Tran S, Boot J R
Eli Lilly and Co., Lilly Research Centre Ltd., Windlesham, Surrey, UK.
Eur J Pharmacol. 1997 Sep 17;335(1):31-6. doi: 10.1016/s0014-2999(97)01174-6.
The omega-conotoxins GVIA, MVIIA, MVIIC and SVIB reduced in a concentration-dependent manner the low frequency electrically stimulated twitch response of the guinea-pig ileum and rat vas deferens. The relative activities of the conotoxins showed some difference between the two preparations in that for ileum it was MVIIA = GVIA > MVIIC = SVIB and for the vas deferens it was MVIIA > GVIA >> SVIB > MVIIC. High frequency electrical stimulation of both preparations resulted in a neurally-mediated omega-conotoxin GVIA resistant component that was sensitive to high concentrations of either omega-conotoxin MVIIC (300 nM- 1 microM) or omega-agatoxin IVA (300 nM-1 microM) but not to omega-conotoxin MVIIA. Lower levels of either omega-conotoxin MVIIC or omega-agatoxin IVA (30-100 nM) failed to significantly affect the omega-conotoxin GVIA resistant component. This omega-conotoxin GVIA resistant component was large in the ileal preparation comprising 30-40% of the maximal response at 20 Hz but relatively small (10%) in the vas deferens. These studies revealed that the N-type voltage-dependent calcium channel (VDCCs) exclusively controls neurotransmission during low frequency stimulation but at higher frequencies there is an additional non-adrenergic, non-cholinergic (NANC) neurotransmission that appears to be regulated via Q-type VDCC.
ω-芋螺毒素GVIA、MVIIA、MVIIC和SVIB以浓度依赖性方式降低豚鼠回肠和大鼠输精管的低频电刺激抽搐反应。两种制剂中芋螺毒素的相对活性存在一些差异,在回肠中为MVIIA = GVIA > MVIIC = SVIB,在输精管中为MVIIA > GVIA >> SVIB > MVIIC。对两种制剂进行高频电刺激均产生一种神经介导的对ω-芋螺毒素GVIA耐药的成分,该成分对高浓度的ω-芋螺毒素MVIIC(300 nM - 1 μM)或ω-阿加毒素IVA(300 nM - 1 μM)敏感,但对ω-芋螺毒素MVIIA不敏感。较低水平的ω-芋螺毒素MVIIC或ω-阿加毒素IVA(30 - 100 nM)未能显著影响对ω-芋螺毒素GVIA耐药的成分。这种对ω-芋螺毒素GVIA耐药的成分在回肠制剂中占比很大,在20 Hz时占最大反应的30 - 40%,但在输精管中相对较小(10%)。这些研究表明,N型电压依赖性钙通道(VDCCs)在低频刺激期间专门控制神经传递,但在较高频率时存在一种额外的非肾上腺素能、非胆碱能(NANC)神经传递,其似乎通过Q型VDCC进行调节。