anti scn11a nav1 9 antibody  (Alomone Labs)


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    Alomone Labs anti scn11a nav1 9 antibody
    mPRMT7 promoted the hyperexcitability of mouse DRG neurons in a <t>SCN11A</t> -dependent manner. Current-clamp responses to 200-ms depolarizing current steps of 50, 100, 150, and 225 pA in representative Scn11a −/− mouse DRG neurons (A-B) and Scn11a +/+ mouse DRG neurons (C-D) expressing the empty vector pcDNA3.1/GFP (mock) and pcDNA3.1-PRMT7/GFP (PRMT7). (E) Rheobase, (F) resting membrane potential (RMP), and (G) V threshold (the threshold at which AP takeoff occurs) were not significantly altered in mock-transfected DRG neurons. Data were statistically analysed by the unpaired Student t test; * P
    Anti Scn11a Nav1 9 Antibody, 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
    https://www.bioz.com/result/anti scn11a nav1 9 antibody/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti scn11a nav1 9 antibody - by Bioz Stars, 2022-07
    93/100 stars

    Images

    1) Product Images from "Protein arginine methyltransferase 7 modulates neuronal excitability by interacting with NaV1.9"

    Article Title: Protein arginine methyltransferase 7 modulates neuronal excitability by interacting with NaV1.9

    Journal: Pain

    doi: 10.1097/j.pain.0000000000002421

    mPRMT7 promoted the hyperexcitability of mouse DRG neurons in a SCN11A -dependent manner. Current-clamp responses to 200-ms depolarizing current steps of 50, 100, 150, and 225 pA in representative Scn11a −/− mouse DRG neurons (A-B) and Scn11a +/+ mouse DRG neurons (C-D) expressing the empty vector pcDNA3.1/GFP (mock) and pcDNA3.1-PRMT7/GFP (PRMT7). (E) Rheobase, (F) resting membrane potential (RMP), and (G) V threshold (the threshold at which AP takeoff occurs) were not significantly altered in mock-transfected DRG neurons. Data were statistically analysed by the unpaired Student t test; * P
    Figure Legend Snippet: mPRMT7 promoted the hyperexcitability of mouse DRG neurons in a SCN11A -dependent manner. Current-clamp responses to 200-ms depolarizing current steps of 50, 100, 150, and 225 pA in representative Scn11a −/− mouse DRG neurons (A-B) and Scn11a +/+ mouse DRG neurons (C-D) expressing the empty vector pcDNA3.1/GFP (mock) and pcDNA3.1-PRMT7/GFP (PRMT7). (E) Rheobase, (F) resting membrane potential (RMP), and (G) V threshold (the threshold at which AP takeoff occurs) were not significantly altered in mock-transfected DRG neurons. Data were statistically analysed by the unpaired Student t test; * P

    Techniques Used: Expressing, Plasmid Preparation, Transfection

    Protein arginine methyltransferase 7 affects the current density of Na V 1.9 by promoting its accumulation on the cell membrane. (A) Representative whole-cell sodium currents evoked by voltage from Scn11a −/− mouse DRG neurons electroporated with SCN11A or SCN11A and PRMT7 . (B) Current–voltage relationships in the indicated experimental groups. The peak current density (normalized by membrane capacitance) was statistically analysed (mock, n = 15; hNa V 1.9, n = 25; and hNa V 1.9 + hPRMT7, n = 23), and significant differences were tested by two-way ANOVA, followed by a post hoc Bonferroni test; infection × voltage: F(32, 948) = 5.846, P
    Figure Legend Snippet: Protein arginine methyltransferase 7 affects the current density of Na V 1.9 by promoting its accumulation on the cell membrane. (A) Representative whole-cell sodium currents evoked by voltage from Scn11a −/− mouse DRG neurons electroporated with SCN11A or SCN11A and PRMT7 . (B) Current–voltage relationships in the indicated experimental groups. The peak current density (normalized by membrane capacitance) was statistically analysed (mock, n = 15; hNa V 1.9, n = 25; and hNa V 1.9 + hPRMT7, n = 23), and significant differences were tested by two-way ANOVA, followed by a post hoc Bonferroni test; infection × voltage: F(32, 948) = 5.846, P

    Techniques Used: Infection

    Interaction and coexpression of Na V 1.9 with PRMT7. Interaction between hLoop1 and full-length hPRMT7 was analysed by GST pull-down assays (A) and reciprocal coimmunoprecipitation assays (B). (C) Interaction between the intracellular domains of hNa V 1.9 and hPRMT7 was examined by coimmunoprecipitation assays. (D) Interaction of mPRMT7 with mNa V 1.9 in mouse DRG tissues was assessed. Scn11a +/+ or Scn11a −/− mouse DRG tissue lysates were immunoprecipitated using anti-mPRMT7 antibodies and control IgG. The precipitates were immunoblotted with the indicated antibodies. (E) Immunohistochemical analysis of mPRMT7/mNa V 1.9 expression in mouse DRG sections. The sections were stained for mPRMT7 (red) and mNa V 1.9 (green) and DAPI (blue). mPRMT7 showed considerable colocalization with mNa V 1.9 in mouse DRG neurons. Scale bars, 50 μm. (F) Percentages of mPRMT7-positive and mNa V 1.9-positive neurons are shown. DAPI, 4,6-diamidino-2-phenylindole; DRG, dorsal root ganglion; GST, glutathione S-transferase; IgG, immunoglobulin G; hNa V 1.9, human hNa V 1.9; PRMT7, protein arginine methyltransferase 7.
    Figure Legend Snippet: Interaction and coexpression of Na V 1.9 with PRMT7. Interaction between hLoop1 and full-length hPRMT7 was analysed by GST pull-down assays (A) and reciprocal coimmunoprecipitation assays (B). (C) Interaction between the intracellular domains of hNa V 1.9 and hPRMT7 was examined by coimmunoprecipitation assays. (D) Interaction of mPRMT7 with mNa V 1.9 in mouse DRG tissues was assessed. Scn11a +/+ or Scn11a −/− mouse DRG tissue lysates were immunoprecipitated using anti-mPRMT7 antibodies and control IgG. The precipitates were immunoblotted with the indicated antibodies. (E) Immunohistochemical analysis of mPRMT7/mNa V 1.9 expression in mouse DRG sections. The sections were stained for mPRMT7 (red) and mNa V 1.9 (green) and DAPI (blue). mPRMT7 showed considerable colocalization with mNa V 1.9 in mouse DRG neurons. Scale bars, 50 μm. (F) Percentages of mPRMT7-positive and mNa V 1.9-positive neurons are shown. DAPI, 4,6-diamidino-2-phenylindole; DRG, dorsal root ganglion; GST, glutathione S-transferase; IgG, immunoglobulin G; hNa V 1.9, human hNa V 1.9; PRMT7, protein arginine methyltransferase 7.

    Techniques Used: Immunoprecipitation, Immunohistochemistry, Expressing, Staining

    DS-437 reduced DRG neuronal excitability and relieved pain hypersensitivity in Scn11a A796G/A796G mice. (A) Current-clamp responses to a 200-ms depolarizing current of 200 pA in representative Scn11a +/+ mouse DRG neurons and Scn11a A796G/A796G mouse DRG neurons with DS-437 or control. (B) Rheobase, (C) resting membrane potential (RMP), and (D) V threshold (the threshold at which AP takeoff occurs) showed no significant changes in DRG neurons treated with or without DS-437. Data were statistically analysed by one-way ANOVA; * P
    Figure Legend Snippet: DS-437 reduced DRG neuronal excitability and relieved pain hypersensitivity in Scn11a A796G/A796G mice. (A) Current-clamp responses to a 200-ms depolarizing current of 200 pA in representative Scn11a +/+ mouse DRG neurons and Scn11a A796G/A796G mouse DRG neurons with DS-437 or control. (B) Rheobase, (C) resting membrane potential (RMP), and (D) V threshold (the threshold at which AP takeoff occurs) showed no significant changes in DRG neurons treated with or without DS-437. Data were statistically analysed by one-way ANOVA; * P

    Techniques Used: Mouse Assay

    2) Product Images from "Antinociceptive Effects of AGAP, a Recombinant Neurotoxic Polypeptide: Possible Involvement of the Tetrodotoxin-Resistant Sodium Channels in Small Dorsal Root Ganglia Neurons"

    Article Title: Antinociceptive Effects of AGAP, a Recombinant Neurotoxic Polypeptide: Possible Involvement of the Tetrodotoxin-Resistant Sodium Channels in Small Dorsal Root Ganglia Neurons

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2016.00496

    Effect of AGAP on the dynamic function of Na V 1.9 channels . 1000 nM AGAP did not significantly affect the voltage-dependence of channel activation or steady-state inactivation. (A,B) Effect of AGAP on steady-state activation kinetics of Na V 1.9 currents. V 1/2 was -38.4 ± 1.5 mV in control conditions and -38.2 ± 3.7 mV in the presence of 1000 nM AGAP. Slope factors were 6.1 ± 0.5 and 7.8 ± 1.1 mV, respectively ( n = 7). (C,D) Steady-state inactivated of Nav1.9 in the absence and presence of AGAP. V 1/2 for inactivation was -67.9 ± 2.2 mV in control conditions and -69.6 ± 2.5 mV in the presence of 1000 nM AGAP. Slope factors were -11.0 ± 1.8 and -12.5 ± 2.0 mV, respectively ( P > 0.05, P values are from unpaired t -test. n = 6).
    Figure Legend Snippet: Effect of AGAP on the dynamic function of Na V 1.9 channels . 1000 nM AGAP did not significantly affect the voltage-dependence of channel activation or steady-state inactivation. (A,B) Effect of AGAP on steady-state activation kinetics of Na V 1.9 currents. V 1/2 was -38.4 ± 1.5 mV in control conditions and -38.2 ± 3.7 mV in the presence of 1000 nM AGAP. Slope factors were 6.1 ± 0.5 and 7.8 ± 1.1 mV, respectively ( n = 7). (C,D) Steady-state inactivated of Nav1.9 in the absence and presence of AGAP. V 1/2 for inactivation was -67.9 ± 2.2 mV in control conditions and -69.6 ± 2.5 mV in the presence of 1000 nM AGAP. Slope factors were -11.0 ± 1.8 and -12.5 ± 2.0 mV, respectively ( P > 0.05, P values are from unpaired t -test. n = 6).

    Techniques Used: Activation Assay

    3) Product Images from "Electroacupuncture Reduces Carrageenan- and CFA-Induced Inflammatory Pain Accompanied by Changing the Expression of Nav1.7 and Nav1.8, rather than Nav1.9, in Mice Dorsal Root Ganglia"

    Article Title: Electroacupuncture Reduces Carrageenan- and CFA-Induced Inflammatory Pain Accompanied by Changing the Expression of Nav1.7 and Nav1.8, rather than Nav1.9, in Mice Dorsal Root Ganglia

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    doi: 10.1155/2013/312184

    Nav1.7 and Nav1.8 protein levels were increased in lumbar DRGs in both intraplantar carrageenan- and CFA-induced inflammation and further attenuated by EA at the ST36 acupoint in mice, but Nav1.9 proteins were not altered. (a) DRGs lysates were immunoreactive with specific antibodies to Nav1.7 and a substantially increased signal at the ipsilateral site, as compared to that of the saline-injected group. Nav1.7 protein levels were attenuated by EA at the ST36 acupoint, as compared to that of the carrageenan- and CFA-induced groups. (b) Nav1.8 displayed similar results to Nav1.7. The protein levels of S-Acu and S-GM were similar to inflamed but not EA group. (c) Nav1.9 protein levels were not changed in both the carrageenan- and CFA-injected sites. Nav1.9 protein levels were not attenuated by EA at the ST36 acupoint, as compared to those of the carrageenan- and CFA-induced groups, either. Nav1.9 proteins were not altered at the ipsilateral site of inflammation and EA stimulation.
    Figure Legend Snippet: Nav1.7 and Nav1.8 protein levels were increased in lumbar DRGs in both intraplantar carrageenan- and CFA-induced inflammation and further attenuated by EA at the ST36 acupoint in mice, but Nav1.9 proteins were not altered. (a) DRGs lysates were immunoreactive with specific antibodies to Nav1.7 and a substantially increased signal at the ipsilateral site, as compared to that of the saline-injected group. Nav1.7 protein levels were attenuated by EA at the ST36 acupoint, as compared to that of the carrageenan- and CFA-induced groups. (b) Nav1.8 displayed similar results to Nav1.7. The protein levels of S-Acu and S-GM were similar to inflamed but not EA group. (c) Nav1.9 protein levels were not changed in both the carrageenan- and CFA-injected sites. Nav1.9 protein levels were not attenuated by EA at the ST36 acupoint, as compared to those of the carrageenan- and CFA-induced groups, either. Nav1.9 proteins were not altered at the ipsilateral site of inflammation and EA stimulation.

    Techniques Used: Mouse Assay, Injection

    Protein levels of Nav1.7, Nav1.8, and Nav1.9 in the L3–L5 DRGs in mice in control, Car, EA, S-Acu, S-GM, CFA, EA, S-Acu, S-GM groups. The percentage of Nav protein levels from lumbar DRGs was presented in each group. * P
    Figure Legend Snippet: Protein levels of Nav1.7, Nav1.8, and Nav1.9 in the L3–L5 DRGs in mice in control, Car, EA, S-Acu, S-GM, CFA, EA, S-Acu, S-GM groups. The percentage of Nav protein levels from lumbar DRGs was presented in each group. * P

    Techniques Used: Mouse Assay

    Nav1.7 and Nav1.8 expressions were increased in ipsilateral DRGs after intraplantar carrageenan injection and further attenuated by EA at the ST36 acupoint in mice, though Nav1.9 was not different. (a)–(c) Nav1.7, Nav1.8, and Nav1.9 immunoreactive neurons were found in lumbar DRGs at the ipsilateral site of the saline-injected group. (d)-(e) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the carrageenan-injected group, but (f) Nav1.9 immunoreactive neurons were not increased. (g)-(h) Carrageenan-induced increases of Nav1.7 and Nav1.8 were attenuated by EA, as compared to those of the carrageenan-induced group. (i) Nav1.9 immunoreactive neurons were not altered by EA at the ipsilateral site of inflammation. (j)-(k) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-Acu group. (l) Nav1.9 immunoreactive neurons were not altered in the S-Acu group. (m)-(n) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-GM group. (o) Nav1.9 immunoreactive neurons were not altered in the S-GM group. Scale bar = 50 um.
    Figure Legend Snippet: Nav1.7 and Nav1.8 expressions were increased in ipsilateral DRGs after intraplantar carrageenan injection and further attenuated by EA at the ST36 acupoint in mice, though Nav1.9 was not different. (a)–(c) Nav1.7, Nav1.8, and Nav1.9 immunoreactive neurons were found in lumbar DRGs at the ipsilateral site of the saline-injected group. (d)-(e) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the carrageenan-injected group, but (f) Nav1.9 immunoreactive neurons were not increased. (g)-(h) Carrageenan-induced increases of Nav1.7 and Nav1.8 were attenuated by EA, as compared to those of the carrageenan-induced group. (i) Nav1.9 immunoreactive neurons were not altered by EA at the ipsilateral site of inflammation. (j)-(k) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-Acu group. (l) Nav1.9 immunoreactive neurons were not altered in the S-Acu group. (m)-(n) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-GM group. (o) Nav1.9 immunoreactive neurons were not altered in the S-GM group. Scale bar = 50 um.

    Techniques Used: Injection, Mouse Assay

    Nav1.7 and Nav1.8 expressions were increased in ipsilateral DRGs after intraplantar CFA injection and further attenuated by EA at the ST36 acupoint in mice, though Nav1.9 was not different. (a)–(c) Nav1.7, Nav1.8, and Nav1.9 immunoreactive neurons were found in lumbar DRGs at the ipsilateral site of the saline-injected group. (d)-(e) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the CFA-injected group, but (f) Nav1.9 immunoreactive neurons were not increased. (g)-(h) CFA-induced increases of Nav1.7 and Nav1.8 were attenuated by EA, as compared to those of the CFA-induced group. (i) Nav1.9 immunoreactive neurons were not altered by EA at the ipsilateral site of inflammation. (j)-(k) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-Acu group. (l) Nav1.9 immunoreactive neurons were not altered in the S-Acu group. (m)-(n) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-GM group. (o) Nav1.9 immunoreactive neurons were not altered in the S-GM group. Scale bar = 50 um.
    Figure Legend Snippet: Nav1.7 and Nav1.8 expressions were increased in ipsilateral DRGs after intraplantar CFA injection and further attenuated by EA at the ST36 acupoint in mice, though Nav1.9 was not different. (a)–(c) Nav1.7, Nav1.8, and Nav1.9 immunoreactive neurons were found in lumbar DRGs at the ipsilateral site of the saline-injected group. (d)-(e) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the CFA-injected group, but (f) Nav1.9 immunoreactive neurons were not increased. (g)-(h) CFA-induced increases of Nav1.7 and Nav1.8 were attenuated by EA, as compared to those of the CFA-induced group. (i) Nav1.9 immunoreactive neurons were not altered by EA at the ipsilateral site of inflammation. (j)-(k) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-Acu group. (l) Nav1.9 immunoreactive neurons were not altered in the S-Acu group. (m)-(n) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-GM group. (o) Nav1.9 immunoreactive neurons were not altered in the S-GM group. Scale bar = 50 um.

    Techniques Used: Injection, Mouse Assay

    4) Product Images from "Ionic Mechanism Underlying Rebound Depolarization in Medial Prefrontal Cortex Pyramidal Neurons"

    Article Title: Ionic Mechanism Underlying Rebound Depolarization in Medial Prefrontal Cortex Pyramidal Neurons

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2018.00093

    Effects of an anti-Nav1.9 channel antibody, IgG and F − on RD in the absence of Ca ++ in the extracellular solution. (Aa) Current protocol applied to evoke RD (compare Figure 1Aa ). (b) Voltage responses to subthreshold −20-pA and threshold 0-pA current pulses lasting 200 ms are shown. Voltage responses were recorded after the 15-min pipette presence of anti-Nav1.9 channel antibody (4 μg/ml, anti-Nav1.9, 15 min). (c) Voltage responses to currents steps shown in (a) after loading the cell for 60 min with anti-Nav1.9 channel antibody (4 μg/ml, anti-Nav1.9, 60 min). In (b,c) are shown recordings obtained from the same neuron. (B) Current protocol applied to evoke RD shown in (b,c) . (a) Voltage response to −20 pA subthreshold and 0 pA threshold current pulses lasting 200 ms recorded after the 15 (b) and 60 min (c) pipette presence of IgG (4 μg/ml; IgG, 15 min and IgG, 60 min, respectively). (C) Mean RD durations after 15-min (a) and 60-min (b) intracellular applications of anti-Nav1.9 antibody (anti-Nav1.9) or IgG (IgG). (D) RD current thresholds recorded during 15, 25 and 35 min in the presence of either only Cl − (control) or Cl − and F − (F − ) in the pipette solution; n.s., non-significant.
    Figure Legend Snippet: Effects of an anti-Nav1.9 channel antibody, IgG and F − on RD in the absence of Ca ++ in the extracellular solution. (Aa) Current protocol applied to evoke RD (compare Figure 1Aa ). (b) Voltage responses to subthreshold −20-pA and threshold 0-pA current pulses lasting 200 ms are shown. Voltage responses were recorded after the 15-min pipette presence of anti-Nav1.9 channel antibody (4 μg/ml, anti-Nav1.9, 15 min). (c) Voltage responses to currents steps shown in (a) after loading the cell for 60 min with anti-Nav1.9 channel antibody (4 μg/ml, anti-Nav1.9, 60 min). In (b,c) are shown recordings obtained from the same neuron. (B) Current protocol applied to evoke RD shown in (b,c) . (a) Voltage response to −20 pA subthreshold and 0 pA threshold current pulses lasting 200 ms recorded after the 15 (b) and 60 min (c) pipette presence of IgG (4 μg/ml; IgG, 15 min and IgG, 60 min, respectively). (C) Mean RD durations after 15-min (a) and 60-min (b) intracellular applications of anti-Nav1.9 antibody (anti-Nav1.9) or IgG (IgG). (D) RD current thresholds recorded during 15, 25 and 35 min in the presence of either only Cl − (control) or Cl − and F − (F − ) in the pipette solution; n.s., non-significant.

    Techniques Used: Transferring

    5) Product Images from "A disease mutation reveals a role for NaV1.9 in acute itch"

    Article Title: A disease mutation reveals a role for NaV1.9 in acute itch

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI122481

    Pruritogens influence NaV 1.9 currents.
    Figure Legend Snippet: Pruritogens influence NaV 1.9 currents.

    Techniques Used:

    Pruritogens influence NaV 1.9 currents.
    Figure Legend Snippet: Pruritogens influence NaV 1.9 currents.

    Techniques Used:

    6) Product Images from "Pattern of Functional TTX-Resistant Sodium Channels Reveals a Developmental Stage of Human iPSC- and ESC-Derived Nociceptors"

    Article Title: Pattern of Functional TTX-Resistant Sodium Channels Reveals a Developmental Stage of Human iPSC- and ESC-Derived Nociceptors

    Journal: Stem Cell Reports

    doi: 10.1016/j.stemcr.2015.07.010

    hPSC-Derived Human Nociceptors Express Three Types of TTXr NAVs (A) mRNA levels of SCN5A , SCN10A , and SCN11A in hPSC-derived nociceptors in comparison to undifferentiated hiPSCs (n ≥ 4 independent experiments, measured as duplicates). (B) Immunofluorescence analysis of hiPSC-derived nociceptors revealed a dotted staining pattern for NAV1.5 and NAV1.9 (scale bars represent 20 μm). (C) Top: schematic voltage protocol for recording of voltage-gated sodium currents. Bottom: representative traces of voltage clamp recordings of HUES6- and hiPSC-derived nociceptors and of heterologously expressed human NAV1.8 and NAV1.5. (D and E) Voltage dependencies of activation (D) and steady-state fast inactivation (E) of HUES6-derived nociceptors (triangles, n = 15 cells of one experiment), hiPSC-derived nociceptors (diamonds, n = 23–26 cells), NAV1.8 (circles, n = 10–13 cells of one experiment), and NAV1.5 (squares, n = 8–10 cells of one experiment) and, shown only in (E), co-expression of NAV1.8 and NAV1.5 (triangles, n = 8 cells of one experiment). All error bars indicate the SEM.
    Figure Legend Snippet: hPSC-Derived Human Nociceptors Express Three Types of TTXr NAVs (A) mRNA levels of SCN5A , SCN10A , and SCN11A in hPSC-derived nociceptors in comparison to undifferentiated hiPSCs (n ≥ 4 independent experiments, measured as duplicates). (B) Immunofluorescence analysis of hiPSC-derived nociceptors revealed a dotted staining pattern for NAV1.5 and NAV1.9 (scale bars represent 20 μm). (C) Top: schematic voltage protocol for recording of voltage-gated sodium currents. Bottom: representative traces of voltage clamp recordings of HUES6- and hiPSC-derived nociceptors and of heterologously expressed human NAV1.8 and NAV1.5. (D and E) Voltage dependencies of activation (D) and steady-state fast inactivation (E) of HUES6-derived nociceptors (triangles, n = 15 cells of one experiment), hiPSC-derived nociceptors (diamonds, n = 23–26 cells), NAV1.8 (circles, n = 10–13 cells of one experiment), and NAV1.5 (squares, n = 8–10 cells of one experiment) and, shown only in (E), co-expression of NAV1.8 and NAV1.5 (triangles, n = 8 cells of one experiment). All error bars indicate the SEM.

    Techniques Used: Derivative Assay, Immunofluorescence, Staining, Activation Assay, Expressing

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    Alomone Labs anti scn11a nav1 9 antibody
    mPRMT7 promoted the hyperexcitability of mouse DRG neurons in a <t>SCN11A</t> -dependent manner. Current-clamp responses to 200-ms depolarizing current steps of 50, 100, 150, and 225 pA in representative Scn11a −/− mouse DRG neurons (A-B) and Scn11a +/+ mouse DRG neurons (C-D) expressing the empty vector pcDNA3.1/GFP (mock) and pcDNA3.1-PRMT7/GFP (PRMT7). (E) Rheobase, (F) resting membrane potential (RMP), and (G) V threshold (the threshold at which AP takeoff occurs) were not significantly altered in mock-transfected DRG neurons. Data were statistically analysed by the unpaired Student t test; * P
    Anti Scn11a Nav1 9 Antibody, 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
    https://www.bioz.com/result/anti scn11a nav1 9 antibody/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti scn11a nav1 9 antibody - by Bioz Stars, 2022-07
    93/100 stars
      Buy from Supplier

    93
    Alomone Labs guinea pig anti nav1 9 polyclonal antibody
    <t>Nav1.9</t> knockout affects ribbon synapse density and survival of spiral ganglion neurons. Representative images of ribbon synapse immunostained with Ctbp2 (green) from WT ( a ) and Nav1.9 −/− mice ( b ). c Quantitative analysis of ribbon synapse counts per IHC from five randomly selected visual fields for each mouse. n = 7 for WT group, n = 5 for Nav1.9 −/− group. * p = 0.034 by Mann–Whitney test. Representative images of spiral ganglion neurons in Rosenthal’s canal from WT ( d ) and Nav1.9 −/− mice ( e ). f Spiral ganglion neuron counts in the basal turn, the middle turn and apical turn together in 3 midmodiolar sections for each animal. n = 5 for WT group, n = 4 for Nav1.9 −/− group. * p = 0.014 by Mann–Whitney test. Data are expressed as mean ± s.d
    Guinea Pig Anti Nav1 9 Polyclonal Antibody, 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
    https://www.bioz.com/result/guinea pig anti nav1 9 polyclonal antibody/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    guinea pig anti nav1 9 polyclonal antibody - by Bioz Stars, 2022-07
    93/100 stars
      Buy from Supplier

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    mPRMT7 promoted the hyperexcitability of mouse DRG neurons in a SCN11A -dependent manner. Current-clamp responses to 200-ms depolarizing current steps of 50, 100, 150, and 225 pA in representative Scn11a −/− mouse DRG neurons (A-B) and Scn11a +/+ mouse DRG neurons (C-D) expressing the empty vector pcDNA3.1/GFP (mock) and pcDNA3.1-PRMT7/GFP (PRMT7). (E) Rheobase, (F) resting membrane potential (RMP), and (G) V threshold (the threshold at which AP takeoff occurs) were not significantly altered in mock-transfected DRG neurons. Data were statistically analysed by the unpaired Student t test; * P

    Journal: Pain

    Article Title: Protein arginine methyltransferase 7 modulates neuronal excitability by interacting with NaV1.9

    doi: 10.1097/j.pain.0000000000002421

    Figure Lengend Snippet: mPRMT7 promoted the hyperexcitability of mouse DRG neurons in a SCN11A -dependent manner. Current-clamp responses to 200-ms depolarizing current steps of 50, 100, 150, and 225 pA in representative Scn11a −/− mouse DRG neurons (A-B) and Scn11a +/+ mouse DRG neurons (C-D) expressing the empty vector pcDNA3.1/GFP (mock) and pcDNA3.1-PRMT7/GFP (PRMT7). (E) Rheobase, (F) resting membrane potential (RMP), and (G) V threshold (the threshold at which AP takeoff occurs) were not significantly altered in mock-transfected DRG neurons. Data were statistically analysed by the unpaired Student t test; * P

    Article Snippet: Proteins were detected using specific antibodies: mouse anti-GST antibody (AE001, ABclonal, Wuhan, China), mouse anti-HA antibody (AE008, ABclonal), mouse anti-GFP antibody (AE012, ABclonal), rabbit anti-PRMT7 (A12159, ABclonal), mouse anti-FLAG antibody (M185-3 L, MBL, Tokyo, Japan), rabbit anti-NaV 1.9 antibody (ASC-017, Alomone Labs, Jerusalem, Israel), rabbit anti-methyl (mono) arginine antibody (ICP0801, ImmuneChem, Burnaby, Canada), control mouse immunoglobulin G (IgG), and rabbit IgG (B900620, 30000-0-AP, ProteinTech, Wuhan, China).

    Techniques: Expressing, Plasmid Preparation, Transfection

    Protein arginine methyltransferase 7 affects the current density of Na V 1.9 by promoting its accumulation on the cell membrane. (A) Representative whole-cell sodium currents evoked by voltage from Scn11a −/− mouse DRG neurons electroporated with SCN11A or SCN11A and PRMT7 . (B) Current–voltage relationships in the indicated experimental groups. The peak current density (normalized by membrane capacitance) was statistically analysed (mock, n = 15; hNa V 1.9, n = 25; and hNa V 1.9 + hPRMT7, n = 23), and significant differences were tested by two-way ANOVA, followed by a post hoc Bonferroni test; infection × voltage: F(32, 948) = 5.846, P

    Journal: Pain

    Article Title: Protein arginine methyltransferase 7 modulates neuronal excitability by interacting with NaV1.9

    doi: 10.1097/j.pain.0000000000002421

    Figure Lengend Snippet: Protein arginine methyltransferase 7 affects the current density of Na V 1.9 by promoting its accumulation on the cell membrane. (A) Representative whole-cell sodium currents evoked by voltage from Scn11a −/− mouse DRG neurons electroporated with SCN11A or SCN11A and PRMT7 . (B) Current–voltage relationships in the indicated experimental groups. The peak current density (normalized by membrane capacitance) was statistically analysed (mock, n = 15; hNa V 1.9, n = 25; and hNa V 1.9 + hPRMT7, n = 23), and significant differences were tested by two-way ANOVA, followed by a post hoc Bonferroni test; infection × voltage: F(32, 948) = 5.846, P

    Article Snippet: Proteins were detected using specific antibodies: mouse anti-GST antibody (AE001, ABclonal, Wuhan, China), mouse anti-HA antibody (AE008, ABclonal), mouse anti-GFP antibody (AE012, ABclonal), rabbit anti-PRMT7 (A12159, ABclonal), mouse anti-FLAG antibody (M185-3 L, MBL, Tokyo, Japan), rabbit anti-NaV 1.9 antibody (ASC-017, Alomone Labs, Jerusalem, Israel), rabbit anti-methyl (mono) arginine antibody (ICP0801, ImmuneChem, Burnaby, Canada), control mouse immunoglobulin G (IgG), and rabbit IgG (B900620, 30000-0-AP, ProteinTech, Wuhan, China).

    Techniques: Infection

    Interaction and coexpression of Na V 1.9 with PRMT7. Interaction between hLoop1 and full-length hPRMT7 was analysed by GST pull-down assays (A) and reciprocal coimmunoprecipitation assays (B). (C) Interaction between the intracellular domains of hNa V 1.9 and hPRMT7 was examined by coimmunoprecipitation assays. (D) Interaction of mPRMT7 with mNa V 1.9 in mouse DRG tissues was assessed. Scn11a +/+ or Scn11a −/− mouse DRG tissue lysates were immunoprecipitated using anti-mPRMT7 antibodies and control IgG. The precipitates were immunoblotted with the indicated antibodies. (E) Immunohistochemical analysis of mPRMT7/mNa V 1.9 expression in mouse DRG sections. The sections were stained for mPRMT7 (red) and mNa V 1.9 (green) and DAPI (blue). mPRMT7 showed considerable colocalization with mNa V 1.9 in mouse DRG neurons. Scale bars, 50 μm. (F) Percentages of mPRMT7-positive and mNa V 1.9-positive neurons are shown. DAPI, 4,6-diamidino-2-phenylindole; DRG, dorsal root ganglion; GST, glutathione S-transferase; IgG, immunoglobulin G; hNa V 1.9, human hNa V 1.9; PRMT7, protein arginine methyltransferase 7.

    Journal: Pain

    Article Title: Protein arginine methyltransferase 7 modulates neuronal excitability by interacting with NaV1.9

    doi: 10.1097/j.pain.0000000000002421

    Figure Lengend Snippet: Interaction and coexpression of Na V 1.9 with PRMT7. Interaction between hLoop1 and full-length hPRMT7 was analysed by GST pull-down assays (A) and reciprocal coimmunoprecipitation assays (B). (C) Interaction between the intracellular domains of hNa V 1.9 and hPRMT7 was examined by coimmunoprecipitation assays. (D) Interaction of mPRMT7 with mNa V 1.9 in mouse DRG tissues was assessed. Scn11a +/+ or Scn11a −/− mouse DRG tissue lysates were immunoprecipitated using anti-mPRMT7 antibodies and control IgG. The precipitates were immunoblotted with the indicated antibodies. (E) Immunohistochemical analysis of mPRMT7/mNa V 1.9 expression in mouse DRG sections. The sections were stained for mPRMT7 (red) and mNa V 1.9 (green) and DAPI (blue). mPRMT7 showed considerable colocalization with mNa V 1.9 in mouse DRG neurons. Scale bars, 50 μm. (F) Percentages of mPRMT7-positive and mNa V 1.9-positive neurons are shown. DAPI, 4,6-diamidino-2-phenylindole; DRG, dorsal root ganglion; GST, glutathione S-transferase; IgG, immunoglobulin G; hNa V 1.9, human hNa V 1.9; PRMT7, protein arginine methyltransferase 7.

    Article Snippet: Proteins were detected using specific antibodies: mouse anti-GST antibody (AE001, ABclonal, Wuhan, China), mouse anti-HA antibody (AE008, ABclonal), mouse anti-GFP antibody (AE012, ABclonal), rabbit anti-PRMT7 (A12159, ABclonal), mouse anti-FLAG antibody (M185-3 L, MBL, Tokyo, Japan), rabbit anti-NaV 1.9 antibody (ASC-017, Alomone Labs, Jerusalem, Israel), rabbit anti-methyl (mono) arginine antibody (ICP0801, ImmuneChem, Burnaby, Canada), control mouse immunoglobulin G (IgG), and rabbit IgG (B900620, 30000-0-AP, ProteinTech, Wuhan, China).

    Techniques: Immunoprecipitation, Immunohistochemistry, Expressing, Staining

    DS-437 reduced DRG neuronal excitability and relieved pain hypersensitivity in Scn11a A796G/A796G mice. (A) Current-clamp responses to a 200-ms depolarizing current of 200 pA in representative Scn11a +/+ mouse DRG neurons and Scn11a A796G/A796G mouse DRG neurons with DS-437 or control. (B) Rheobase, (C) resting membrane potential (RMP), and (D) V threshold (the threshold at which AP takeoff occurs) showed no significant changes in DRG neurons treated with or without DS-437. Data were statistically analysed by one-way ANOVA; * P

    Journal: Pain

    Article Title: Protein arginine methyltransferase 7 modulates neuronal excitability by interacting with NaV1.9

    doi: 10.1097/j.pain.0000000000002421

    Figure Lengend Snippet: DS-437 reduced DRG neuronal excitability and relieved pain hypersensitivity in Scn11a A796G/A796G mice. (A) Current-clamp responses to a 200-ms depolarizing current of 200 pA in representative Scn11a +/+ mouse DRG neurons and Scn11a A796G/A796G mouse DRG neurons with DS-437 or control. (B) Rheobase, (C) resting membrane potential (RMP), and (D) V threshold (the threshold at which AP takeoff occurs) showed no significant changes in DRG neurons treated with or without DS-437. Data were statistically analysed by one-way ANOVA; * P

    Article Snippet: Proteins were detected using specific antibodies: mouse anti-GST antibody (AE001, ABclonal, Wuhan, China), mouse anti-HA antibody (AE008, ABclonal), mouse anti-GFP antibody (AE012, ABclonal), rabbit anti-PRMT7 (A12159, ABclonal), mouse anti-FLAG antibody (M185-3 L, MBL, Tokyo, Japan), rabbit anti-NaV 1.9 antibody (ASC-017, Alomone Labs, Jerusalem, Israel), rabbit anti-methyl (mono) arginine antibody (ICP0801, ImmuneChem, Burnaby, Canada), control mouse immunoglobulin G (IgG), and rabbit IgG (B900620, 30000-0-AP, ProteinTech, Wuhan, China).

    Techniques: Mouse Assay

    Effect of AGAP on the dynamic function of Na V 1.9 channels . 1000 nM AGAP did not significantly affect the voltage-dependence of channel activation or steady-state inactivation. (A,B) Effect of AGAP on steady-state activation kinetics of Na V 1.9 currents. V 1/2 was -38.4 ± 1.5 mV in control conditions and -38.2 ± 3.7 mV in the presence of 1000 nM AGAP. Slope factors were 6.1 ± 0.5 and 7.8 ± 1.1 mV, respectively ( n = 7). (C,D) Steady-state inactivated of Nav1.9 in the absence and presence of AGAP. V 1/2 for inactivation was -67.9 ± 2.2 mV in control conditions and -69.6 ± 2.5 mV in the presence of 1000 nM AGAP. Slope factors were -11.0 ± 1.8 and -12.5 ± 2.0 mV, respectively ( P > 0.05, P values are from unpaired t -test. n = 6).

    Journal: Frontiers in Pharmacology

    Article Title: Antinociceptive Effects of AGAP, a Recombinant Neurotoxic Polypeptide: Possible Involvement of the Tetrodotoxin-Resistant Sodium Channels in Small Dorsal Root Ganglia Neurons

    doi: 10.3389/fphar.2016.00496

    Figure Lengend Snippet: Effect of AGAP on the dynamic function of Na V 1.9 channels . 1000 nM AGAP did not significantly affect the voltage-dependence of channel activation or steady-state inactivation. (A,B) Effect of AGAP on steady-state activation kinetics of Na V 1.9 currents. V 1/2 was -38.4 ± 1.5 mV in control conditions and -38.2 ± 3.7 mV in the presence of 1000 nM AGAP. Slope factors were 6.1 ± 0.5 and 7.8 ± 1.1 mV, respectively ( n = 7). (C,D) Steady-state inactivated of Nav1.9 in the absence and presence of AGAP. V 1/2 for inactivation was -67.9 ± 2.2 mV in control conditions and -69.6 ± 2.5 mV in the presence of 1000 nM AGAP. Slope factors were -11.0 ± 1.8 and -12.5 ± 2.0 mV, respectively ( P > 0.05, P values are from unpaired t -test. n = 6).

    Article Snippet: Primary antibodies targeting rat NaV 1.8 (1:200; Alomone), NaV1.9 (1:200; Alomone) and NF200 (1:200; Sigma) were performed for immunohistochemistry overnight at 4°C.

    Techniques: Activation Assay

    Nav1.7 and Nav1.8 protein levels were increased in lumbar DRGs in both intraplantar carrageenan- and CFA-induced inflammation and further attenuated by EA at the ST36 acupoint in mice, but Nav1.9 proteins were not altered. (a) DRGs lysates were immunoreactive with specific antibodies to Nav1.7 and a substantially increased signal at the ipsilateral site, as compared to that of the saline-injected group. Nav1.7 protein levels were attenuated by EA at the ST36 acupoint, as compared to that of the carrageenan- and CFA-induced groups. (b) Nav1.8 displayed similar results to Nav1.7. The protein levels of S-Acu and S-GM were similar to inflamed but not EA group. (c) Nav1.9 protein levels were not changed in both the carrageenan- and CFA-injected sites. Nav1.9 protein levels were not attenuated by EA at the ST36 acupoint, as compared to those of the carrageenan- and CFA-induced groups, either. Nav1.9 proteins were not altered at the ipsilateral site of inflammation and EA stimulation.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Electroacupuncture Reduces Carrageenan- and CFA-Induced Inflammatory Pain Accompanied by Changing the Expression of Nav1.7 and Nav1.8, rather than Nav1.9, in Mice Dorsal Root Ganglia

    doi: 10.1155/2013/312184

    Figure Lengend Snippet: Nav1.7 and Nav1.8 protein levels were increased in lumbar DRGs in both intraplantar carrageenan- and CFA-induced inflammation and further attenuated by EA at the ST36 acupoint in mice, but Nav1.9 proteins were not altered. (a) DRGs lysates were immunoreactive with specific antibodies to Nav1.7 and a substantially increased signal at the ipsilateral site, as compared to that of the saline-injected group. Nav1.7 protein levels were attenuated by EA at the ST36 acupoint, as compared to that of the carrageenan- and CFA-induced groups. (b) Nav1.8 displayed similar results to Nav1.7. The protein levels of S-Acu and S-GM were similar to inflamed but not EA group. (c) Nav1.9 protein levels were not changed in both the carrageenan- and CFA-injected sites. Nav1.9 protein levels were not attenuated by EA at the ST36 acupoint, as compared to those of the carrageenan- and CFA-induced groups, either. Nav1.9 proteins were not altered at the ipsilateral site of inflammation and EA stimulation.

    Article Snippet: DRGs were incubated with primary antibodies prepared in blocking solution at 4°C overnight against Nav1.7 (1 : 1000, Alomone), Nav1.8 (1 : 1000, Alomone), and Nav1.9 (1 : 1000, Alomone).

    Techniques: Mouse Assay, Injection

    Protein levels of Nav1.7, Nav1.8, and Nav1.9 in the L3–L5 DRGs in mice in control, Car, EA, S-Acu, S-GM, CFA, EA, S-Acu, S-GM groups. The percentage of Nav protein levels from lumbar DRGs was presented in each group. * P

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Electroacupuncture Reduces Carrageenan- and CFA-Induced Inflammatory Pain Accompanied by Changing the Expression of Nav1.7 and Nav1.8, rather than Nav1.9, in Mice Dorsal Root Ganglia

    doi: 10.1155/2013/312184

    Figure Lengend Snippet: Protein levels of Nav1.7, Nav1.8, and Nav1.9 in the L3–L5 DRGs in mice in control, Car, EA, S-Acu, S-GM, CFA, EA, S-Acu, S-GM groups. The percentage of Nav protein levels from lumbar DRGs was presented in each group. * P

    Article Snippet: DRGs were incubated with primary antibodies prepared in blocking solution at 4°C overnight against Nav1.7 (1 : 1000, Alomone), Nav1.8 (1 : 1000, Alomone), and Nav1.9 (1 : 1000, Alomone).

    Techniques: Mouse Assay

    Nav1.7 and Nav1.8 expressions were increased in ipsilateral DRGs after intraplantar carrageenan injection and further attenuated by EA at the ST36 acupoint in mice, though Nav1.9 was not different. (a)–(c) Nav1.7, Nav1.8, and Nav1.9 immunoreactive neurons were found in lumbar DRGs at the ipsilateral site of the saline-injected group. (d)-(e) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the carrageenan-injected group, but (f) Nav1.9 immunoreactive neurons were not increased. (g)-(h) Carrageenan-induced increases of Nav1.7 and Nav1.8 were attenuated by EA, as compared to those of the carrageenan-induced group. (i) Nav1.9 immunoreactive neurons were not altered by EA at the ipsilateral site of inflammation. (j)-(k) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-Acu group. (l) Nav1.9 immunoreactive neurons were not altered in the S-Acu group. (m)-(n) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-GM group. (o) Nav1.9 immunoreactive neurons were not altered in the S-GM group. Scale bar = 50 um.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Electroacupuncture Reduces Carrageenan- and CFA-Induced Inflammatory Pain Accompanied by Changing the Expression of Nav1.7 and Nav1.8, rather than Nav1.9, in Mice Dorsal Root Ganglia

    doi: 10.1155/2013/312184

    Figure Lengend Snippet: Nav1.7 and Nav1.8 expressions were increased in ipsilateral DRGs after intraplantar carrageenan injection and further attenuated by EA at the ST36 acupoint in mice, though Nav1.9 was not different. (a)–(c) Nav1.7, Nav1.8, and Nav1.9 immunoreactive neurons were found in lumbar DRGs at the ipsilateral site of the saline-injected group. (d)-(e) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the carrageenan-injected group, but (f) Nav1.9 immunoreactive neurons were not increased. (g)-(h) Carrageenan-induced increases of Nav1.7 and Nav1.8 were attenuated by EA, as compared to those of the carrageenan-induced group. (i) Nav1.9 immunoreactive neurons were not altered by EA at the ipsilateral site of inflammation. (j)-(k) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-Acu group. (l) Nav1.9 immunoreactive neurons were not altered in the S-Acu group. (m)-(n) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-GM group. (o) Nav1.9 immunoreactive neurons were not altered in the S-GM group. Scale bar = 50 um.

    Article Snippet: DRGs were incubated with primary antibodies prepared in blocking solution at 4°C overnight against Nav1.7 (1 : 1000, Alomone), Nav1.8 (1 : 1000, Alomone), and Nav1.9 (1 : 1000, Alomone).

    Techniques: Injection, Mouse Assay

    Nav1.7 and Nav1.8 expressions were increased in ipsilateral DRGs after intraplantar CFA injection and further attenuated by EA at the ST36 acupoint in mice, though Nav1.9 was not different. (a)–(c) Nav1.7, Nav1.8, and Nav1.9 immunoreactive neurons were found in lumbar DRGs at the ipsilateral site of the saline-injected group. (d)-(e) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the CFA-injected group, but (f) Nav1.9 immunoreactive neurons were not increased. (g)-(h) CFA-induced increases of Nav1.7 and Nav1.8 were attenuated by EA, as compared to those of the CFA-induced group. (i) Nav1.9 immunoreactive neurons were not altered by EA at the ipsilateral site of inflammation. (j)-(k) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-Acu group. (l) Nav1.9 immunoreactive neurons were not altered in the S-Acu group. (m)-(n) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-GM group. (o) Nav1.9 immunoreactive neurons were not altered in the S-GM group. Scale bar = 50 um.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Electroacupuncture Reduces Carrageenan- and CFA-Induced Inflammatory Pain Accompanied by Changing the Expression of Nav1.7 and Nav1.8, rather than Nav1.9, in Mice Dorsal Root Ganglia

    doi: 10.1155/2013/312184

    Figure Lengend Snippet: Nav1.7 and Nav1.8 expressions were increased in ipsilateral DRGs after intraplantar CFA injection and further attenuated by EA at the ST36 acupoint in mice, though Nav1.9 was not different. (a)–(c) Nav1.7, Nav1.8, and Nav1.9 immunoreactive neurons were found in lumbar DRGs at the ipsilateral site of the saline-injected group. (d)-(e) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the CFA-injected group, but (f) Nav1.9 immunoreactive neurons were not increased. (g)-(h) CFA-induced increases of Nav1.7 and Nav1.8 were attenuated by EA, as compared to those of the CFA-induced group. (i) Nav1.9 immunoreactive neurons were not altered by EA at the ipsilateral site of inflammation. (j)-(k) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-Acu group. (l) Nav1.9 immunoreactive neurons were not altered in the S-Acu group. (m)-(n) Nav1.7 and Nav1.8 immunoreactive neurons were increased in the S-GM group. (o) Nav1.9 immunoreactive neurons were not altered in the S-GM group. Scale bar = 50 um.

    Article Snippet: DRGs were incubated with primary antibodies prepared in blocking solution at 4°C overnight against Nav1.7 (1 : 1000, Alomone), Nav1.8 (1 : 1000, Alomone), and Nav1.9 (1 : 1000, Alomone).

    Techniques: Injection, Mouse Assay

    Nav1.9 knockout affects ribbon synapse density and survival of spiral ganglion neurons. Representative images of ribbon synapse immunostained with Ctbp2 (green) from WT ( a ) and Nav1.9 −/− mice ( b ). c Quantitative analysis of ribbon synapse counts per IHC from five randomly selected visual fields for each mouse. n = 7 for WT group, n = 5 for Nav1.9 −/− group. * p = 0.034 by Mann–Whitney test. Representative images of spiral ganglion neurons in Rosenthal’s canal from WT ( d ) and Nav1.9 −/− mice ( e ). f Spiral ganglion neuron counts in the basal turn, the middle turn and apical turn together in 3 midmodiolar sections for each animal. n = 5 for WT group, n = 4 for Nav1.9 −/− group. * p = 0.014 by Mann–Whitney test. Data are expressed as mean ± s.d

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: Nav1.9 knockout affects ribbon synapse density and survival of spiral ganglion neurons. Representative images of ribbon synapse immunostained with Ctbp2 (green) from WT ( a ) and Nav1.9 −/− mice ( b ). c Quantitative analysis of ribbon synapse counts per IHC from five randomly selected visual fields for each mouse. n = 7 for WT group, n = 5 for Nav1.9 −/− group. * p = 0.034 by Mann–Whitney test. Representative images of spiral ganglion neurons in Rosenthal’s canal from WT ( d ) and Nav1.9 −/− mice ( e ). f Spiral ganglion neuron counts in the basal turn, the middle turn and apical turn together in 3 midmodiolar sections for each animal. n = 5 for WT group, n = 4 for Nav1.9 −/− group. * p = 0.014 by Mann–Whitney test. Data are expressed as mean ± s.d

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: Knock-Out, Mouse Assay, Immunohistochemistry, MANN-WHITNEY

    Nav1.9 knockout does not affect the morphology of hair cells. a The digital image of a dissected cochlea including the hook region (left) from a 4 months old mouse. Schematic drawing of the same cochlea with percent distance from the apex plotted (right). b Scale is showing frequency, percent distance from the apex, and distance (mm), according to Müller et al. [ 22 ]: x = 100 − (156.53 − 82.46 * log(F)). The full basilar membrane length is 6.3 mm for this particular cochlea. C, Images of organ of Cortis from 4 months old mice stained by DAPI (blue), with the apical turn (0–25% distance from the apex), the middle turn (30–55% distance from the apex) and the basal turn (60–85% distance from the apex). d Images of the organ of Corti of Nav1.9 −/− mice at postnatal ages of 2 months by SEM, containing the apical turn ( b1 – b3 ), the middle turn ( b4 – b6 ), and the basal turn ( b7 – b9 )

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: Nav1.9 knockout does not affect the morphology of hair cells. a The digital image of a dissected cochlea including the hook region (left) from a 4 months old mouse. Schematic drawing of the same cochlea with percent distance from the apex plotted (right). b Scale is showing frequency, percent distance from the apex, and distance (mm), according to Müller et al. [ 22 ]: x = 100 − (156.53 − 82.46 * log(F)). The full basilar membrane length is 6.3 mm for this particular cochlea. C, Images of organ of Cortis from 4 months old mice stained by DAPI (blue), with the apical turn (0–25% distance from the apex), the middle turn (30–55% distance from the apex) and the basal turn (60–85% distance from the apex). d Images of the organ of Corti of Nav1.9 −/− mice at postnatal ages of 2 months by SEM, containing the apical turn ( b1 – b3 ), the middle turn ( b4 – b6 ), and the basal turn ( b7 – b9 )

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: Knock-Out, Mouse Assay, Staining

    CRISPR/Cas 9-mediated generation of a Nav1.9 −/− mouse model. a A representative illustration of the CRISPR/Cas9 targeting strategy for generating Nav1.9 knockout (KO) mice. The Cas9 mRNA and two single guide RNAs targeting a region from SCN11A exon 3 to 5, were microinjected into mouse zygotes. b Schematic diagram of primer pair design for PCR genotyping, a representative PCR genotyping result for Nav1.9 wild-type (WT), homozygous (Nav1.9 −/− ) and heterozygous (Nav1.9 +/− ), the region of junction of DSB is absent in the WT mice. Primer 2: primer pairs containing forward primer and KO specific reverse primer; Primer 1: primer pairs containing forward primer and WT specific reverse primer. c This successfully eliminated all of exon 3, 4 and 5, as confirmed by Sanger sequencing, induces reading frame shift and thus a premature translational- termination codon during the truncated protein expression. d The protein expression of Nav1.9 in the cochleas of Nav1.9 −/− mice (n = 3) or WT mice (n = 4) was measured by western blot

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: CRISPR/Cas 9-mediated generation of a Nav1.9 −/− mouse model. a A representative illustration of the CRISPR/Cas9 targeting strategy for generating Nav1.9 knockout (KO) mice. The Cas9 mRNA and two single guide RNAs targeting a region from SCN11A exon 3 to 5, were microinjected into mouse zygotes. b Schematic diagram of primer pair design for PCR genotyping, a representative PCR genotyping result for Nav1.9 wild-type (WT), homozygous (Nav1.9 −/− ) and heterozygous (Nav1.9 +/− ), the region of junction of DSB is absent in the WT mice. Primer 2: primer pairs containing forward primer and KO specific reverse primer; Primer 1: primer pairs containing forward primer and WT specific reverse primer. c This successfully eliminated all of exon 3, 4 and 5, as confirmed by Sanger sequencing, induces reading frame shift and thus a premature translational- termination codon during the truncated protein expression. d The protein expression of Nav1.9 in the cochleas of Nav1.9 −/− mice (n = 3) or WT mice (n = 4) was measured by western blot

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: CRISPR, Knock-Out, Mouse Assay, Polymerase Chain Reaction, Sequencing, Expressing, Western Blot

    Distribution of Nav1.9 in primary auditory afferents. a The voltage-gated sodium channel Nav1.9 and Nav1.1 mRNA levels in modiolus of WT ICR mice at the postnatal 0, 7th, 14th, 21th, 28th and 60th day. Each time point contains 5 mice. * p = 0.028, ** p = 0.004. b A schematic representing the localization of Nav1.9 channels at primary afferent peripheral nerve endings on hair cells in cochlea, in SGN somata, in the auditory nerve located within the modiolus, and in the cochlear nuclei. c Nav1.9 is present in cochlea basilar membrane by surface preparation technique and immunofluorescence staining in cryo-section. c1 Horizontal section showing three rows of OHCs and one row of IHCs. In a linear distribution below the IHCs, Nav1.9 (purple) is in the afferent endings beneath the IHC bases. Also stained are the afferent radial fibers leading through the tunnel of Corti to their first hemi-nodes beneath the foramina nervosa. Scales = 75 μm. c2 The diagram of the cochlea’s afferent innervations pattern. c3 Nav1.9 is in the nerve endings of internal spiral fibers or radial fibers beneath IHC (red), the cilia of which exhibit phalloidin labeling (green). Scales = 50 μm. c4 The high magnification image of c3. Scale = 10 μm. d The expression of Nav1.9 in the SGNs of P60 WT mouse was measured by immunofluorescence. Nav1.9, MBP, and cell nucleus are stained as red, green and blue, respectively. e Some neurons from the dorsal cochlear nucleus are labeled by Nav1.9 (red)

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: Distribution of Nav1.9 in primary auditory afferents. a The voltage-gated sodium channel Nav1.9 and Nav1.1 mRNA levels in modiolus of WT ICR mice at the postnatal 0, 7th, 14th, 21th, 28th and 60th day. Each time point contains 5 mice. * p = 0.028, ** p = 0.004. b A schematic representing the localization of Nav1.9 channels at primary afferent peripheral nerve endings on hair cells in cochlea, in SGN somata, in the auditory nerve located within the modiolus, and in the cochlear nuclei. c Nav1.9 is present in cochlea basilar membrane by surface preparation technique and immunofluorescence staining in cryo-section. c1 Horizontal section showing three rows of OHCs and one row of IHCs. In a linear distribution below the IHCs, Nav1.9 (purple) is in the afferent endings beneath the IHC bases. Also stained are the afferent radial fibers leading through the tunnel of Corti to their first hemi-nodes beneath the foramina nervosa. Scales = 75 μm. c2 The diagram of the cochlea’s afferent innervations pattern. c3 Nav1.9 is in the nerve endings of internal spiral fibers or radial fibers beneath IHC (red), the cilia of which exhibit phalloidin labeling (green). Scales = 50 μm. c4 The high magnification image of c3. Scale = 10 μm. d The expression of Nav1.9 in the SGNs of P60 WT mouse was measured by immunofluorescence. Nav1.9, MBP, and cell nucleus are stained as red, green and blue, respectively. e Some neurons from the dorsal cochlear nucleus are labeled by Nav1.9 (red)

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: Mouse Assay, Immunofluorescence, Staining, Immunohistochemistry, Labeling, Expressing

    Auditory compound action potentials are affected by Nav1.9 knockout. Nav1.9 knockout induces higher CAP P1 threshold, * p = 0.013 with Mann–Whitney test ( a ), lower CAP P1 amplitude, * p = 0.041 with independent samples t test ( b ), compared with WT group; c the CAP P1 latency is not affected at the time point of postnatal day 60, p = 0.242 with independent samples t test. d Representative CAP waveforms from a WT mouse. e Representative CAP waveforms from a Nav1.9 −/− mice. Data are expressed as mean ± s.d

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: Auditory compound action potentials are affected by Nav1.9 knockout. Nav1.9 knockout induces higher CAP P1 threshold, * p = 0.013 with Mann–Whitney test ( a ), lower CAP P1 amplitude, * p = 0.041 with independent samples t test ( b ), compared with WT group; c the CAP P1 latency is not affected at the time point of postnatal day 60, p = 0.242 with independent samples t test. d Representative CAP waveforms from a WT mouse. e Representative CAP waveforms from a Nav1.9 −/− mice. Data are expressed as mean ± s.d

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: Knock-Out, MANN-WHITNEY, Mouse Assay

    Audiological characterization of Nav1.9 −/− mice. a Mean ABR thresholds of six wild-type, four heterozygous and seven homozygous versus sound frequency, ** p = 0.002, ** p = 0.001 at 12 kHz compared with homozygous, * p = 0.01, *** p = 0.000 at 16 kHz compared with homozygous by one-way ANOVA with Bonferroni’s post-hoc test. b Example of ABR waveforms at 16 kHz in one ear of a wild-type superimposed on an example of ABR waveforms in one ear of Nav1.9 −/− mice. c ABR thresholds of WT and homozygous mice of postnatal day 21 to 60 at 8 kHz. p = 0.807 at P21; p = 0.932 at P30; p = 0.504 with independent samples t test; n.s.: not significant. d ABR threshold of WT and homozygous mice of postnatal day 21 to 60 at 16 kHz. * p = 0.016, ** p = 0.006, *** p = 0.000 with Mann–Whitney test. Data are expressed as mean ± s.d

    Journal: BMC Neuroscience

    Article Title: SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves

    doi: 10.1186/s12868-021-00613-8

    Figure Lengend Snippet: Audiological characterization of Nav1.9 −/− mice. a Mean ABR thresholds of six wild-type, four heterozygous and seven homozygous versus sound frequency, ** p = 0.002, ** p = 0.001 at 12 kHz compared with homozygous, * p = 0.01, *** p = 0.000 at 16 kHz compared with homozygous by one-way ANOVA with Bonferroni’s post-hoc test. b Example of ABR waveforms at 16 kHz in one ear of a wild-type superimposed on an example of ABR waveforms in one ear of Nav1.9 −/− mice. c ABR thresholds of WT and homozygous mice of postnatal day 21 to 60 at 8 kHz. p = 0.807 at P21; p = 0.932 at P30; p = 0.504 with independent samples t test; n.s.: not significant. d ABR threshold of WT and homozygous mice of postnatal day 21 to 60 at 16 kHz. * p = 0.016, ** p = 0.006, *** p = 0.000 with Mann–Whitney test. Data are expressed as mean ± s.d

    Article Snippet: Immunohistochemistry and synaptic counts After washes with 0.1% Triton X-100 in PBS, sections on adhesion microscope slides were blocked with 10% normal goat serum (ZLI-9021, ZSGB-BIO) and incubated with rabbit anti-SCN11A polyclonal antibody (AT322395, 1:200, OriGene, Rockville, MD), guinea pig anti-Nav1.9 polyclonal antibody (AGP-030, 1:200, alomone labs, Israel), mouse anti-CtBP2 (612044, 1:100, BD Biosciences), in 10% goat serum diluted in 0.1 M PBS at 4 ℃ overnight and then incubated with secondary antibodies containing anti-mouse Alexa Fluo™ 488 (lot 1810918, 1:400, goat, Thermo Fisher), anti-rabbit Alexa Fluor™ 568 (lot 1494753, 1:400, goat, Thermo Fisher), or anti-guinea pig Alexa FluroTM647 (A-21450, 1:400, goat, Thermo Fisher).

    Techniques: Mouse Assay, MANN-WHITNEY