bay k8644  (Alomone Labs)


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    Structured Review

    Alomone Labs bay k8644
    In (a) we show the percentage of singly- and polyinnervated NMJ after 4 applications over the LAL surface (one application every day between P5–P8 (observation at P9) of one of the following VGCC inhibitor substances: nitrendipine (NT 1 μM, an L-type channel blocker), ω-conotoxin-GVIA (ω-CON 1 μM, N-type channel blocker), and ω-agatoxin-IVA (ω-AGA 100 nM, P/Q-type blocker). Also, the L activator <t>Bay-K8644</t> (5 μM), the P/Q- and N-type activator GV-58 (20 μM), and the intracellular calcium chelator BAPTA-AM (5 μM). The histogram in ( b ) shows the percentage of S1-S4 clusters in the untreated control mice (PBS) and after the 4 applications of the aforesaid substances. Data were presented as percentages of NMJ ± SD. Fisher’s test: * p
    Bay K8644, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bay k8644/product/Alomone Labs
    Average 94 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    bay k8644 - by Bioz Stars, 2022-12
    94/100 stars

    Images

    1) Product Images from "Involvement of the Voltage-Gated Calcium Channels L- P/Q- and N-Types in Synapse Elimination During Neuromuscular Junction Development"

    Article Title: Involvement of the Voltage-Gated Calcium Channels L- P/Q- and N-Types in Synapse Elimination During Neuromuscular Junction Development

    Journal: Molecular Neurobiology

    doi: 10.1007/s12035-022-02818-2

    In (a) we show the percentage of singly- and polyinnervated NMJ after 4 applications over the LAL surface (one application every day between P5–P8 (observation at P9) of one of the following VGCC inhibitor substances: nitrendipine (NT 1 μM, an L-type channel blocker), ω-conotoxin-GVIA (ω-CON 1 μM, N-type channel blocker), and ω-agatoxin-IVA (ω-AGA 100 nM, P/Q-type blocker). Also, the L activator Bay-K8644 (5 μM), the P/Q- and N-type activator GV-58 (20 μM), and the intracellular calcium chelator BAPTA-AM (5 μM). The histogram in ( b ) shows the percentage of S1-S4 clusters in the untreated control mice (PBS) and after the 4 applications of the aforesaid substances. Data were presented as percentages of NMJ ± SD. Fisher’s test: * p
    Figure Legend Snippet: In (a) we show the percentage of singly- and polyinnervated NMJ after 4 applications over the LAL surface (one application every day between P5–P8 (observation at P9) of one of the following VGCC inhibitor substances: nitrendipine (NT 1 μM, an L-type channel blocker), ω-conotoxin-GVIA (ω-CON 1 μM, N-type channel blocker), and ω-agatoxin-IVA (ω-AGA 100 nM, P/Q-type blocker). Also, the L activator Bay-K8644 (5 μM), the P/Q- and N-type activator GV-58 (20 μM), and the intracellular calcium chelator BAPTA-AM (5 μM). The histogram in ( b ) shows the percentage of S1-S4 clusters in the untreated control mice (PBS) and after the 4 applications of the aforesaid substances. Data were presented as percentages of NMJ ± SD. Fisher’s test: * p

    Techniques Used: Mouse Assay

    2) Product Images from "Involvement of the Voltage-Gated Calcium Channels L- P/Q- and N-Types in Synapse Elimination During Neuromuscular Junction Development"

    Article Title: Involvement of the Voltage-Gated Calcium Channels L- P/Q- and N-Types in Synapse Elimination During Neuromuscular Junction Development

    Journal: Molecular Neurobiology

    doi: 10.1007/s12035-022-02818-2

    In (a) we show the percentage of singly- and polyinnervated NMJ after 4 applications over the LAL surface (one application every day between P5–P8 (observation at P9) of one of the following VGCC inhibitor substances: nitrendipine (NT 1 μM, an L-type channel blocker), ω-conotoxin-GVIA (ω-CON 1 μM, N-type channel blocker), and ω-agatoxin-IVA (ω-AGA 100 nM, P/Q-type blocker). Also, the L activator Bay-K8644 (5 μM), the P/Q- and N-type activator GV-58 (20 μM), and the intracellular calcium chelator BAPTA-AM (5 μM). The histogram in ( b ) shows the percentage of S1-S4 clusters in the untreated control mice (PBS) and after the 4 applications of the aforesaid substances. Data were presented as percentages of NMJ ± SD. Fisher’s test: * p
    Figure Legend Snippet: In (a) we show the percentage of singly- and polyinnervated NMJ after 4 applications over the LAL surface (one application every day between P5–P8 (observation at P9) of one of the following VGCC inhibitor substances: nitrendipine (NT 1 μM, an L-type channel blocker), ω-conotoxin-GVIA (ω-CON 1 μM, N-type channel blocker), and ω-agatoxin-IVA (ω-AGA 100 nM, P/Q-type blocker). Also, the L activator Bay-K8644 (5 μM), the P/Q- and N-type activator GV-58 (20 μM), and the intracellular calcium chelator BAPTA-AM (5 μM). The histogram in ( b ) shows the percentage of S1-S4 clusters in the untreated control mice (PBS) and after the 4 applications of the aforesaid substances. Data were presented as percentages of NMJ ± SD. Fisher’s test: * p

    Techniques Used: Mouse Assay

    3) Product Images from "Pharmacological Dissection of the Crosstalk between NaV and CaV Channels in GH3b6 Cells"

    Article Title: Pharmacological Dissection of the Crosstalk between NaV and CaV Channels in GH3b6 Cells

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms23020827

    Effects of BIII 890CL on Ca 2+ responses triggered by VTD or Bay K8644. ( A ) Representative Fura-2 fluorescence kinetic traces illustrating Ca 2+ response induced by 10 µM of VTD, alone or co-injected with 1 µM of TTX or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. ( B ) Concentration–inhibition relationship of VTD-induced Ca 2+ responses by BIII 890CL, (IC50 = 1.47 ± 0.18 µM, Hill slope = 1.26 ± 0.23, R 2 = 0.94). ( C ) Representative Fura-2 fluorescence kinetics traces illustrating Ca 2+ response induced by 1 µM of Bay K8644, a specific L-type Ca V channel activator, alone or co-injected with 10 µM of nifedipine or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. Data represent the mean ± SEM ( n = 3) of recordings of two independent experiments.
    Figure Legend Snippet: Effects of BIII 890CL on Ca 2+ responses triggered by VTD or Bay K8644. ( A ) Representative Fura-2 fluorescence kinetic traces illustrating Ca 2+ response induced by 10 µM of VTD, alone or co-injected with 1 µM of TTX or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. ( B ) Concentration–inhibition relationship of VTD-induced Ca 2+ responses by BIII 890CL, (IC50 = 1.47 ± 0.18 µM, Hill slope = 1.26 ± 0.23, R 2 = 0.94). ( C ) Representative Fura-2 fluorescence kinetics traces illustrating Ca 2+ response induced by 1 µM of Bay K8644, a specific L-type Ca V channel activator, alone or co-injected with 10 µM of nifedipine or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. Data represent the mean ± SEM ( n = 3) of recordings of two independent experiments.

    Techniques Used: Fluorescence, Injection, Negative Control, Concentration Assay, Inhibition

    4) Product Images from "Pharmacological Dissection of the Crosstalk between NaV and CaV Channels in GH3b6 Cells"

    Article Title: Pharmacological Dissection of the Crosstalk between NaV and CaV Channels in GH3b6 Cells

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms23020827

    Effects of BIII 890CL on Ca 2+ responses triggered by VTD or Bay K8644. ( A ) Representative Fura-2 fluorescence kinetic traces illustrating Ca 2+ response induced by 10 µM of VTD, alone or co-injected with 1 µM of TTX or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. ( B ) Concentration–inhibition relationship of VTD-induced Ca 2+ responses by BIII 890CL, (IC50 = 1.47 ± 0.18 µM, Hill slope = 1.26 ± 0.23, R 2 = 0.94). ( C ) Representative Fura-2 fluorescence kinetics traces illustrating Ca 2+ response induced by 1 µM of Bay K8644, a specific L-type Ca V channel activator, alone or co-injected with 10 µM of nifedipine or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. Data represent the mean ± SEM ( n = 3) of recordings of two independent experiments.
    Figure Legend Snippet: Effects of BIII 890CL on Ca 2+ responses triggered by VTD or Bay K8644. ( A ) Representative Fura-2 fluorescence kinetic traces illustrating Ca 2+ response induced by 10 µM of VTD, alone or co-injected with 1 µM of TTX or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. ( B ) Concentration–inhibition relationship of VTD-induced Ca 2+ responses by BIII 890CL, (IC50 = 1.47 ± 0.18 µM, Hill slope = 1.26 ± 0.23, R 2 = 0.94). ( C ) Representative Fura-2 fluorescence kinetics traces illustrating Ca 2+ response induced by 1 µM of Bay K8644, a specific L-type Ca V channel activator, alone or co-injected with 10 µM of nifedipine or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. Data represent the mean ± SEM ( n = 3) of recordings of two independent experiments.

    Techniques Used: Fluorescence, Injection, Negative Control, Concentration Assay, Inhibition

    5) Product Images from "Kv2.1 mediates spatial and functional coupling of L-type calcium channels and ryanodine receptors in neurons"

    Article Title: Kv2.1 mediates spatial and functional coupling of L-type calcium channels and ryanodine receptors in neurons

    Journal: bioRxiv

    doi: 10.1101/702514

    Kv2.1 expression increases the frequency of LTCC- and RyR-mediated sparks reconstituted in HEK293T cells. (A) TIRF image of a HEK293T cell expressing Cav1.2, RyR2, STAC1, and the LTCC auxiliary subunits β3 and α2δ1, and loaded with Cal-590 AM. (B-C) TIRF images of HEK293T cells additionally coexpressing Kv2.1. Dashed line indicates ROI depicted in corresponding kymographs (scale bar in panels A-C: 10 µm). (D-F) Kymograph showing the localized Ca 2+ release events detected in the ROI on the cell in panels A-C, respectively. In (F), 100 µM tetracaine was added at the indicated time point. (G) Kymograph showing the localized Ca 2+ release events detected in a cell treated with 500 nM Bay K8644 at the indicated time point. (H) Illustration of the membrane topology of a single Kv2.1 α subunit depicting the locations of the P404W and S586A point mutations. (I) Summary data of the amplitude, frequency and spatial spread (width) of all sparks recorded from HEK293T cells expressing Cav1.2, RyR2, and auxiliary subunits, without (control) or with addition of the indicated Kv2.1 isoforms. Each point corresponds to a single cell (width: *p=0.048; amplitude: **p
    Figure Legend Snippet: Kv2.1 expression increases the frequency of LTCC- and RyR-mediated sparks reconstituted in HEK293T cells. (A) TIRF image of a HEK293T cell expressing Cav1.2, RyR2, STAC1, and the LTCC auxiliary subunits β3 and α2δ1, and loaded with Cal-590 AM. (B-C) TIRF images of HEK293T cells additionally coexpressing Kv2.1. Dashed line indicates ROI depicted in corresponding kymographs (scale bar in panels A-C: 10 µm). (D-F) Kymograph showing the localized Ca 2+ release events detected in the ROI on the cell in panels A-C, respectively. In (F), 100 µM tetracaine was added at the indicated time point. (G) Kymograph showing the localized Ca 2+ release events detected in a cell treated with 500 nM Bay K8644 at the indicated time point. (H) Illustration of the membrane topology of a single Kv2.1 α subunit depicting the locations of the P404W and S586A point mutations. (I) Summary data of the amplitude, frequency and spatial spread (width) of all sparks recorded from HEK293T cells expressing Cav1.2, RyR2, and auxiliary subunits, without (control) or with addition of the indicated Kv2.1 isoforms. Each point corresponds to a single cell (width: *p=0.048; amplitude: **p

    Techniques Used: Expressing

    6) Product Images from "Role of age, Rho‐kinase 2 expression, and G protein‐mediated signaling in the myogenic response in mouse small mesenteric arteries. Role of age, Rho‐kinase 2 expression, and G protein‐mediated signaling in the myogenic response in mouse small mesenteric arteries"

    Article Title: Role of age, Rho‐kinase 2 expression, and G protein‐mediated signaling in the myogenic response in mouse small mesenteric arteries. Role of age, Rho‐kinase 2 expression, and G protein‐mediated signaling in the myogenic response in mouse small mesenteric arteries

    Journal: Physiological Reports

    doi: 10.14814/phy2.13863

    (A) Effect of the L‐type Ca 2+ channel agonist BayK 8644 (2 μ mol L −1 ) on MT . A total of five vessels from five young mice were tested. (B) In a parallel series of experiment the effect of the ROCK 2 inhibitor KD 025 (5 μ mol L −1 ) in the presence of BayK 8644 was investigated. A total of five vessels from four young mice were tested. (C) For comparison, the effect of ROCK 2 inhibition with KD 025 (5 μ mol L −1 ) was tested in a small pial arteries from three healthy Göttingen minipigs. This original trace showing a pial vessel that develops MT at 60, 90 and 120 mm Hg, and MT is strongly inhibited by direct bath application of KD 025. Note that the full effect of KD 025 takes 5–10 min to be established. (D) The same experiment but with results for all three minipigs depicted as myogenic tone. Also shown is the effect of washout (15–20 min) of the drug. (E) Active vasoconstriction to direct bath application of ET ‐1 (20 and 50 nmol L −1 ) in small pial arteries from three minipigs pressurized at 60 mm Hg. Potent inhibition of vascular tone is induced by KD 025, and the remainder of tone is abolished by direct bath application of the L‐type antagonist nifedipine (10 μ mol L −1 ).
    Figure Legend Snippet: (A) Effect of the L‐type Ca 2+ channel agonist BayK 8644 (2 μ mol L −1 ) on MT . A total of five vessels from five young mice were tested. (B) In a parallel series of experiment the effect of the ROCK 2 inhibitor KD 025 (5 μ mol L −1 ) in the presence of BayK 8644 was investigated. A total of five vessels from four young mice were tested. (C) For comparison, the effect of ROCK 2 inhibition with KD 025 (5 μ mol L −1 ) was tested in a small pial arteries from three healthy Göttingen minipigs. This original trace showing a pial vessel that develops MT at 60, 90 and 120 mm Hg, and MT is strongly inhibited by direct bath application of KD 025. Note that the full effect of KD 025 takes 5–10 min to be established. (D) The same experiment but with results for all three minipigs depicted as myogenic tone. Also shown is the effect of washout (15–20 min) of the drug. (E) Active vasoconstriction to direct bath application of ET ‐1 (20 and 50 nmol L −1 ) in small pial arteries from three minipigs pressurized at 60 mm Hg. Potent inhibition of vascular tone is induced by KD 025, and the remainder of tone is abolished by direct bath application of the L‐type antagonist nifedipine (10 μ mol L −1 ).

    Techniques Used: Mouse Assay, Inhibition

    7) Product Images from "Dynamics of Insulin Secretion from EndoC-βH1 β-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues"

    Article Title: Dynamics of Insulin Secretion from EndoC-βH1 β-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues

    Journal: Journal of Diabetes Research

    doi: 10.1155/2017/2309630

    Kinetic profiles of insulin secretion from perifused EndoC- β H1  β -cell pseudoislets in response to a 30 min stimulation with glibenclamide (10  μ M) (a) ( n  = 5) as well as with Bay K 8644 (1  μ M) (b) ( n  = 5) in the presence of glucose (10 mM) (a) ( n  = 7). After a 20 min preperifusion phase with basal glucose (3 mM), a 30 min stimulation period and thereafter a return of the perifusion to basal glucose medium for another 30 min are depicted. Shown are means ± SEM of insulin release rates expressed as ng/min and per 100 pseudoislets (PI).
    Figure Legend Snippet: Kinetic profiles of insulin secretion from perifused EndoC- β H1 β -cell pseudoislets in response to a 30 min stimulation with glibenclamide (10  μ M) (a) ( n = 5) as well as with Bay K 8644 (1  μ M) (b) ( n = 5) in the presence of glucose (10 mM) (a) ( n = 7). After a 20 min preperifusion phase with basal glucose (3 mM), a 30 min stimulation period and thereafter a return of the perifusion to basal glucose medium for another 30 min are depicted. Shown are means ± SEM of insulin release rates expressed as ng/min and per 100 pseudoislets (PI).

    Techniques Used:

    8) Product Images from "Dynamics of Insulin Secretion from EndoC-βH1 β-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues"

    Article Title: Dynamics of Insulin Secretion from EndoC-βH1 β-Cell Pseudoislets in Response to Glucose and Other Nutrient and Nonnutrient Secretagogues

    Journal: Journal of Diabetes Research

    doi: 10.1155/2017/2309630

    Kinetic profiles of insulin secretion from perifused EndoC- β H1  β -cell pseudoislets in response to a 30 min stimulation with glibenclamide (10  μ M) (a) ( n  = 5) as well as with Bay K 8644 (1  μ M) (b) ( n  = 5) in the presence of glucose (10 mM) (a) ( n  = 7). After a 20 min preperifusion phase with basal glucose (3 mM), a 30 min stimulation period and thereafter a return of the perifusion to basal glucose medium for another 30 min are depicted. Shown are means ± SEM of insulin release rates expressed as ng/min and per 100 pseudoislets (PI).
    Figure Legend Snippet: Kinetic profiles of insulin secretion from perifused EndoC- β H1 β -cell pseudoislets in response to a 30 min stimulation with glibenclamide (10  μ M) (a) ( n = 5) as well as with Bay K 8644 (1  μ M) (b) ( n = 5) in the presence of glucose (10 mM) (a) ( n = 7). After a 20 min preperifusion phase with basal glucose (3 mM), a 30 min stimulation period and thereafter a return of the perifusion to basal glucose medium for another 30 min are depicted. Shown are means ± SEM of insulin release rates expressed as ng/min and per 100 pseudoislets (PI).

    Techniques Used:

    9) Product Images from "Differential outgrowth of axons and their branches is regulated by localized calcium transients"

    Article Title: Differential outgrowth of axons and their branches is regulated by localized calcium transients

    Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

    doi: 10.1523/JNEUROSCI.4548-07.2008

    Bath application of BayK 8644 increases differential process outgrowth. A, Timelapse images of a cortical neuron exposed to BayK for 8 hours, showing extension of the primary axon extends and retraction of the branch. B, C, Phase images showing the effect
    Figure Legend Snippet: Bath application of BayK 8644 increases differential process outgrowth. A, Timelapse images of a cortical neuron exposed to BayK for 8 hours, showing extension of the primary axon extends and retraction of the branch. B, C, Phase images showing the effect

    Techniques Used:

    Bath application of BayK 8644 induces localized calcium transients. A, DIC (left) and fluorescence images (right) of a cortical neuron exposed to BayK 8644. Bath application of BayK at 0:00 induced high frequency localized calcium transients primarily
    Figure Legend Snippet: Bath application of BayK 8644 induces localized calcium transients. A, DIC (left) and fluorescence images (right) of a cortical neuron exposed to BayK 8644. Bath application of BayK at 0:00 induced high frequency localized calcium transients primarily

    Techniques Used: Fluorescence

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    Alomone Labs bay k8644
    In (a) we show the percentage of singly- and polyinnervated NMJ after 4 applications over the LAL surface (one application every day between P5–P8 (observation at P9) of one of the following VGCC inhibitor substances: nitrendipine (NT 1 μM, an L-type channel blocker), ω-conotoxin-GVIA (ω-CON 1 μM, N-type channel blocker), and ω-agatoxin-IVA (ω-AGA 100 nM, P/Q-type blocker). Also, the L activator <t>Bay-K8644</t> (5 μM), the P/Q- and N-type activator GV-58 (20 μM), and the intracellular calcium chelator BAPTA-AM (5 μM). The histogram in ( b ) shows the percentage of S1-S4 clusters in the untreated control mice (PBS) and after the 4 applications of the aforesaid substances. Data were presented as percentages of NMJ ± SD. Fisher’s test: * p
    Bay K8644, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bay k8644/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bay k8644 - by Bioz Stars, 2022-12
    94/100 stars
      Buy from Supplier

    Image Search Results


    In (a) we show the percentage of singly- and polyinnervated NMJ after 4 applications over the LAL surface (one application every day between P5–P8 (observation at P9) of one of the following VGCC inhibitor substances: nitrendipine (NT 1 μM, an L-type channel blocker), ω-conotoxin-GVIA (ω-CON 1 μM, N-type channel blocker), and ω-agatoxin-IVA (ω-AGA 100 nM, P/Q-type blocker). Also, the L activator Bay-K8644 (5 μM), the P/Q- and N-type activator GV-58 (20 μM), and the intracellular calcium chelator BAPTA-AM (5 μM). The histogram in ( b ) shows the percentage of S1-S4 clusters in the untreated control mice (PBS) and after the 4 applications of the aforesaid substances. Data were presented as percentages of NMJ ± SD. Fisher’s test: * p

    Journal: Molecular Neurobiology

    Article Title: Involvement of the Voltage-Gated Calcium Channels L- P/Q- and N-Types in Synapse Elimination During Neuromuscular Junction Development

    doi: 10.1007/s12035-022-02818-2

    Figure Lengend Snippet: In (a) we show the percentage of singly- and polyinnervated NMJ after 4 applications over the LAL surface (one application every day between P5–P8 (observation at P9) of one of the following VGCC inhibitor substances: nitrendipine (NT 1 μM, an L-type channel blocker), ω-conotoxin-GVIA (ω-CON 1 μM, N-type channel blocker), and ω-agatoxin-IVA (ω-AGA 100 nM, P/Q-type blocker). Also, the L activator Bay-K8644 (5 μM), the P/Q- and N-type activator GV-58 (20 μM), and the intracellular calcium chelator BAPTA-AM (5 μM). The histogram in ( b ) shows the percentage of S1-S4 clusters in the untreated control mice (PBS) and after the 4 applications of the aforesaid substances. Data were presented as percentages of NMJ ± SD. Fisher’s test: * p

    Article Snippet: The working solutions used were Bay-K8644, 5 µM, and GV-58, 20 µM.

    Techniques: Mouse Assay

    Effects of BIII 890CL on Ca 2+ responses triggered by VTD or Bay K8644. ( A ) Representative Fura-2 fluorescence kinetic traces illustrating Ca 2+ response induced by 10 µM of VTD, alone or co-injected with 1 µM of TTX or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. ( B ) Concentration–inhibition relationship of VTD-induced Ca 2+ responses by BIII 890CL, (IC50 = 1.47 ± 0.18 µM, Hill slope = 1.26 ± 0.23, R 2 = 0.94). ( C ) Representative Fura-2 fluorescence kinetics traces illustrating Ca 2+ response induced by 1 µM of Bay K8644, a specific L-type Ca V channel activator, alone or co-injected with 10 µM of nifedipine or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. Data represent the mean ± SEM ( n = 3) of recordings of two independent experiments.

    Journal: International Journal of Molecular Sciences

    Article Title: Pharmacological Dissection of the Crosstalk between NaV and CaV Channels in GH3b6 Cells

    doi: 10.3390/ijms23020827

    Figure Lengend Snippet: Effects of BIII 890CL on Ca 2+ responses triggered by VTD or Bay K8644. ( A ) Representative Fura-2 fluorescence kinetic traces illustrating Ca 2+ response induced by 10 µM of VTD, alone or co-injected with 1 µM of TTX or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. ( B ) Concentration–inhibition relationship of VTD-induced Ca 2+ responses by BIII 890CL, (IC50 = 1.47 ± 0.18 µM, Hill slope = 1.26 ± 0.23, R 2 = 0.94). ( C ) Representative Fura-2 fluorescence kinetics traces illustrating Ca 2+ response induced by 1 µM of Bay K8644, a specific L-type Ca V channel activator, alone or co-injected with 10 µM of nifedipine or with 10 or 1 µM of BIII 890 CL or with BI 55CL (10 and 1 µM), used as a negative control. Data represent the mean ± SEM ( n = 3) of recordings of two independent experiments.

    Article Snippet: After a 30 s baseline, NaV activators including VTD, BTX, Tf2, PbTx-2, β-PMTX, and deltamethrin and Bay K8644 were automatically injected, and the fluorescence emission spectra were monitored for 320 s at an acquisition frequency of 0.25 Hz.

    Techniques: Fluorescence, Injection, Negative Control, Concentration Assay, Inhibition