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通过激活节后毒蕈碱M1受体介导自主神经节中突触传递的调节。

Modulation of synaptic transmission in autonomic ganglia mediated via the activation of postganglionic muscarinic M1 receptors.

作者信息

Galvan M

机构信息

Department of Pharmacology, Byk Gulden Pharmaceuticals, Konstanz, FRG.

出版信息

Pharmacology. 1988;37 Suppl 1:11-6. doi: 10.1159/000138501.

Abstract

The facilitatory actions of muscarine on synaptic transmission were measured in rat superior cervical ganglia in vitro. Muscarine (300 nmol/l) induced increases in submaximal population action potentials, which were mimicked by the M1 receptor agonist McN-A-343 (1 mumol/l) and antagonized by the M1 receptor antagonist pirenzepine (100 nmol/l) and telenzepine (100 nmol/l), but not by the M2 receptor antagonist AF-DX 116 (1 mumol/l). Slow excitatory postsynaptic potentials recorded from curarized rabbit isolated superior cervical ganglia were also blocked by telenzepine (300 nmol/l) but not by AF-DX 116 (3 mumol/l). It is concluded that M1 receptors mediate the excitatory actions of muscarinic agonists in these sympathetic ganglia.

摘要

在体外对大鼠颈上神经节中毒蕈碱对突触传递的促进作用进行了测定。毒蕈碱(300 nmol/l)可使阈下复合动作电位增加,该作用可被M1受体激动剂 McN - A - 343(1 μmol/l)模拟,并被M1受体拮抗剂哌仑西平(100 nmol/l)和替仑西平(100 nmol/l)拮抗,但不被M2受体拮抗剂AF - DX 116(1 μmol/l)拮抗。从箭毒处理的兔离体颈上神经节记录到的慢兴奋性突触后电位也被替仑西平(300 nmol/l)阻断,但不被AF - DX 116(3 μmol/l)阻断。得出结论:M1受体介导了毒蕈碱激动剂在这些交感神经节中的兴奋作用。

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