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ω conotoxin mviic  (Alomone Labs)
94
Alomone Labs ω conotoxin mviic
Ca V 2.1 channels provide a trigger for LTX N4C -induced bursts of exocytosis, while Ca V 1 channels modify their dynamics. Mouse neuromuscular preparations were incubated in 2 mM Ca 2+ and stimulated by 0.25 nM LTX N4C . ( a , b ) Average MEPP frequencies induced by LTX N4C before or after the application of Ca v channel inhibitors: 10 μM nimodipine ( n = 6; N = 32) to block Ca V 1 channels ( a ), or 1 <t>μM</t> <t>ω-conotoxin</t> <t>MVIIC</t> ( n = 4; N = 36) to block Ca V 2.1/2.2 channels ( b ). ( c ) ω-Conotoxin MVIIC significantly reduces MEPP frequencies within the IBIs of LTX N4C -induced bursts; n = 5. ( d , e ) Average MEPP frequencies induced by LTX N4C after the application of more selective Ca V 2 channel inhibitors: 50 nM ω-conotoxin GVIA ( n = 4; N = 32) to block Ca V 2.2 channels ( d ), or 200 nM ω-agatoxin IVA ( n = 6; N = 31) to block Ca V 2.1 channels ( e ). ( f ) Ca V 2.1 blockers only affect LTX N4C actions if added before the toxin, but fail to do so when added after LTX N4C ; n = 10; N = 67. ( g ) ω-Agatoxin IVA (200 nM) blocks all LTX N4C -induced increase in MEPP frequency when added together with or after the G αq blocker UBO-QIC; n = 4; N = 32. ( h , i ) The Ca V 2 agonist GV-58 (50 μM) increases the basal spontaneous MEPP frequency ( h ), but does not affect the average MEPP frequency induced by LTX N4C ; n = 3; N = 36. However, GV-58 significantly increases MEPP frequency within IBIs ( i ); n = 3; N = 36. Symbols next to bars indicate statistical significance compared to respective controls; other comparisons are shown by lines: *, p < 0.05; **, p < 0.01; ***, p < 0.001; #, p < 0.0001; NS, not significant. ( j ) LTX N4C fails to induce any changes in Ca 2+ cyt in nerve terminals pretreated with ω-conotoxin MVIIC. Muscle preparations were preloaded with Fluo-4-AM (see ) and treated with 1 μM ω-conotoxin MVIIC, followed by the addition of 0.25 nM LTX N4C and recording of intracellular fluorescence.
ω Conotoxin Mviic, 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/product/c-150s/%CF%89-Conotoxin+MVIIC/pmc13162755-87-32-36
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mhz cutoff frequency  (Mini-Circuits)
95
Mini-Circuits mhz cutoff frequency
Ca V 2.1 channels provide a trigger for LTX N4C -induced bursts of exocytosis, while Ca V 1 channels modify their dynamics. Mouse neuromuscular preparations were incubated in 2 mM Ca 2+ and stimulated by 0.25 nM LTX N4C . ( a , b ) Average MEPP frequencies induced by LTX N4C before or after the application of Ca v channel inhibitors: 10 μM nimodipine ( n = 6; N = 32) to block Ca V 1 channels ( a ), or 1 <t>μM</t> <t>ω-conotoxin</t> <t>MVIIC</t> ( n = 4; N = 36) to block Ca V 2.1/2.2 channels ( b ). ( c ) ω-Conotoxin MVIIC significantly reduces MEPP frequencies within the IBIs of LTX N4C -induced bursts; n = 5. ( d , e ) Average MEPP frequencies induced by LTX N4C after the application of more selective Ca V 2 channel inhibitors: 50 nM ω-conotoxin GVIA ( n = 4; N = 32) to block Ca V 2.2 channels ( d ), or 200 nM ω-agatoxin IVA ( n = 6; N = 31) to block Ca V 2.1 channels ( e ). ( f ) Ca V 2.1 blockers only affect LTX N4C actions if added before the toxin, but fail to do so when added after LTX N4C ; n = 10; N = 67. ( g ) ω-Agatoxin IVA (200 nM) blocks all LTX N4C -induced increase in MEPP frequency when added together with or after the G αq blocker UBO-QIC; n = 4; N = 32. ( h , i ) The Ca V 2 agonist GV-58 (50 μM) increases the basal spontaneous MEPP frequency ( h ), but does not affect the average MEPP frequency induced by LTX N4C ; n = 3; N = 36. However, GV-58 significantly increases MEPP frequency within IBIs ( i ); n = 3; N = 36. Symbols next to bars indicate statistical significance compared to respective controls; other comparisons are shown by lines: *, p < 0.05; **, p < 0.01; ***, p < 0.001; #, p < 0.0001; NS, not significant. ( j ) LTX N4C fails to induce any changes in Ca 2+ cyt in nerve terminals pretreated with ω-conotoxin MVIIC. Muscle preparations were preloaded with Fluo-4-AM (see ) and treated with 1 μM ω-conotoxin MVIIC, followed by the addition of 0.25 nM LTX N4C and recording of intracellular fluorescence.
Mhz Cutoff Frequency, supplied by Mini-Circuits, 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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slp  (Mini-Circuits)
95
Mini-Circuits slp
Ca V 2.1 channels provide a trigger for LTX N4C -induced bursts of exocytosis, while Ca V 1 channels modify their dynamics. Mouse neuromuscular preparations were incubated in 2 mM Ca 2+ and stimulated by 0.25 nM LTX N4C . ( a , b ) Average MEPP frequencies induced by LTX N4C before or after the application of Ca v channel inhibitors: 10 μM nimodipine ( n = 6; N = 32) to block Ca V 1 channels ( a ), or 1 <t>μM</t> <t>ω-conotoxin</t> <t>MVIIC</t> ( n = 4; N = 36) to block Ca V 2.1/2.2 channels ( b ). ( c ) ω-Conotoxin MVIIC significantly reduces MEPP frequencies within the IBIs of LTX N4C -induced bursts; n = 5. ( d , e ) Average MEPP frequencies induced by LTX N4C after the application of more selective Ca V 2 channel inhibitors: 50 nM ω-conotoxin GVIA ( n = 4; N = 32) to block Ca V 2.2 channels ( d ), or 200 nM ω-agatoxin IVA ( n = 6; N = 31) to block Ca V 2.1 channels ( e ). ( f ) Ca V 2.1 blockers only affect LTX N4C actions if added before the toxin, but fail to do so when added after LTX N4C ; n = 10; N = 67. ( g ) ω-Agatoxin IVA (200 nM) blocks all LTX N4C -induced increase in MEPP frequency when added together with or after the G αq blocker UBO-QIC; n = 4; N = 32. ( h , i ) The Ca V 2 agonist GV-58 (50 μM) increases the basal spontaneous MEPP frequency ( h ), but does not affect the average MEPP frequency induced by LTX N4C ; n = 3; N = 36. However, GV-58 significantly increases MEPP frequency within IBIs ( i ); n = 3; N = 36. Symbols next to bars indicate statistical significance compared to respective controls; other comparisons are shown by lines: *, p < 0.05; **, p < 0.01; ***, p < 0.001; #, p < 0.0001; NS, not significant. ( j ) LTX N4C fails to induce any changes in Ca 2+ cyt in nerve terminals pretreated with ω-conotoxin MVIIC. Muscle preparations were preloaded with Fluo-4-AM (see ) and treated with 1 μM ω-conotoxin MVIIC, followed by the addition of 0.25 nM LTX N4C and recording of intracellular fluorescence.
Slp, supplied by Mini-Circuits, 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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transparent tube axegen mct 150 c 7 fluo 8 calcium flux abeam ab112129 assay reagent 8 hepes gibco  (Thermo Fisher)
99
Thermo Fisher transparent tube axegen mct 150 c 7 fluo 8 calcium flux abeam ab112129 assay reagent 8 hepes gibco
Ca V 2.1 channels provide a trigger for LTX N4C -induced bursts of exocytosis, while Ca V 1 channels modify their dynamics. Mouse neuromuscular preparations were incubated in 2 mM Ca 2+ and stimulated by 0.25 nM LTX N4C . ( a , b ) Average MEPP frequencies induced by LTX N4C before or after the application of Ca v channel inhibitors: 10 μM nimodipine ( n = 6; N = 32) to block Ca V 1 channels ( a ), or 1 <t>μM</t> <t>ω-conotoxin</t> <t>MVIIC</t> ( n = 4; N = 36) to block Ca V 2.1/2.2 channels ( b ). ( c ) ω-Conotoxin MVIIC significantly reduces MEPP frequencies within the IBIs of LTX N4C -induced bursts; n = 5. ( d , e ) Average MEPP frequencies induced by LTX N4C after the application of more selective Ca V 2 channel inhibitors: 50 nM ω-conotoxin GVIA ( n = 4; N = 32) to block Ca V 2.2 channels ( d ), or 200 nM ω-agatoxin IVA ( n = 6; N = 31) to block Ca V 2.1 channels ( e ). ( f ) Ca V 2.1 blockers only affect LTX N4C actions if added before the toxin, but fail to do so when added after LTX N4C ; n = 10; N = 67. ( g ) ω-Agatoxin IVA (200 nM) blocks all LTX N4C -induced increase in MEPP frequency when added together with or after the G αq blocker UBO-QIC; n = 4; N = 32. ( h , i ) The Ca V 2 agonist GV-58 (50 μM) increases the basal spontaneous MEPP frequency ( h ), but does not affect the average MEPP frequency induced by LTX N4C ; n = 3; N = 36. However, GV-58 significantly increases MEPP frequency within IBIs ( i ); n = 3; N = 36. Symbols next to bars indicate statistical significance compared to respective controls; other comparisons are shown by lines: *, p < 0.05; **, p < 0.01; ***, p < 0.001; #, p < 0.0001; NS, not significant. ( j ) LTX N4C fails to induce any changes in Ca 2+ cyt in nerve terminals pretreated with ω-conotoxin MVIIC. Muscle preparations were preloaded with Fluo-4-AM (see ) and treated with 1 μM ω-conotoxin MVIIC, followed by the addition of 0.25 nM LTX N4C and recording of intracellular fluorescence.
Transparent Tube Axegen Mct 150 C 7 Fluo 8 Calcium Flux Abeam Ab112129 Assay Reagent 8 Hepes Gibco, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/c-150s/HEPES/us12583846-453-56-70
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myc 150 monoclonal santa cruz biotechnology sc  (Santa Cruz Biotechnology)
96
Santa Cruz Biotechnology myc 150 monoclonal santa cruz biotechnology sc
Ca V 2.1 channels provide a trigger for LTX N4C -induced bursts of exocytosis, while Ca V 1 channels modify their dynamics. Mouse neuromuscular preparations were incubated in 2 mM Ca 2+ and stimulated by 0.25 nM LTX N4C . ( a , b ) Average MEPP frequencies induced by LTX N4C before or after the application of Ca v channel inhibitors: 10 μM nimodipine ( n = 6; N = 32) to block Ca V 1 channels ( a ), or 1 <t>μM</t> <t>ω-conotoxin</t> <t>MVIIC</t> ( n = 4; N = 36) to block Ca V 2.1/2.2 channels ( b ). ( c ) ω-Conotoxin MVIIC significantly reduces MEPP frequencies within the IBIs of LTX N4C -induced bursts; n = 5. ( d , e ) Average MEPP frequencies induced by LTX N4C after the application of more selective Ca V 2 channel inhibitors: 50 nM ω-conotoxin GVIA ( n = 4; N = 32) to block Ca V 2.2 channels ( d ), or 200 nM ω-agatoxin IVA ( n = 6; N = 31) to block Ca V 2.1 channels ( e ). ( f ) Ca V 2.1 blockers only affect LTX N4C actions if added before the toxin, but fail to do so when added after LTX N4C ; n = 10; N = 67. ( g ) ω-Agatoxin IVA (200 nM) blocks all LTX N4C -induced increase in MEPP frequency when added together with or after the G αq blocker UBO-QIC; n = 4; N = 32. ( h , i ) The Ca V 2 agonist GV-58 (50 μM) increases the basal spontaneous MEPP frequency ( h ), but does not affect the average MEPP frequency induced by LTX N4C ; n = 3; N = 36. However, GV-58 significantly increases MEPP frequency within IBIs ( i ); n = 3; N = 36. Symbols next to bars indicate statistical significance compared to respective controls; other comparisons are shown by lines: *, p < 0.05; **, p < 0.01; ***, p < 0.001; #, p < 0.0001; NS, not significant. ( j ) LTX N4C fails to induce any changes in Ca 2+ cyt in nerve terminals pretreated with ω-conotoxin MVIIC. Muscle preparations were preloaded with Fluo-4-AM (see ) and treated with 1 μM ω-conotoxin MVIIC, followed by the addition of 0.25 nM LTX N4C and recording of intracellular fluorescence.
Myc 150 Monoclonal Santa Cruz Biotechnology Sc, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/c-150s/c-Myc+Antibody/us12578341-107-66-69
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low pass filter  (Mini-Circuits)
95
Mini-Circuits low pass filter
Ca V 2.1 channels provide a trigger for LTX N4C -induced bursts of exocytosis, while Ca V 1 channels modify their dynamics. Mouse neuromuscular preparations were incubated in 2 mM Ca 2+ and stimulated by 0.25 nM LTX N4C . ( a , b ) Average MEPP frequencies induced by LTX N4C before or after the application of Ca v channel inhibitors: 10 μM nimodipine ( n = 6; N = 32) to block Ca V 1 channels ( a ), or 1 <t>μM</t> <t>ω-conotoxin</t> <t>MVIIC</t> ( n = 4; N = 36) to block Ca V 2.1/2.2 channels ( b ). ( c ) ω-Conotoxin MVIIC significantly reduces MEPP frequencies within the IBIs of LTX N4C -induced bursts; n = 5. ( d , e ) Average MEPP frequencies induced by LTX N4C after the application of more selective Ca V 2 channel inhibitors: 50 nM ω-conotoxin GVIA ( n = 4; N = 32) to block Ca V 2.2 channels ( d ), or 200 nM ω-agatoxin IVA ( n = 6; N = 31) to block Ca V 2.1 channels ( e ). ( f ) Ca V 2.1 blockers only affect LTX N4C actions if added before the toxin, but fail to do so when added after LTX N4C ; n = 10; N = 67. ( g ) ω-Agatoxin IVA (200 nM) blocks all LTX N4C -induced increase in MEPP frequency when added together with or after the G αq blocker UBO-QIC; n = 4; N = 32. ( h , i ) The Ca V 2 agonist GV-58 (50 μM) increases the basal spontaneous MEPP frequency ( h ), but does not affect the average MEPP frequency induced by LTX N4C ; n = 3; N = 36. However, GV-58 significantly increases MEPP frequency within IBIs ( i ); n = 3; N = 36. Symbols next to bars indicate statistical significance compared to respective controls; other comparisons are shown by lines: *, p < 0.05; **, p < 0.01; ***, p < 0.001; #, p < 0.0001; NS, not significant. ( j ) LTX N4C fails to induce any changes in Ca 2+ cyt in nerve terminals pretreated with ω-conotoxin MVIIC. Muscle preparations were preloaded with Fluo-4-AM (see ) and treated with 1 μM ω-conotoxin MVIIC, followed by the addition of 0.25 nM LTX N4C and recording of intracellular fluorescence.
Low Pass Filter, supplied by Mini-Circuits, 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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s parameter data  (Mini-Circuits)
94
Mini-Circuits s parameter data
Ca V 2.1 channels provide a trigger for LTX N4C -induced bursts of exocytosis, while Ca V 1 channels modify their dynamics. Mouse neuromuscular preparations were incubated in 2 mM Ca 2+ and stimulated by 0.25 nM LTX N4C . ( a , b ) Average MEPP frequencies induced by LTX N4C before or after the application of Ca v channel inhibitors: 10 μM nimodipine ( n = 6; N = 32) to block Ca V 1 channels ( a ), or 1 <t>μM</t> <t>ω-conotoxin</t> <t>MVIIC</t> ( n = 4; N = 36) to block Ca V 2.1/2.2 channels ( b ). ( c ) ω-Conotoxin MVIIC significantly reduces MEPP frequencies within the IBIs of LTX N4C -induced bursts; n = 5. ( d , e ) Average MEPP frequencies induced by LTX N4C after the application of more selective Ca V 2 channel inhibitors: 50 nM ω-conotoxin GVIA ( n = 4; N = 32) to block Ca V 2.2 channels ( d ), or 200 nM ω-agatoxin IVA ( n = 6; N = 31) to block Ca V 2.1 channels ( e ). ( f ) Ca V 2.1 blockers only affect LTX N4C actions if added before the toxin, but fail to do so when added after LTX N4C ; n = 10; N = 67. ( g ) ω-Agatoxin IVA (200 nM) blocks all LTX N4C -induced increase in MEPP frequency when added together with or after the G αq blocker UBO-QIC; n = 4; N = 32. ( h , i ) The Ca V 2 agonist GV-58 (50 μM) increases the basal spontaneous MEPP frequency ( h ), but does not affect the average MEPP frequency induced by LTX N4C ; n = 3; N = 36. However, GV-58 significantly increases MEPP frequency within IBIs ( i ); n = 3; N = 36. Symbols next to bars indicate statistical significance compared to respective controls; other comparisons are shown by lines: *, p < 0.05; **, p < 0.01; ***, p < 0.001; #, p < 0.0001; NS, not significant. ( j ) LTX N4C fails to induce any changes in Ca 2+ cyt in nerve terminals pretreated with ω-conotoxin MVIIC. Muscle preparations were preloaded with Fluo-4-AM (see ) and treated with 1 μM ω-conotoxin MVIIC, followed by the addition of 0.25 nM LTX N4C and recording of intracellular fluorescence.
S Parameter Data, supplied by Mini-Circuits, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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minicircuits slp 450 lowpass filters  (Mini-Circuits)
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Mini-Circuits minicircuits slp 450 lowpass filters
Ca V 2.1 channels provide a trigger for LTX N4C -induced bursts of exocytosis, while Ca V 1 channels modify their dynamics. Mouse neuromuscular preparations were incubated in 2 mM Ca 2+ and stimulated by 0.25 nM LTX N4C . ( a , b ) Average MEPP frequencies induced by LTX N4C before or after the application of Ca v channel inhibitors: 10 μM nimodipine ( n = 6; N = 32) to block Ca V 1 channels ( a ), or 1 <t>μM</t> <t>ω-conotoxin</t> <t>MVIIC</t> ( n = 4; N = 36) to block Ca V 2.1/2.2 channels ( b ). ( c ) ω-Conotoxin MVIIC significantly reduces MEPP frequencies within the IBIs of LTX N4C -induced bursts; n = 5. ( d , e ) Average MEPP frequencies induced by LTX N4C after the application of more selective Ca V 2 channel inhibitors: 50 nM ω-conotoxin GVIA ( n = 4; N = 32) to block Ca V 2.2 channels ( d ), or 200 nM ω-agatoxin IVA ( n = 6; N = 31) to block Ca V 2.1 channels ( e ). ( f ) Ca V 2.1 blockers only affect LTX N4C actions if added before the toxin, but fail to do so when added after LTX N4C ; n = 10; N = 67. ( g ) ω-Agatoxin IVA (200 nM) blocks all LTX N4C -induced increase in MEPP frequency when added together with or after the G αq blocker UBO-QIC; n = 4; N = 32. ( h , i ) The Ca V 2 agonist GV-58 (50 μM) increases the basal spontaneous MEPP frequency ( h ), but does not affect the average MEPP frequency induced by LTX N4C ; n = 3; N = 36. However, GV-58 significantly increases MEPP frequency within IBIs ( i ); n = 3; N = 36. Symbols next to bars indicate statistical significance compared to respective controls; other comparisons are shown by lines: *, p < 0.05; **, p < 0.01; ***, p < 0.001; #, p < 0.0001; NS, not significant. ( j ) LTX N4C fails to induce any changes in Ca 2+ cyt in nerve terminals pretreated with ω-conotoxin MVIIC. Muscle preparations were preloaded with Fluo-4-AM (see ) and treated with 1 μM ω-conotoxin MVIIC, followed by the addition of 0.25 nM LTX N4C and recording of intracellular fluorescence.
Minicircuits Slp 450 Lowpass Filters, supplied by Mini-Circuits, 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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Image Search Results


Ca V 2.1 channels provide a trigger for LTX N4C -induced bursts of exocytosis, while Ca V 1 channels modify their dynamics. Mouse neuromuscular preparations were incubated in 2 mM Ca 2+ and stimulated by 0.25 nM LTX N4C . ( a , b ) Average MEPP frequencies induced by LTX N4C before or after the application of Ca v channel inhibitors: 10 μM nimodipine ( n = 6; N = 32) to block Ca V 1 channels ( a ), or 1 μM ω-conotoxin MVIIC ( n = 4; N = 36) to block Ca V 2.1/2.2 channels ( b ). ( c ) ω-Conotoxin MVIIC significantly reduces MEPP frequencies within the IBIs of LTX N4C -induced bursts; n = 5. ( d , e ) Average MEPP frequencies induced by LTX N4C after the application of more selective Ca V 2 channel inhibitors: 50 nM ω-conotoxin GVIA ( n = 4; N = 32) to block Ca V 2.2 channels ( d ), or 200 nM ω-agatoxin IVA ( n = 6; N = 31) to block Ca V 2.1 channels ( e ). ( f ) Ca V 2.1 blockers only affect LTX N4C actions if added before the toxin, but fail to do so when added after LTX N4C ; n = 10; N = 67. ( g ) ω-Agatoxin IVA (200 nM) blocks all LTX N4C -induced increase in MEPP frequency when added together with or after the G αq blocker UBO-QIC; n = 4; N = 32. ( h , i ) The Ca V 2 agonist GV-58 (50 μM) increases the basal spontaneous MEPP frequency ( h ), but does not affect the average MEPP frequency induced by LTX N4C ; n = 3; N = 36. However, GV-58 significantly increases MEPP frequency within IBIs ( i ); n = 3; N = 36. Symbols next to bars indicate statistical significance compared to respective controls; other comparisons are shown by lines: *, p < 0.05; **, p < 0.01; ***, p < 0.001; #, p < 0.0001; NS, not significant. ( j ) LTX N4C fails to induce any changes in Ca 2+ cyt in nerve terminals pretreated with ω-conotoxin MVIIC. Muscle preparations were preloaded with Fluo-4-AM (see ) and treated with 1 μM ω-conotoxin MVIIC, followed by the addition of 0.25 nM LTX N4C and recording of intracellular fluorescence.

Journal: Cells

Article Title: Latrophilin-1-Mediated G αq Signaling, Store-Operated Ca 2+ Entry, and Ca V 2.1 Activation Control Spontaneous Exocytosis at the Mouse Neuromuscular Junction

doi: 10.3390/cells15090821

Figure Lengend Snippet: Ca V 2.1 channels provide a trigger for LTX N4C -induced bursts of exocytosis, while Ca V 1 channels modify their dynamics. Mouse neuromuscular preparations were incubated in 2 mM Ca 2+ and stimulated by 0.25 nM LTX N4C . ( a , b ) Average MEPP frequencies induced by LTX N4C before or after the application of Ca v channel inhibitors: 10 μM nimodipine ( n = 6; N = 32) to block Ca V 1 channels ( a ), or 1 μM ω-conotoxin MVIIC ( n = 4; N = 36) to block Ca V 2.1/2.2 channels ( b ). ( c ) ω-Conotoxin MVIIC significantly reduces MEPP frequencies within the IBIs of LTX N4C -induced bursts; n = 5. ( d , e ) Average MEPP frequencies induced by LTX N4C after the application of more selective Ca V 2 channel inhibitors: 50 nM ω-conotoxin GVIA ( n = 4; N = 32) to block Ca V 2.2 channels ( d ), or 200 nM ω-agatoxin IVA ( n = 6; N = 31) to block Ca V 2.1 channels ( e ). ( f ) Ca V 2.1 blockers only affect LTX N4C actions if added before the toxin, but fail to do so when added after LTX N4C ; n = 10; N = 67. ( g ) ω-Agatoxin IVA (200 nM) blocks all LTX N4C -induced increase in MEPP frequency when added together with or after the G αq blocker UBO-QIC; n = 4; N = 32. ( h , i ) The Ca V 2 agonist GV-58 (50 μM) increases the basal spontaneous MEPP frequency ( h ), but does not affect the average MEPP frequency induced by LTX N4C ; n = 3; N = 36. However, GV-58 significantly increases MEPP frequency within IBIs ( i ); n = 3; N = 36. Symbols next to bars indicate statistical significance compared to respective controls; other comparisons are shown by lines: *, p < 0.05; **, p < 0.01; ***, p < 0.001; #, p < 0.0001; NS, not significant. ( j ) LTX N4C fails to induce any changes in Ca 2+ cyt in nerve terminals pretreated with ω-conotoxin MVIIC. Muscle preparations were preloaded with Fluo-4-AM (see ) and treated with 1 μM ω-conotoxin MVIIC, followed by the addition of 0.25 nM LTX N4C and recording of intracellular fluorescence.

Article Snippet: Tetramethylrhodamine-conjugated α-bungarotoxin (αBuTX), αBuTX Alexa Fluor 546, Alexa Fluor 647 labeling kit, and Fluo-4 acetoxymethyl (AM) ester were from Thermo-Fisher Scientific (UK Life Technologies Limited, Paisley, UK). ω-Agatoxin IVA, ω-conotoxin GVIA, and ω-conotoxin MVIIC were from Alomone Labs (Jerusalem, Israel).

Techniques: Incubation, Blocking Assay, Fluorescence