mviia  (Alomone Labs)


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    Alomone Labs mviia
    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin <t>MVIIA</t> for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer <t>without</t> <t>ω-conotoxins:</t> c: < stimulation buffer without ω-conotoxins; p < 0.05.
    Mviia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 85 stars, based on 1 article reviews
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    mviia - by Bioz Stars, 2023-09
    85/100 stars

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    1) Product Images from "Cell-Based Reporter Release Assay to Determine the Activity of Calcium-Dependent Neurotoxins and Neuroactive Pharmaceuticals"

    Article Title: Cell-Based Reporter Release Assay to Determine the Activity of Calcium-Dependent Neurotoxins and Neuroactive Pharmaceuticals

    Journal: Toxins

    doi: 10.3390/toxins13040247

    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin MVIIA for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer without ω-conotoxins: c: < stimulation buffer without ω-conotoxins; p < 0.05.
    Figure Legend Snippet: Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin MVIIA for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer without ω-conotoxins: c: < stimulation buffer without ω-conotoxins; p < 0.05.

    Techniques Used: Inhibition, Luciferase, Stable Transfection, Expressing, Cell Culture, Incubation, Activity Assay

    mviia  (Alomone Labs)


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    Potency of Ca V 2.2 channel inhibition and side effects of intraplantar administration <t>of</t> <t>ω-conotoxins.</t> ( A ) Representative concentration response curves for inhibition of KCl evoked Ca V 2.2 response in SH-SY5Y cells. Potency of GVIA (IC 50 11.2 ± 3.3 nM), <t>MVIIA</t> (IC 50 6.8 ± 2.1 nM), and CVIF (IC 50 10.0 ± 3.1 nM) determined from three independent experiments each conducted in triplicate. ( B , C ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change mechanical and thermal PWTs compared to healthy control group ( n = 18) ( p > 0.05). ( D – F ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change foot slips, distance covered, and ataxia index in the parallel rod floor test compared with healthy control mice ( n = 18) ( p > 0.05). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test.
    Mviia, 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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    1) Product Images from "Subcutaneous ω-Conotoxins Alleviate Mechanical Pain in Rodent Models of Acute Peripheral Neuropathy"

    Article Title: Subcutaneous ω-Conotoxins Alleviate Mechanical Pain in Rodent Models of Acute Peripheral Neuropathy

    Journal: Marine Drugs

    doi: 10.3390/md19020106

    Potency of Ca V 2.2 channel inhibition and side effects of intraplantar administration of ω-conotoxins. ( A ) Representative concentration response curves for inhibition of KCl evoked Ca V 2.2 response in SH-SY5Y cells. Potency of GVIA (IC 50 11.2 ± 3.3 nM), MVIIA (IC 50 6.8 ± 2.1 nM), and CVIF (IC 50 10.0 ± 3.1 nM) determined from three independent experiments each conducted in triplicate. ( B , C ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change mechanical and thermal PWTs compared to healthy control group ( n = 18) ( p > 0.05). ( D – F ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change foot slips, distance covered, and ataxia index in the parallel rod floor test compared with healthy control mice ( n = 18) ( p > 0.05). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test.
    Figure Legend Snippet: Potency of Ca V 2.2 channel inhibition and side effects of intraplantar administration of ω-conotoxins. ( A ) Representative concentration response curves for inhibition of KCl evoked Ca V 2.2 response in SH-SY5Y cells. Potency of GVIA (IC 50 11.2 ± 3.3 nM), MVIIA (IC 50 6.8 ± 2.1 nM), and CVIF (IC 50 10.0 ± 3.1 nM) determined from three independent experiments each conducted in triplicate. ( B , C ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change mechanical and thermal PWTs compared to healthy control group ( n = 18) ( p > 0.05). ( D – F ) Intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF ( n = 6 per group) in naïve C57BL6/J mice did not significantly change foot slips, distance covered, and ataxia index in the parallel rod floor test compared with healthy control mice ( n = 18) ( p > 0.05). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test.

    Techniques Used: Inhibition, Concentration Assay, Injection

    Analgesic effects of ω-conotoxins on surgery-induced mechanical and thermal allodynia. ( A ) Surgery-induced mechanical allodynia developed 24 h after surgery. Paw withdrawal thresholds were significantly lowered in the surgery group compared with naïve mice ( p < 0.0001; n = 12 per group). Compared with vehicle control, the PWTs of post-surgery mice increased significantly after intraplantar injection of 0.6, 2.0, and 6.0 pmol/paw (30, 100, and 300 nM MVIIA; 20 µL) MVIIA ( p < 0.05; p < 0.0001; p < 0.0001, respectively; n = 6 per group), but remained unchanged after intraplantar injection of 6.0 pmol/paw (300 nM; 20 µL) GVIA and CVIF ( p > 0.05; n = 6 per group). ( B ) The thermal thresholds of mice 24 h after surgery were significantly lower, compared with naïve mice ( p < 0.05; n = 18). However, the intraplantar injection of 2.0 pmol/paw (100 nM; 20 µL) GVIA, MVIIA, and CVIF did not reverse thermal allodynia in mice 24 h after surgery compared to vehicle control group ( p > 0.05; n = 6 per group). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test; * p < 0.05; **** p < 0.0001 compared with vehicle control group (except where indicated otherwise).
    Figure Legend Snippet: Analgesic effects of ω-conotoxins on surgery-induced mechanical and thermal allodynia. ( A ) Surgery-induced mechanical allodynia developed 24 h after surgery. Paw withdrawal thresholds were significantly lowered in the surgery group compared with naïve mice ( p < 0.0001; n = 12 per group). Compared with vehicle control, the PWTs of post-surgery mice increased significantly after intraplantar injection of 0.6, 2.0, and 6.0 pmol/paw (30, 100, and 300 nM MVIIA; 20 µL) MVIIA ( p < 0.05; p < 0.0001; p < 0.0001, respectively; n = 6 per group), but remained unchanged after intraplantar injection of 6.0 pmol/paw (300 nM; 20 µL) GVIA and CVIF ( p > 0.05; n = 6 per group). ( B ) The thermal thresholds of mice 24 h after surgery were significantly lower, compared with naïve mice ( p < 0.05; n = 18). However, the intraplantar injection of 2.0 pmol/paw (100 nM; 20 µL) GVIA, MVIIA, and CVIF did not reverse thermal allodynia in mice 24 h after surgery compared to vehicle control group ( p > 0.05; n = 6 per group). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test; * p < 0.05; **** p < 0.0001 compared with vehicle control group (except where indicated otherwise).

    Techniques Used: Injection

    Analgesic effects of ω-conotoxins in oxaliplatin-induced mechanical allodynia. ( A ) Mechanical allodynia developed 24 h after intraplantar administration of 40 µg/paw oxaliplatin. Paw withdrawal thresholds were significantly reduced in oxaliplatin injected group compared to naïve mice ( p < 0.0001; n = 18 per group). Administration of 6 pmol/paw (300 nM; 20 µL) GVIA and MVIIA significantly increased the PWTs of oxaliplatin-treated mice compared to vehicle control group ( p < 0.05, p < 0.0001 n = 6 per group). However, 6 pmol/paw (300 nM; 20 µL) CVIF did not significantly change PWTs compared to vehicle control mice ( p > 0.05; n = 6 per group). ( B ) Dose response curves of the antiallodynic effect of GVIA and MVIIA on oxaliplatin-induced mechanical allodynia. The ED 50 of GVIA and MVIIA was found to be 1.8 pmol/paw and 0.8 pmol/paw, respectively. Data indicated by the hexagons are from two doses (2 and 6 pmol/paw) (100 and 300 nM; 20 µL) of CVIF ( n = 6 per data point). ( C ) Time course of action of GVIA and MVIIA in the OIPN model. Paw withdrawal thresholds were measured after intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA and MVIIA. 300 nM GVIA significantly increased PWTs at 10 ( p < 0.01; n = 6 per group) and 30 min ( p < 0.05; n = 6 per group) after injection while 300 nM MVIIA significantly increased PWTs only at 10 min ( p < 0.01; n = 6 per group) after injection, compared with vehicle control group. The increase in mechanical PWTs produced by GVIA and MVIIA gradually returned to pre-injection levels at 120–180 min after treatment. ( D ) Contralateral administration of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF, 24 h after intraplantar administration of oxaliplatin, did not significantly change mechanical PWTs compared to vehicle treated control group ( p > 0.05; n = 6 per group). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test, or two-way ANOVA with Sidak’s post-test as appropriate; * p < 0.05; ** p < 0.01, **** p < 0.0001 compared with vehicle control (except where indicated otherwise).
    Figure Legend Snippet: Analgesic effects of ω-conotoxins in oxaliplatin-induced mechanical allodynia. ( A ) Mechanical allodynia developed 24 h after intraplantar administration of 40 µg/paw oxaliplatin. Paw withdrawal thresholds were significantly reduced in oxaliplatin injected group compared to naïve mice ( p < 0.0001; n = 18 per group). Administration of 6 pmol/paw (300 nM; 20 µL) GVIA and MVIIA significantly increased the PWTs of oxaliplatin-treated mice compared to vehicle control group ( p < 0.05, p < 0.0001 n = 6 per group). However, 6 pmol/paw (300 nM; 20 µL) CVIF did not significantly change PWTs compared to vehicle control mice ( p > 0.05; n = 6 per group). ( B ) Dose response curves of the antiallodynic effect of GVIA and MVIIA on oxaliplatin-induced mechanical allodynia. The ED 50 of GVIA and MVIIA was found to be 1.8 pmol/paw and 0.8 pmol/paw, respectively. Data indicated by the hexagons are from two doses (2 and 6 pmol/paw) (100 and 300 nM; 20 µL) of CVIF ( n = 6 per data point). ( C ) Time course of action of GVIA and MVIIA in the OIPN model. Paw withdrawal thresholds were measured after intraplantar injection of 6 pmol/paw (300 nM; 20 µL) GVIA and MVIIA. 300 nM GVIA significantly increased PWTs at 10 ( p < 0.01; n = 6 per group) and 30 min ( p < 0.05; n = 6 per group) after injection while 300 nM MVIIA significantly increased PWTs only at 10 min ( p < 0.01; n = 6 per group) after injection, compared with vehicle control group. The increase in mechanical PWTs produced by GVIA and MVIIA gradually returned to pre-injection levels at 120–180 min after treatment. ( D ) Contralateral administration of 6 pmol/paw (300 nM; 20 µL) GVIA, MVIIA, and CVIF, 24 h after intraplantar administration of oxaliplatin, did not significantly change mechanical PWTs compared to vehicle treated control group ( p > 0.05; n = 6 per group). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test, or two-way ANOVA with Sidak’s post-test as appropriate; * p < 0.05; ** p < 0.01, **** p < 0.0001 compared with vehicle control (except where indicated otherwise).

    Techniques Used: Injection, Produced

    Analgesic effects of ω-conotoxins in cisplatin-induced mechanical allodynia. Cisplatin-induced mechanical allodynia developed 24 h after intraplantar administration of 40 µg/paw cisplatin. Paw withdrawal thresholds were significantly reduced in cisplatin injected group compared to naïve mice ( p < 0.0001; one-way ANOVA; n = 18 per group). Intraplantar injection of 2 pmol/paw (100 nM; 20 µL) GVIA, MVIIA, and CVIF did not significantly change the PWTs in cisplatin-treated mice compared to vehicle control mice ( p > 0.05; n = 6 per group). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test, **** p < 0.0001 compared with vehicle control (except where indicated otherwise).
    Figure Legend Snippet: Analgesic effects of ω-conotoxins in cisplatin-induced mechanical allodynia. Cisplatin-induced mechanical allodynia developed 24 h after intraplantar administration of 40 µg/paw cisplatin. Paw withdrawal thresholds were significantly reduced in cisplatin injected group compared to naïve mice ( p < 0.0001; one-way ANOVA; n = 18 per group). Intraplantar injection of 2 pmol/paw (100 nM; 20 µL) GVIA, MVIIA, and CVIF did not significantly change the PWTs in cisplatin-treated mice compared to vehicle control mice ( p > 0.05; n = 6 per group). All data are presented as mean ± SEM. Statistical significance was determined using one-way ANOVA with Dunnett’s post-test, **** p < 0.0001 compared with vehicle control (except where indicated otherwise).

    Techniques Used: Injection

    ω conotoxin mviia  (Alomone Labs)


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    Alomone Labs mviia
    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin <t>MVIIA</t> for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer <t>without</t> <t>ω-conotoxins:</t> c: < stimulation buffer without ω-conotoxins; p < 0.05.
    Mviia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin <t>MVIIA</t> for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer <t>without</t> <t>ω-conotoxins:</t> c: < stimulation buffer without ω-conotoxins; p < 0.05.
    ω Conotoxin Mviia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin <t>MVIIA</t> for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer <t>without</t> <t>ω-conotoxins:</t> c: < stimulation buffer without ω-conotoxins; p < 0.05.
    Conotoxin Mviia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs ω ctx mviia
    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin <t>MVIIA</t> for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer <t>without</t> <t>ω-conotoxins:</t> c: < stimulation buffer without ω-conotoxins; p < 0.05.
    ω Ctx Mviia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs conotoxins mviia
    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin <t>MVIIA</t> for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer <t>without</t> <t>ω-conotoxins:</t> c: < stimulation buffer without ω-conotoxins; p < 0.05.
    Conotoxins Mviia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    conotoxins mviia - by Bioz Stars, 2023-09
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    Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin MVIIA for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer without ω-conotoxins: c: < stimulation buffer without ω-conotoxins; p < 0.05.

    Journal: Toxins

    Article Title: Cell-Based Reporter Release Assay to Determine the Activity of Calcium-Dependent Neurotoxins and Neuroactive Pharmaceuticals

    doi: 10.3390/toxins13040247

    Figure Lengend Snippet: Inhibition of luciferase release by N-Type VGCC inhibitors. SIMA cells stably expressing hPOMC1-26 GLuc were cultured and differentiated as described in the methods section. After removing the medium, cells were washed with fresh medium and incubated in differentiation medium with different concentrations of N-type VGCC inhibitors ω-conotoxin GVIA or ω-conotoxin MVIIA for 10 min. Cells were then incubated for three minutes with non-depolarizing (Na + , control, not shown) or depolarizing (K + , stimulated) balanced salt solution in the presence of different ω-conotoxin concentrations. Cell culture supernatants were centrifuged, and luciferase activity was determined in the cell culture supernatants. Values are means ± SEM of at least three independent experiments. Statistics: Student’s t-test for unpaired samples, a: > control buffer without ω-conotoxins: c: < stimulation buffer without ω-conotoxins; p < 0.05.

    Article Snippet: Neurotoxins and neuroactive pharmaceuticals used: carbachol, atropine, verapamil, nifedipine, thrimethadione and zonisamide were from Sigma-Aldrich (Taufkirchen, Germany); α-Latrotoxin (ALX-630-027) was from Enzo Life Science (Lörrach, Germany); ω-conotoxins GVIA and MVIIA were from Alamone labs (Jerusalem, Israel); agatoxin and SNX-482 were from tebu-bio (Offenbach, Germany).

    Techniques: Inhibition, Luciferase, Stable Transfection, Expressing, Cell Culture, Incubation, Activity Assay