Jiang Z G, Dun N J
Brain Res. 1986 Aug 27;381(1):182-6. doi: 10.1016/0006-8993(86)90710-9.
In addition to depolarizing the ventral horn cells including antidromically identified motoneurons in thin transverse neonatal rat spinal cord slice preparations, exogenously applied acetylcholine (ACh) suppressed the amplitude of excitatory postsynaptic potentials (EPSPs) either occurring spontaneously or elicited by stimulation of dorsal rootlets. A reduction of EPSPs could still be detected when the ACh-induced depolarization was nullified by hyperpolarizing current. Atropine but not D-tubocurarine effectively antagonized the depolarization and synaptic depression caused by ACh. While depressing the EPSPs, ACh had no appreciable effect on membrane depolarizations elicited by glutamate. Methacholine mimicked the depolarizing and synaptic depressant effects of ACh. The results suggest that muscarinic agonists inhibit synaptic transmission of ventral horn neurons including motoneurons by a presynaptic mechanism in reducing the output of excitatory transmitters.
除了使新生大鼠脊髓薄片横切标本中包括逆向鉴定的运动神经元在内的腹角细胞去极化外，外源性应用乙酰胆碱（ACh）还可抑制自发出现的或由背根小束刺激诱发的兴奋性突触后电位（EPSP）的幅度。当通过超极化电流消除ACh诱导的去极化时，仍可检测到EPSP的降低。阿托品而非筒箭毒碱可有效拮抗ACh引起的去极化和突触抑制。在抑制EPSP的同时，ACh对谷氨酸引起的膜去极化没有明显影响。醋甲胆碱模拟了ACh的去极化和突触抑制作用。结果表明，毒蕈碱激动剂通过减少兴奋性递质的释放，以突触前机制抑制包括运动神经元在内的腹角神经元的突触传递。
