Wessler I, Dooley D J, Lohr B
Department of Pharmacology, University of Mainz, Germany.
Eur J Pharmacol. 1995 May 4;278(1):83-6. doi: 10.1016/0014-2999(95)00133-6.
In the present experiments it was tested whether omega-agatoxin-IVA, a peptide blocking P-type voltage-dependent Ca2+ channels, inhibits the evoked release of newly synthesized [3H]acetylcholine from the rat phrenic nerve. Release of [3H]acetylcholine was evoked by electrical stimulation of the isolated phrenic nerve (100 or 750 pulses at 5 Hz). omega-Agatoxin-IVA inhibited evoked [3H]acetylcholine release in a concentration-related manner; inhibition started at a concentration of 30 nM with complete block occurring at 500 nM. In conclusion, the present experiments demonstrate that omega-agatoxin-IVA-sensitive P-type Ca2+ channels are critically involved in the regulation of stimulus-induced transmitter release at mammalian motor endplates.
在本实验中，检测了一种阻断P型电压依赖性Ca2+通道的肽——ω-芋螺毒素-IVA是否抑制大鼠膈神经新合成的[3H]乙酰胆碱的诱发释放。通过电刺激分离的膈神经（5Hz下100或750个脉冲）诱发[3H]乙酰胆碱的释放。ω-芋螺毒素-IVA以浓度相关的方式抑制诱发的[3H]乙酰胆碱释放；抑制作用在30 nM的浓度时开始，在500 nM时完全阻断。总之，本实验表明，ω-芋螺毒素-IVA敏感的P型Ca2+通道在哺乳动物运动终板刺激诱导的递质释放调节中起关键作用。
