P型钙通道阻滞剂ω-芋螺毒素IVA对小鼠运动神经乙酰胆碱释放的抑制作用。
Inhibition of acetylcholine release from mouse motor nerve by a P-type calcium channel blocker, omega-agatoxin IVA.
作者信息
Hong S J, Chang C C
机构信息
Department of Pharmacology, College of Medicine, National Taiwan University, Taipei.
出版信息
J Physiol. 1995 Jan 15;482 ( Pt 2)(Pt 2):283-90. doi: 10.1113/jphysiol.1995.sp020517.
Abstract
- The effects were studied of the central neurone P-type Ca2+ channel blockers, omega-agatoxin IVA, omega-conotoxin MVIIC (polypeptide toxins) and synthetic funnel-web spider polyamine toxin on acetylcholine release from mouse motor nerve. 2. omega-Agatoxin IVA decreased the quantal content of endplate potentials and blocked synaptic transmission in the nanomolar range in a reversible manner, whereas the other toxins depressed transmission in the hundred micromolar range. 3. The polyamine toxin, but not the polypeptide toxins, decreased the amplitude of the miniature endplate potential. The increase in the frequency of miniature endplate potentials evoked by high [K+], but not that evoked by alpha-latrotoxin, was effectively antagonized by omega-agatoxin IVA. 4. In the presence of omega-agatoxin IVA, high frequency nerve stimulation produced facilitation of endplate currents and tetanic contractions. 5. The results suggest that, under physiological conditions, the Ca2+ necessary for nerve action potential-evoked acetylcholine release is translocated via a subtype of the P-type Ca2+ channel sensitive to omega-agatoxin IVA.
摘要
- 研究了中枢神经元P型钙离子通道阻滞剂ω-芋螺毒素IVA、ω-芋螺毒素MVIIC（多肽毒素）以及合成的漏斗网蜘蛛多胺毒素对小鼠运动神经乙酰胆碱释放的影响。2. ω-芋螺毒素IVA以可逆方式在纳摩尔范围内降低终板电位的量子含量并阻断突触传递，而其他毒素在百微摩尔范围内抑制传递。3. 多胺毒素而非多肽毒素降低了微小终板电位的幅度。ω-芋螺毒素IVA有效拮抗了高[K⁺]诱发的微小终板电位频率增加，但对α-银环蛇毒素诱发的频率增加无拮抗作用。4. 在存在ω-芋螺毒素IVA的情况下，高频神经刺激产生终板电流易化和强直收缩。5. 结果表明，在生理条件下，神经动作电位诱发乙酰胆碱释放所需的钙离子通过对ω-芋螺毒素IVA敏感的P型钙离子通道亚型转运。
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