ω conotoxin gvia  (Alomone Labs)


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    Alomone Labs ω conotoxin gvia
    ω Conotoxin Gvia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ω conotoxin gvia  (Alomone Labs)


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    Alomone Labs ω conotoxin gvia
    ω Conotoxin Gvia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ω conotoxin gvia  (Alomone Labs)


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    Alomone Labs ω conotoxin gvia
    ω Conotoxin Gvia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    conotoxin giiib c 270  (Alomone Labs)


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    Alomone Labs conotoxin giiib c 270
    Conotoxin Giiib C 270, 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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    muscle sodium channel blocker  (Alomone Labs)


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    Alomone Labs muscle sodium channel blocker
    Muscle Sodium Channel Blocker, 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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    ω conotoxin gvia  (Alomone Labs)


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    Alomone Labs ω conotoxin gvia
    ( A ) Isolated magnocellular neurons were identified as either vasopressin or oxytocin by their presence or absence of the GFP signal. Scale bar = 10 µm. ( B ) The current-voltage relationships show no difference between whole-cell calcium currents (WCCC) of vasopressin and oxytocin neurons (n = 20 each). ( C ) Normalized conductance (G/G max , fitted using Boltzmann equation) showed no significant change with or without TG. ( D ) Examples of two neurons (both oxytocin neurons), one vehicle treated (•) and one 50 min after pre-treating with thapsigargin (○). The steady-state Ca 2+ current is plotted against time following treatment with channel toxins (in order: 1 µM nicardipine; 200 nM ω-agatoxin IV; 500 <t>nM</t> <t>ω-conotoxin</t> <t>GVIA).</t> The current measured after each toxin was subtracted from that evoked before each treatment to determine the current carried by L-, P/Q- and N-type channels. The remaining current was attributed to R-type channels. ( E ) Examples of N-, L- and WCCC elicited by voltage steps in controls and TG treated cells. ( F ) The resulting current density for each current type normalised for the peak maximal current was averaged (n = 5) to give the average current density from neurons treated with vehicle or thapsigargin. ( G ) In a subsequent experiment L- or N-type channel toxins were administered, alternating the order (n = 5 for each condition). Mean±S.E.M are shown and compared by t-test. * P <0.05 vs control.
    ω Conotoxin Gvia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 95 stars, based on 1 article reviews
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    Images

    1) Product Images from "The Involvement of Voltage-Operated Calcium Channels in Somato-Dendritic Oxytocin Release"

    Article Title: The Involvement of Voltage-Operated Calcium Channels in Somato-Dendritic Oxytocin Release

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0025366

    ( A ) Isolated magnocellular neurons were identified as either vasopressin or oxytocin by their presence or absence of the GFP signal. Scale bar = 10 µm. ( B ) The current-voltage relationships show no difference between whole-cell calcium currents (WCCC) of vasopressin and oxytocin neurons (n = 20 each). ( C ) Normalized conductance (G/G max , fitted using Boltzmann equation) showed no significant change with or without TG. ( D ) Examples of two neurons (both oxytocin neurons), one vehicle treated (•) and one 50 min after pre-treating with thapsigargin (○). The steady-state Ca 2+ current is plotted against time following treatment with channel toxins (in order: 1 µM nicardipine; 200 nM ω-agatoxin IV; 500 nM ω-conotoxin GVIA). The current measured after each toxin was subtracted from that evoked before each treatment to determine the current carried by L-, P/Q- and N-type channels. The remaining current was attributed to R-type channels. ( E ) Examples of N-, L- and WCCC elicited by voltage steps in controls and TG treated cells. ( F ) The resulting current density for each current type normalised for the peak maximal current was averaged (n = 5) to give the average current density from neurons treated with vehicle or thapsigargin. ( G ) In a subsequent experiment L- or N-type channel toxins were administered, alternating the order (n = 5 for each condition). Mean±S.E.M are shown and compared by t-test. * P <0.05 vs control.
    Figure Legend Snippet: ( A ) Isolated magnocellular neurons were identified as either vasopressin or oxytocin by their presence or absence of the GFP signal. Scale bar = 10 µm. ( B ) The current-voltage relationships show no difference between whole-cell calcium currents (WCCC) of vasopressin and oxytocin neurons (n = 20 each). ( C ) Normalized conductance (G/G max , fitted using Boltzmann equation) showed no significant change with or without TG. ( D ) Examples of two neurons (both oxytocin neurons), one vehicle treated (•) and one 50 min after pre-treating with thapsigargin (○). The steady-state Ca 2+ current is plotted against time following treatment with channel toxins (in order: 1 µM nicardipine; 200 nM ω-agatoxin IV; 500 nM ω-conotoxin GVIA). The current measured after each toxin was subtracted from that evoked before each treatment to determine the current carried by L-, P/Q- and N-type channels. The remaining current was attributed to R-type channels. ( E ) Examples of N-, L- and WCCC elicited by voltage steps in controls and TG treated cells. ( F ) The resulting current density for each current type normalised for the peak maximal current was averaged (n = 5) to give the average current density from neurons treated with vehicle or thapsigargin. ( G ) In a subsequent experiment L- or N-type channel toxins were administered, alternating the order (n = 5 for each condition). Mean±S.E.M are shown and compared by t-test. * P <0.05 vs control.

    Techniques Used: Isolation

    ω conotoxin mviic  (Alomone Labs)


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    Alomone Labs ω conotoxin mviic
    ω Conotoxin Mviic, 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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    ω conotoxin mviic  (Alomone Labs)


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    Alomone Labs ω conotoxin mviic
    Spontaneous calcium transients and growth cone turning are sensitive to blockage of store-operated channels . (A) Individual control morphant growth cones exhibited sparse spontaneous calcium transients, occurring at a rate of approximately one transient per three minutes. (B) Homer1 morphant growth cones exhibited significantly greater frequency, at a rate of at least one spontaneous transient per minute. (C) A trace from a single Homer1 morphant growth cone showed a decrease in spontaneous calcium transient frequency in the presence of bath applied SKF-96365. (D) Quantification of spontaneous calcium transient frequencies in Homer1 morphant growth cones. Removing calcium from the media (Ca free) or bath application of La 3+ (La) or SKF-96365 (SKF) reduced spontaneous transient frequencies in Homer1 morphant growth cones to control (ctrl) levels. Bath application of a voltage-gated calcium channel (VGCC) inhibitor cocktail or nifedipine alone had little effect on the frequency of spontaneous calcium transients in Homer1 morphant growth cones. (E) Calcium-dependent brain derived neurotrophic factor (BDNF)-induced turning is mediated through store-operated channels. BDNF attraction was abolished when TRPC channels were inactivated with bath application of SKF-96365 or La 3+ . Inhibition of VGCCs with nifedipine <t>or</t> <t>ω-conotoxin-MVIIC</t> had no effect on control and Homer1 morphant growth cone turning. (F) Inhibition of store-operated channels did not alter axon extension rates. Error bars indicate standard error of the mean. Cocktail = nifedipine, ω-conotoxin-MVIIC plus Ni ++ . The scale bar in (C) applies also to (A, B).
    ω Conotoxin Mviic, 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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    ω conotoxin mviic - by Bioz Stars, 2023-03
    93/100 stars

    Images

    1) Product Images from "Homer regulates calcium signalling in growth cone turning"

    Article Title: Homer regulates calcium signalling in growth cone turning

    Journal: Neural Development

    doi: 10.1186/1749-8104-4-29

    Spontaneous calcium transients and growth cone turning are sensitive to blockage of store-operated channels . (A) Individual control morphant growth cones exhibited sparse spontaneous calcium transients, occurring at a rate of approximately one transient per three minutes. (B) Homer1 morphant growth cones exhibited significantly greater frequency, at a rate of at least one spontaneous transient per minute. (C) A trace from a single Homer1 morphant growth cone showed a decrease in spontaneous calcium transient frequency in the presence of bath applied SKF-96365. (D) Quantification of spontaneous calcium transient frequencies in Homer1 morphant growth cones. Removing calcium from the media (Ca free) or bath application of La 3+ (La) or SKF-96365 (SKF) reduced spontaneous transient frequencies in Homer1 morphant growth cones to control (ctrl) levels. Bath application of a voltage-gated calcium channel (VGCC) inhibitor cocktail or nifedipine alone had little effect on the frequency of spontaneous calcium transients in Homer1 morphant growth cones. (E) Calcium-dependent brain derived neurotrophic factor (BDNF)-induced turning is mediated through store-operated channels. BDNF attraction was abolished when TRPC channels were inactivated with bath application of SKF-96365 or La 3+ . Inhibition of VGCCs with nifedipine or ω-conotoxin-MVIIC had no effect on control and Homer1 morphant growth cone turning. (F) Inhibition of store-operated channels did not alter axon extension rates. Error bars indicate standard error of the mean. Cocktail = nifedipine, ω-conotoxin-MVIIC plus Ni ++ . The scale bar in (C) applies also to (A, B).
    Figure Legend Snippet: Spontaneous calcium transients and growth cone turning are sensitive to blockage of store-operated channels . (A) Individual control morphant growth cones exhibited sparse spontaneous calcium transients, occurring at a rate of approximately one transient per three minutes. (B) Homer1 morphant growth cones exhibited significantly greater frequency, at a rate of at least one spontaneous transient per minute. (C) A trace from a single Homer1 morphant growth cone showed a decrease in spontaneous calcium transient frequency in the presence of bath applied SKF-96365. (D) Quantification of spontaneous calcium transient frequencies in Homer1 morphant growth cones. Removing calcium from the media (Ca free) or bath application of La 3+ (La) or SKF-96365 (SKF) reduced spontaneous transient frequencies in Homer1 morphant growth cones to control (ctrl) levels. Bath application of a voltage-gated calcium channel (VGCC) inhibitor cocktail or nifedipine alone had little effect on the frequency of spontaneous calcium transients in Homer1 morphant growth cones. (E) Calcium-dependent brain derived neurotrophic factor (BDNF)-induced turning is mediated through store-operated channels. BDNF attraction was abolished when TRPC channels were inactivated with bath application of SKF-96365 or La 3+ . Inhibition of VGCCs with nifedipine or ω-conotoxin-MVIIC had no effect on control and Homer1 morphant growth cone turning. (F) Inhibition of store-operated channels did not alter axon extension rates. Error bars indicate standard error of the mean. Cocktail = nifedipine, ω-conotoxin-MVIIC plus Ni ++ . The scale bar in (C) applies also to (A, B).

    Techniques Used: Derivative Assay, Inhibition

    n type calcium channel inhibitor α conotoxin  (Alomone Labs)


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    Alomone Labs n type calcium channel inhibitor α conotoxin
    N Type Calcium Channel Inhibitor α Conotoxin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    conotoxin gvia  (Alomone Labs)


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    Alomone Labs conotoxin gvia
    Summary of the compounds and antiepileptic drugs evaluated in the calcium oscillations assay.
    Conotoxin Gvia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 86 stars, based on 1 article reviews
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    86/100 stars

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    1) Product Images from "New In Vitro Phenotypic Assay for Epilepsy: Fluorescent Measurement of Synchronized Neuronal Calcium Oscillations"

    Article Title: New In Vitro Phenotypic Assay for Epilepsy: Fluorescent Measurement of Synchronized Neuronal Calcium Oscillations

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0084755

    Summary of the compounds and antiepileptic drugs evaluated in the calcium oscillations assay.
    Figure Legend Snippet: Summary of the compounds and antiepileptic drugs evaluated in the calcium oscillations assay.

    Techniques Used:

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    Alomone Labs ω conotoxin gvia
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    conotoxin giiib c 270  (Alomone Labs)
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    Alomone Labs conotoxin giiib c 270
    Conotoxin Giiib C 270, 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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    ω conotoxin mviic  (Alomone Labs)
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    Alomone Labs ω conotoxin mviic
    ω Conotoxin Mviic, 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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    n type calcium channel inhibitor α conotoxin  (Alomone Labs)
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    Alomone Labs n type calcium channel inhibitor α conotoxin
    N Type Calcium Channel Inhibitor α Conotoxin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    conotoxin gvia  (Alomone Labs)
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    Alomone Labs conotoxin gvia
    Summary of the compounds and antiepileptic drugs evaluated in the calcium oscillations assay.
    Conotoxin Gvia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Summary of the compounds and antiepileptic drugs evaluated in the calcium oscillations assay.

    Journal: PLoS ONE

    Article Title: New In Vitro Phenotypic Assay for Epilepsy: Fluorescent Measurement of Synchronized Neuronal Calcium Oscillations

    doi: 10.1371/journal.pone.0084755

    Figure Lengend Snippet: Summary of the compounds and antiepileptic drugs evaluated in the calcium oscillations assay.

    Article Snippet: Diazepam was from Fragon; phenytoin from Fluka; conotoxin GVIA and TTX from Alomone Labs; gabapentin from TCI Chemicals; and levetiracetam and retigabine were synthetized at UCB.

    Techniques: