (30 μM), imipramine (100 μM), fluvoxamine (100 μM), or mianserin (100 μM) in HEK293T cells. (B) Enhancement of BDNF mRNA expression by sertraline, fluoxetine, imipramine, fluvoxamine, or mianserin in astrocytes. Astrocytes were treated with each antidepressant (30 μM) for 8 h and the BDNF mRNA expression was analyzed by RT-PCR. The BDNF mRNA levels are expressed as the ratio to GAPDH mRNA. Each point represents the mean ± SEM of six separate experiments. ∗ P

    Techniques Used: Inhibition, Expressing, Reverse Transcription Polymerase Chain Reaction

    Effects of Kir4.1 knockdown on BDNF and other neurotrophic factors in astrocytes. Effects of Kir4.1 siRNA transfection on BDNF mRNA (A) and protein levels (B) . The BDNF mRNA levels and protein levels were analyzed by RT-PCR and ELISA, respectively, in astrocytes at 24 or 48 h after the transfection of Kir4.1 siRNA. (C) Effects of Kir4.1 siRNA transfection on mRNA levels of GDNF, CNTF, and NGF. The GDNF, CNTF, or NGF mRNA level was analyzed by RT-PCR in astrocytes at 24 or 48 h after transfection of Kir4.1 siRNA. The mRNA and protein levels are expressed as the ratio to GAPDH mRNA and β-actin protein, respectively. Each point represents the mean ± SEM of 5–6 separate experiments. ∗ P
    Figure Legend Snippet: Effects of Kir4.1 knockdown on BDNF and other neurotrophic factors in astrocytes. Effects of Kir4.1 siRNA transfection on BDNF mRNA (A) and protein levels (B) . The BDNF mRNA levels and protein levels were analyzed by RT-PCR and ELISA, respectively, in astrocytes at 24 or 48 h after the transfection of Kir4.1 siRNA. (C) Effects of Kir4.1 siRNA transfection on mRNA levels of GDNF, CNTF, and NGF. The GDNF, CNTF, or NGF mRNA level was analyzed by RT-PCR in astrocytes at 24 or 48 h after transfection of Kir4.1 siRNA. The mRNA and protein levels are expressed as the ratio to GAPDH mRNA and β-actin protein, respectively. Each point represents the mean ± SEM of 5–6 separate experiments. ∗ P

    Techniques Used: Transfection, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    Knockdown of Kir4.1 channels in astrocytes transfected with Kir4.1 siRNA. Kir4.1 mRNA levels (A) and protein levels (B) were analyzed by RT-PCR or Western blotting, respectively, at 24 or 48 h after transfection of Kir4.1 siRNA. The Kir4.1 mRNA and protein levels are expressed as the ratio to GAPDH mRNA and β-actin protein, respectively. Each point represents the mean ± SEM of 5–6 separate experiments. ∗ P
    Figure Legend Snippet: Knockdown of Kir4.1 channels in astrocytes transfected with Kir4.1 siRNA. Kir4.1 mRNA levels (A) and protein levels (B) were analyzed by RT-PCR or Western blotting, respectively, at 24 or 48 h after transfection of Kir4.1 siRNA. The Kir4.1 mRNA and protein levels are expressed as the ratio to GAPDH mRNA and β-actin protein, respectively. Each point represents the mean ± SEM of 5–6 separate experiments. ∗ P

    Techniques Used: Transfection, Reverse Transcription Polymerase Chain Reaction, Western Blot

    Effects of U0126, SB202190, and SP600125 on BDNF mRNA induction by Kir4.1 knockdown in astrocytes. Astrocytes were pretreated with 10 μM U0126, 10 μM SB202190, or 10 μM SP600125 for 30 min, and transfected with Kir4.1 siRNA or a negative control. The mRNA expression of Kir4.1 (A) or BDNF (B) was analyzed by RT-PCR in astrocytes at 24 h after transfection of Kir4.1 siRNA. The mRNA levels are expressed as the ratio to GAPDH mRNA. Each point represents the mean ± SEM of 5–6 separate experiments. ∗ P
    Figure Legend Snippet: Effects of U0126, SB202190, and SP600125 on BDNF mRNA induction by Kir4.1 knockdown in astrocytes. Astrocytes were pretreated with 10 μM U0126, 10 μM SB202190, or 10 μM SP600125 for 30 min, and transfected with Kir4.1 siRNA or a negative control. The mRNA expression of Kir4.1 (A) or BDNF (B) was analyzed by RT-PCR in astrocytes at 24 h after transfection of Kir4.1 siRNA. The mRNA levels are expressed as the ratio to GAPDH mRNA. Each point represents the mean ± SEM of 5–6 separate experiments. ∗ P

    Techniques Used: Transfection, Negative Control, Expressing, Reverse Transcription Polymerase Chain Reaction

    Expression patterns of Kir4.1 channels and BDNF in cultured astrocytes. (A) Representative images of double-immunofluorescent staining for GFAP and Kir4.1 (a) , GFAP and BDNF (b) , or Kir4.1 and BDNF (c) in single astrocytes. (B) Clustered astrocytes stained for GFAP and BDNF in culture preparations. Lower panels showed magnified images of region indicated by squares (a–d) . Scale bar: 50 μm ( Aa , Ab , and B ) or 25 μm (Ac) .
    Figure Legend Snippet: Expression patterns of Kir4.1 channels and BDNF in cultured astrocytes. (A) Representative images of double-immunofluorescent staining for GFAP and Kir4.1 (a) , GFAP and BDNF (b) , or Kir4.1 and BDNF (c) in single astrocytes. (B) Clustered astrocytes stained for GFAP and BDNF in culture preparations. Lower panels showed magnified images of region indicated by squares (a–d) . Scale bar: 50 μm ( Aa , Ab , and B ) or 25 μm (Ac) .

    Techniques Used: Expressing, Cell Culture, Staining

    Schematic drawing illustrating the effects of the Kir4.1 inhibition on the BDNF expression in astrocytes. Inhibition (blockade and knockdown) of Kir4.1 channels activates the Ras/Raf/MEK/ERK signaling pathway and enhances BDNF expression in astrocytes, which modulates the development of epilepsy (epileptogenesis) and other neuropsychiatric disorders (e.g., major depression).
    Figure Legend Snippet: Schematic drawing illustrating the effects of the Kir4.1 inhibition on the BDNF expression in astrocytes. Inhibition (blockade and knockdown) of Kir4.1 channels activates the Ras/Raf/MEK/ERK signaling pathway and enhances BDNF expression in astrocytes, which modulates the development of epilepsy (epileptogenesis) and other neuropsychiatric disorders (e.g., major depression).

    Techniques Used: Inhibition, Expressing

    17) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    18) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    19) Product Images from "Neuroimmune–Glia Interactions in the Sensory Ganglia Account for the Development of Acute Herpetic Neuralgia"

    Article Title: Neuroimmune–Glia Interactions in the Sensory Ganglia Account for the Development of Acute Herpetic Neuralgia

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.2233-16.2017

    Kir4.1 expression in SGCs is downregulated during acute herpetic neuralgia. A , Relative mRNA expression of Kcnj10 in infected DRGs (L3–L6) up to 21 dpi ( n = 7 for each time point). B , Representative immunofluorescence for Kir4.1 immunoreactivity in DRGs slices from naive and HSV-1-infected mice (7 dpi). C , Representative and densitometric quantification of Western blotting of Kir4.1 protein expression in DRGs ( n = 4 per group) from naive and HSV-1-infected mice (7 dpi). D , Naive mice ( n = 5 per group) were treated daily with ShRNA-Kir4.1 or ShRNA-control for 5 consecutive days (indicated arrows). The mechanical nociceptive threshold was determined 0 to 8 after treatment. E , Representative and desintometric quantification of Western blotting of Kir4.1 protein expression in DRGs ( n = 5 per group) from naive or ShRNA treated mice Data are expressed as the mean ± SEM. * p
    Figure Legend Snippet: Kir4.1 expression in SGCs is downregulated during acute herpetic neuralgia. A , Relative mRNA expression of Kcnj10 in infected DRGs (L3–L6) up to 21 dpi ( n = 7 for each time point). B , Representative immunofluorescence for Kir4.1 immunoreactivity in DRGs slices from naive and HSV-1-infected mice (7 dpi). C , Representative and densitometric quantification of Western blotting of Kir4.1 protein expression in DRGs ( n = 4 per group) from naive and HSV-1-infected mice (7 dpi). D , Naive mice ( n = 5 per group) were treated daily with ShRNA-Kir4.1 or ShRNA-control for 5 consecutive days (indicated arrows). The mechanical nociceptive threshold was determined 0 to 8 after treatment. E , Representative and desintometric quantification of Western blotting of Kir4.1 protein expression in DRGs ( n = 5 per group) from naive or ShRNA treated mice Data are expressed as the mean ± SEM. * p

    Techniques Used: Expressing, Infection, Immunofluorescence, Mouse Assay, Western Blot, shRNA

    Schematic representation of neuroimmune interactions occurring at the sensory ganglia that account for the development of acute herpetic neuralgia. HSV-1 replicates in the sensory ganglia that leads to the induction of a local inflammatory/immune response. It is characterized by the infiltration of leukocytes (mainly macrophages and neutrophils) that in turn mediate the production of TNF. The TNF/TNFR1 signaling in SGCs finally downregulates the expression of Kir4.1, which contributes indirectly to enhance primary sensory neurons excitability and finally to the development of herpetic neuralgia.
    Figure Legend Snippet: Schematic representation of neuroimmune interactions occurring at the sensory ganglia that account for the development of acute herpetic neuralgia. HSV-1 replicates in the sensory ganglia that leads to the induction of a local inflammatory/immune response. It is characterized by the infiltration of leukocytes (mainly macrophages and neutrophils) that in turn mediate the production of TNF. The TNF/TNFR1 signaling in SGCs finally downregulates the expression of Kir4.1, which contributes indirectly to enhance primary sensory neurons excitability and finally to the development of herpetic neuralgia.

    Techniques Used: Expressing

    TNF/TNR1 signaling downmodulates the expression of Kir4.1 in SGCs, which might account for herpetic neuralgia. A , Representative imunofluorescence for Kir4.1 and TNFR1 immunoreactivity in DRGs slices from naive mice. B , Relative mRNA expression of Kcnj10 in DRGs (L3–L6) from infected WT and Tnfr1 −/− mice ( n = 6 per group) at 7 dpi. C , Representative and densitometric quantification of Western blotting of Kir4.1 protein expression in DRGs ( n = 4 per group) from WT and Tnfr1 −/− mice infected with HSV-1 (7 dpi). D , Relative mRNA expression of Kcnj10 in culture of mice SGCs after stimulation with recombinant TNF. Data are expressed as the mean ± SEM. * p
    Figure Legend Snippet: TNF/TNR1 signaling downmodulates the expression of Kir4.1 in SGCs, which might account for herpetic neuralgia. A , Representative imunofluorescence for Kir4.1 and TNFR1 immunoreactivity in DRGs slices from naive mice. B , Relative mRNA expression of Kcnj10 in DRGs (L3–L6) from infected WT and Tnfr1 −/− mice ( n = 6 per group) at 7 dpi. C , Representative and densitometric quantification of Western blotting of Kir4.1 protein expression in DRGs ( n = 4 per group) from WT and Tnfr1 −/− mice infected with HSV-1 (7 dpi). D , Relative mRNA expression of Kcnj10 in culture of mice SGCs after stimulation with recombinant TNF. Data are expressed as the mean ± SEM. * p

    Techniques Used: Expressing, Mouse Assay, Infection, Western Blot, Recombinant

    20) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    21) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    22) Product Images from "Development of functional units within trigeminal ganglia correlates with increased expression of proteins involved in neuron-glia interactions"

    Article Title: Development of functional units within trigeminal ganglia correlates with increased expression of proteins involved in neuron-glia interactions

    Journal: Neuron glia biology

    doi: 10.1017/S1740925X10000232

    Temporal and spatial expression of Neurofilament 200 and Kir4.1 in trigeminal ganglia during postnatal development
    Figure Legend Snippet: Temporal and spatial expression of Neurofilament 200 and Kir4.1 in trigeminal ganglia during postnatal development

    Techniques Used: Expressing

    23) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    24) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    25) Product Images from "Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors"

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    Journal:

    doi: 10.1002/jcp.21169

    Effects of SP on the single channel activity of Kir4.1-Kir5.1
    Figure Legend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Techniques Used: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH
    Figure Legend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Techniques Used: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons
    Figure Legend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Techniques Used: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH
    Figure Legend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Techniques Used:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi
    Figure Legend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Techniques Used:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters
    Figure Legend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Techniques Used:

    26) Product Images from "Development of functional units within trigeminal ganglia correlates with increased expression of proteins involved in neuron-glia interactions"

    Article Title: Development of functional units within trigeminal ganglia correlates with increased expression of proteins involved in neuron-glia interactions

    Journal: Neuron glia biology

    doi: 10.1017/S1740925X10000232

    Temporal and spatial expression of Neurofilament 200 and Kir4.1 in trigeminal ganglia during postnatal development
    Figure Legend Snippet: Temporal and spatial expression of Neurofilament 200 and Kir4.1 in trigeminal ganglia during postnatal development

    Techniques Used: Expressing

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    Alomone Labs kir4 1 ab
    In vivo intravitreal application of <t>Kir4.1-Ab:carrier</t> reduces STR and PhNR electronegative ERG potentials in RCS rat. ( A ) STR and PhNR were diminished in the eye of a 15-wk-old rat injected with Kir4.1-Ab:carrier (red) relative to the contralateral IgG:carrier control eye (black). ( B ) Light-adapted ERG responses (stimulus intensity 0.6 log cd-s/m 2 ) before (black) and 2 h after injection in a representative RCS rat at 14 wk of age. One eye was injected with Kir4.1-Ab:carrier (red) and the contralateral control eye with rabbit IgG:carrier (gray). PhNR amplitudes were decreased by 29 ± 5% ( n = 3) compared with the same eye baseline, whereas no change in PhNR amplitude was seen in the contralateral control eyes.
    Kir4 1 Ab, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    In vivo intravitreal application of Kir4.1-Ab:carrier reduces STR and PhNR electronegative ERG potentials in RCS rat. ( A ) STR and PhNR were diminished in the eye of a 15-wk-old rat injected with Kir4.1-Ab:carrier (red) relative to the contralateral IgG:carrier control eye (black). ( B ) Light-adapted ERG responses (stimulus intensity 0.6 log cd-s/m 2 ) before (black) and 2 h after injection in a representative RCS rat at 14 wk of age. One eye was injected with Kir4.1-Ab:carrier (red) and the contralateral control eye with rabbit IgG:carrier (gray). PhNR amplitudes were decreased by 29 ± 5% ( n = 3) compared with the same eye baseline, whereas no change in PhNR amplitude was seen in the contralateral control eyes.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Probing potassium channel function in vivo by intracellular delivery of antibodies in a rat model of retinal neurodegeneration

    doi: 10.1073/pnas.0913472107

    Figure Lengend Snippet: In vivo intravitreal application of Kir4.1-Ab:carrier reduces STR and PhNR electronegative ERG potentials in RCS rat. ( A ) STR and PhNR were diminished in the eye of a 15-wk-old rat injected with Kir4.1-Ab:carrier (red) relative to the contralateral IgG:carrier control eye (black). ( B ) Light-adapted ERG responses (stimulus intensity 0.6 log cd-s/m 2 ) before (black) and 2 h after injection in a representative RCS rat at 14 wk of age. One eye was injected with Kir4.1-Ab:carrier (red) and the contralateral control eye with rabbit IgG:carrier (gray). PhNR amplitudes were decreased by 29 ± 5% ( n = 3) compared with the same eye baseline, whereas no change in PhNR amplitude was seen in the contralateral control eyes.

    Article Snippet: Primary antibodies were polyclonal rabbit anti-human Kir2.1-Ab and Kir4.1-Ab (1:50 dilution; Alomone Labs), monoclonal mouse anti-human protein kinase C alpha (PKCα-Ab 1:200; Santa Cruz Biotechnology) to label rod BCs , monoclonal mouse anti-human protein kinase C beta (PKCβ-Ab, 1:200; Santa Cruz Biotechnology) to label cone BCs , polyclonal guinea-pig anti-rat vesicular glutamate transporter 1 (VGLUT1-Ab, 1:5,000; Chemicon) to label rod and cone BCs , polyclonal goat anti-human synapsin Ia/b-Ab (1:50; Santa Cruz Biotechnology) and IIa-Ab (1:100; Santa Cruz Biotechnology) as amacrine cell markers that label phosphoproteins of conventional synapses but not ribbon-containing terminals , and polyclonal GFAP-Ab (Sigma, 1:200) as Müller cell marker.

    Techniques: In Vivo, Injection

    IHC of rat retina shows Kir4.1 colocalization with Müller cell GFAP marker. ( A ) Conventional postmortem double labeling with Kir4.1-Ab (red) and GFAP-Ab (green) shows colocalization with Müller cells in a dystrophic 14 wk-old RCS retina. ( B ) In vivo intravitreal application of Kir4.1-Ab:carrier complex gives prominent labeling of Müller cell endfeet with extensions along Müller cell processes in the IPL (red) in a 15-wk-old dystrophic RCS rat and colocalizes with GFAP (green). GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; ONL, outer nuclear layer.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Probing potassium channel function in vivo by intracellular delivery of antibodies in a rat model of retinal neurodegeneration

    doi: 10.1073/pnas.0913472107

    Figure Lengend Snippet: IHC of rat retina shows Kir4.1 colocalization with Müller cell GFAP marker. ( A ) Conventional postmortem double labeling with Kir4.1-Ab (red) and GFAP-Ab (green) shows colocalization with Müller cells in a dystrophic 14 wk-old RCS retina. ( B ) In vivo intravitreal application of Kir4.1-Ab:carrier complex gives prominent labeling of Müller cell endfeet with extensions along Müller cell processes in the IPL (red) in a 15-wk-old dystrophic RCS rat and colocalizes with GFAP (green). GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; ONL, outer nuclear layer.

    Article Snippet: Primary antibodies were polyclonal rabbit anti-human Kir2.1-Ab and Kir4.1-Ab (1:50 dilution; Alomone Labs), monoclonal mouse anti-human protein kinase C alpha (PKCα-Ab 1:200; Santa Cruz Biotechnology) to label rod BCs , monoclonal mouse anti-human protein kinase C beta (PKCβ-Ab, 1:200; Santa Cruz Biotechnology) to label cone BCs , polyclonal guinea-pig anti-rat vesicular glutamate transporter 1 (VGLUT1-Ab, 1:5,000; Chemicon) to label rod and cone BCs , polyclonal goat anti-human synapsin Ia/b-Ab (1:50; Santa Cruz Biotechnology) and IIa-Ab (1:100; Santa Cruz Biotechnology) as amacrine cell markers that label phosphoproteins of conventional synapses but not ribbon-containing terminals , and polyclonal GFAP-Ab (Sigma, 1:200) as Müller cell marker.

    Techniques: Immunohistochemistry, Marker, Labeling, In Vivo

    Immunohistochemical analysis of Kir4.1- and GFAP-immunoreactivity (IR)-positive cells in pilocarpine-inducedTLE rats. (A) Schematic illustrations of the brain sections selected for quantitative analysis of Kir4.1- and GFAP-IR-positive cells. Squares in each section indicate the area analyzed for counting of Kir4.1- and GFAP-IR-positive cells. The distance from the Bregma is shown on the bottom of each section. MC, motor cortex; SC, sensory cortex; AID, agranular insular cortex; Pir, piriform cortex; dmST, vmST, dlST and vlST, dorsomedial, ventromedial, dorsolateral, and ventrolateral striatum, respectively; AcbC and AcbSh, core and shell regions of nucleus accumbens, respectively; Ect-PRh, ectorhinal–perirhinal cortex; MePV and MePD, medial amygdaloid nucleus, posteroventral and posterodorsal part; BLP, basolateral amygdaloid nucleus, posterior part; BMP, basomedial amygdaloid nucleus, posterior part; PMCo, posteromedial cortical amygdaloid nucleus; CA1, CA3, and DG: CA1, CA3, and dentate gyrus of the hippocampus. (B) Representative photographs illustrating the Kir4.1 (upper panels)- and GFAP (lower panels)-positive cells in the sensory cortex (SC) and the medial amygdaloid nucleus, posterodorsal part (MePD). Scale bar: 50 μ m.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Expressional analysis of the astrocytic Kir4.1 channel in a pilocarpine-induced temporal lobe epilepsy model

    doi: 10.3389/fncel.2013.00104

    Figure Lengend Snippet: Immunohistochemical analysis of Kir4.1- and GFAP-immunoreactivity (IR)-positive cells in pilocarpine-inducedTLE rats. (A) Schematic illustrations of the brain sections selected for quantitative analysis of Kir4.1- and GFAP-IR-positive cells. Squares in each section indicate the area analyzed for counting of Kir4.1- and GFAP-IR-positive cells. The distance from the Bregma is shown on the bottom of each section. MC, motor cortex; SC, sensory cortex; AID, agranular insular cortex; Pir, piriform cortex; dmST, vmST, dlST and vlST, dorsomedial, ventromedial, dorsolateral, and ventrolateral striatum, respectively; AcbC and AcbSh, core and shell regions of nucleus accumbens, respectively; Ect-PRh, ectorhinal–perirhinal cortex; MePV and MePD, medial amygdaloid nucleus, posteroventral and posterodorsal part; BLP, basolateral amygdaloid nucleus, posterior part; BMP, basomedial amygdaloid nucleus, posterior part; PMCo, posteromedial cortical amygdaloid nucleus; CA1, CA3, and DG: CA1, CA3, and dentate gyrus of the hippocampus. (B) Representative photographs illustrating the Kir4.1 (upper panels)- and GFAP (lower panels)-positive cells in the sensory cortex (SC) and the medial amygdaloid nucleus, posterodorsal part (MePD). Scale bar: 50 μ m.

    Article Snippet: The primary antibodies used were a rabbit polyclonal antibody against Kir4.1 (1:500, Alomone Labs., Jerusalem, Israel), a goat polyclonal antibody against Kir5.1 (N-12; 1:400, Santa Cruz Biotechnology), a goat polyclonal antibody against Kir2.1 (1:400, Santa Cruz Biotechnology) and mouse monoclonal antibodies against β-actin (1:1000, Sigma-Aldrich).

    Techniques: Immunohistochemistry

    Western blot analysis for Kir4.1, Kir5.1 and Kir2.1 expression in pilocarpine-inducedTLE rats. (A) Representative Western blots visualizing Kir4.1, Kir5.1, and Kir2.1 expression in the frontal cortex (fCx), occipito-temporal cortex (otCx), striatum (St), and hypothalamus (Ht). (B–D) Regional expression of Kir4.1 (B) , Kir5.1 (C) , and Kir2.1 (D) in pilocarpine-induced TLE rats. Kir expression was expressed as relative optical density (ROD) to β-actin. fCx, frontal cortex; ptCx, parieto-temporal cortex; otCx, occipito-temporal cortex; St, striatum; Hpc, hippocampus; Th, thalamus; Ht, hypothalamus; Mid, midbrain; P/MO, pons/medulla oblongata; Cer, cerebellum. Each column represents the mean ± SEM of four animals. * P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Expressional analysis of the astrocytic Kir4.1 channel in a pilocarpine-induced temporal lobe epilepsy model

    doi: 10.3389/fncel.2013.00104

    Figure Lengend Snippet: Western blot analysis for Kir4.1, Kir5.1 and Kir2.1 expression in pilocarpine-inducedTLE rats. (A) Representative Western blots visualizing Kir4.1, Kir5.1, and Kir2.1 expression in the frontal cortex (fCx), occipito-temporal cortex (otCx), striatum (St), and hypothalamus (Ht). (B–D) Regional expression of Kir4.1 (B) , Kir5.1 (C) , and Kir2.1 (D) in pilocarpine-induced TLE rats. Kir expression was expressed as relative optical density (ROD) to β-actin. fCx, frontal cortex; ptCx, parieto-temporal cortex; otCx, occipito-temporal cortex; St, striatum; Hpc, hippocampus; Th, thalamus; Ht, hypothalamus; Mid, midbrain; P/MO, pons/medulla oblongata; Cer, cerebellum. Each column represents the mean ± SEM of four animals. * P

    Article Snippet: The primary antibodies used were a rabbit polyclonal antibody against Kir4.1 (1:500, Alomone Labs., Jerusalem, Israel), a goat polyclonal antibody against Kir5.1 (N-12; 1:400, Santa Cruz Biotechnology), a goat polyclonal antibody against Kir2.1 (1:400, Santa Cruz Biotechnology) and mouse monoclonal antibodies against β-actin (1:1000, Sigma-Aldrich).

    Techniques: Western Blot, Expressing

    Topographical expression of Kir4.1 and GFAP in the cortical regions of pilocarpine-inducedTLE rats. (A,B) Number of Kir4.1 (A) - or GFAP (B) -immunoreactivity (IR)-positive cells. (C) Relative Kir4.1 expression ratios in astrocytes. A pair of successive slices in each region from the same animal was stained with anti-Kir4.1 or anti-GFAP antibody. The Kir4.1 expression ratios were calculated as the ratios of Kir4.1-positive astrocytes relative to the total number of astrocytes (Kir4.1-positive cells/GFAP-positive cells) in each animal. MC, motor cortex; SC, sensory cortex; AID, agranular insular cortex, dorsal part; Ect-PRh, ectorhinal-perirhinal cortex; Pir, piriform cortex. Each column represents the mean ± S.E.M. of seven animals. * P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Expressional analysis of the astrocytic Kir4.1 channel in a pilocarpine-induced temporal lobe epilepsy model

    doi: 10.3389/fncel.2013.00104

    Figure Lengend Snippet: Topographical expression of Kir4.1 and GFAP in the cortical regions of pilocarpine-inducedTLE rats. (A,B) Number of Kir4.1 (A) - or GFAP (B) -immunoreactivity (IR)-positive cells. (C) Relative Kir4.1 expression ratios in astrocytes. A pair of successive slices in each region from the same animal was stained with anti-Kir4.1 or anti-GFAP antibody. The Kir4.1 expression ratios were calculated as the ratios of Kir4.1-positive astrocytes relative to the total number of astrocytes (Kir4.1-positive cells/GFAP-positive cells) in each animal. MC, motor cortex; SC, sensory cortex; AID, agranular insular cortex, dorsal part; Ect-PRh, ectorhinal-perirhinal cortex; Pir, piriform cortex. Each column represents the mean ± S.E.M. of seven animals. * P

    Article Snippet: The primary antibodies used were a rabbit polyclonal antibody against Kir4.1 (1:500, Alomone Labs., Jerusalem, Israel), a goat polyclonal antibody against Kir5.1 (N-12; 1:400, Santa Cruz Biotechnology), a goat polyclonal antibody against Kir2.1 (1:400, Santa Cruz Biotechnology) and mouse monoclonal antibodies against β-actin (1:1000, Sigma-Aldrich).

    Techniques: Expressing, Staining

    Topographical expression of Kir4.1 and GFAP in the basal ganglia and limbic regions of pilocarpine-inducedTLE rats. (A,B) Number of Kir4.1 (A) - or GFAP (B) -immunoreactivity (IR)-positive cells. (C) Relative Kir4.1 expression ratios in astrocytes. A pair of successive slices in each region from the same animal was stained with anti-Kir4.1 or anti-GFAP antibody. The Kir4.1 expression ratios were calculated as the ratios of Kir4.1-positive astrocytes relative to the total number of astrocytes (Kir4.1Kir4.1-positive cells/GFAP-positive cells) in each animal. dmST, vmST, dlST, and vlST, dorsomedial, ventromedial, dorsolateral, and ventrolateral striatum, respectively; AcbC and AcbSh, core and shell regions of the nucleus accumbens, respectively; MePV and MePD, medial amygdaloid nucleus, posteroventral and posterodorsal part; BLP, basolateral amygdaloid nucleus, posterior part; BMP, basomedial amygdaloid nucleus, posterior part; PMCo, posteromedial cortical amygdaloid nucleus; CA1, CA3, and DG, CA1, CA3, and dentate gyrus of the hippocampus. Each column represents the mean ± SEM of seven animals. * P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Expressional analysis of the astrocytic Kir4.1 channel in a pilocarpine-induced temporal lobe epilepsy model

    doi: 10.3389/fncel.2013.00104

    Figure Lengend Snippet: Topographical expression of Kir4.1 and GFAP in the basal ganglia and limbic regions of pilocarpine-inducedTLE rats. (A,B) Number of Kir4.1 (A) - or GFAP (B) -immunoreactivity (IR)-positive cells. (C) Relative Kir4.1 expression ratios in astrocytes. A pair of successive slices in each region from the same animal was stained with anti-Kir4.1 or anti-GFAP antibody. The Kir4.1 expression ratios were calculated as the ratios of Kir4.1-positive astrocytes relative to the total number of astrocytes (Kir4.1Kir4.1-positive cells/GFAP-positive cells) in each animal. dmST, vmST, dlST, and vlST, dorsomedial, ventromedial, dorsolateral, and ventrolateral striatum, respectively; AcbC and AcbSh, core and shell regions of the nucleus accumbens, respectively; MePV and MePD, medial amygdaloid nucleus, posteroventral and posterodorsal part; BLP, basolateral amygdaloid nucleus, posterior part; BMP, basomedial amygdaloid nucleus, posterior part; PMCo, posteromedial cortical amygdaloid nucleus; CA1, CA3, and DG, CA1, CA3, and dentate gyrus of the hippocampus. Each column represents the mean ± SEM of seven animals. * P

    Article Snippet: The primary antibodies used were a rabbit polyclonal antibody against Kir4.1 (1:500, Alomone Labs., Jerusalem, Israel), a goat polyclonal antibody against Kir5.1 (N-12; 1:400, Santa Cruz Biotechnology), a goat polyclonal antibody against Kir2.1 (1:400, Santa Cruz Biotechnology) and mouse monoclonal antibodies against β-actin (1:1000, Sigma-Aldrich).

    Techniques: Expressing, Staining

    Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Journal:

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    doi: 10.1002/jcp.21169

    Figure Lengend Snippet: Effects of SP on the single channel activity of Kir4.1-Kir5.1

    Article Snippet: The Kir4.1 and Kir5.1 subunits are expressed in brainstem neurons.

    Techniques: Activity Assay

    Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Journal:

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    doi: 10.1002/jcp.21169

    Figure Lengend Snippet: Involvement of PKC in the Kir4.1-Kir5.1 inhibition by SP, DOI and TRH

    Article Snippet: The Kir4.1 and Kir5.1 subunits are expressed in brainstem neurons.

    Techniques: Inhibition

    Expression of Kir4.1-Kir5.1 in brainstem neurons

    Journal:

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    doi: 10.1002/jcp.21169

    Figure Lengend Snippet: Expression of Kir4.1-Kir5.1 in brainstem neurons

    Article Snippet: The Kir4.1 and Kir5.1 subunits are expressed in brainstem neurons.

    Techniques: Expressing

    Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Journal:

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    doi: 10.1002/jcp.21169

    Figure Lengend Snippet: Kir4.1-Kir5.1 channel is inhibited by SP, DOI, and TRH

    Article Snippet: The Kir4.1 and Kir5.1 subunits are expressed in brainstem neurons.

    Techniques:

    Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Journal:

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    doi: 10.1002/jcp.21169

    Figure Lengend Snippet: Independent regulation of the Kir4.1-Kir5.1 channel by neurotransmitters and pHi

    Article Snippet: The Kir4.1 and Kir5.1 subunits are expressed in brainstem neurons.

    Techniques:

    PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Journal:

    Article Title: Modulation of the Heteromeric Kir4.1-Kir5.1 Channel by Multiple Neurotransmitters via Gαq-coupled Receptors

    doi: 10.1002/jcp.21169

    Figure Lengend Snippet: PKC involvement in the modulation of the Kir4.1-Kir5.1 channel by the neurotransmitters

    Article Snippet: The Kir4.1 and Kir5.1 subunits are expressed in brainstem neurons.

    Techniques: