摘要
β-蝮蛇毒素(β-agkistrodotoxin简写β-AgTX)对骨胳肌神经肌肉接头的作用已有实验分析,本文则观察了β-AgTX对蟾蜍交感神经节胆碱能性和非胆碱能性突触电位的作用。结果表明,β-AgTX对胆碱能性快兴奋性突触后电位(f-EPSP)和由压力微量注射ACh产生的ACh电位快成分有可逆性抑制作用,且对f-EPSP的幅值抑制率明显大于对ACh电位的抑制率,方差分析显示β-AgTX对f-EPSP和对ACh电位的抑制之间的差异显著(P<0.01)。β-AgTX对非胆碱能性迟慢兴奋性突触后电位(1s-EPSP)无明显作用。本结果提示β-AgTX可能是通过抑制节前神经末梢释放AGh的突触前机制和占据突触后N型胆碱能受体影响ACh的作用之突触后机制,抑制蟾蜍交感神经节的胆碱能性传递过程。
The effects of β-agkistrodotoxin (β-AgTX) on synaptic transmission ofthe toad sympathetic ganglia were investigated by intracellular recording tech-niques. Superfusion of β-AgTX (30 μg/ml, 5--15 min) reversibly inhibitedthe cholinergic fast excitatory postsynaptic potential (f-EPSP, n=16) and thefast components of acetylcholine(ACh) potential induced by micropressure adminis-tration of ACh (n=24). Comparison of β-AgTX effect in the same cell groupshowed significantly different inhibition rates on f-EPSP (77.2±27.7%) andACh potential (25.5±17.5%) (n=6, P<0.01, F test). During application ofβ-AgTX (30 or 50 μg/ml) for 15--30 min, no detectable change was found innon-cholinergic late slow EPSPs (n=22). The results suggest that β-AgTXselectively inhibits the cholinergic transmission of the toad sympathetic gangliaby both presynaptic and postsynaptic mechanism.
出处
《生理学报》
CAS
CSCD
北大核心
1992年第2期149-156,共8页
Acta Physiologica Sinica
关键词
β-蝮蛇毒素
突触传递
交感神经节
β-agkistrodotoxin
synaptic transmission
sympathetic ganglion
toad
acetylcholine potential
