Newberry N R, Connolly G P
Merck Sharp and Dohme Research Laboratories, Neuroscience Research Centre, Essex, U.K.
Neuropharmacology. 1989 May;28(5):487-93. doi: 10.1016/0028-3908(89)90084-1.
Selective antagonists have been used to classify the muscarinic receptors involved in the slow excitatory postsynaptic potential and slow inhibitory postsynaptic potential of the superior cervical ganglia of the rat, as recorded in 1 microM neostigmine, using a grease-gap method. Cardioselective M2 antagonists, e.g. AF-DX 116, depressed the slow inhibitory postsynaptic potential and enhanced the slow excitatory postsynaptic potential. The M1 selective antagonist pirenzepine depressed both potentials equally. The high potency of pirenzepine against the slow excitatory postsynaptic potential, however, indicates that it is mediated by M1 receptors. The slow excitatory and inhibitory postsynaptic potentials were found to be pharmacologically similar to the muscarinic agonist-induced depolarisation and hyperpolarisation of this preparation, respectively. The actions of two muscarinic agonists on the postsynaptic potentials were also studied. It is concluded that the slow excitatory postsynaptic potential is mediated by M1 receptors and the slow inhibitory postsynaptic potential by cardiac-like M2 receptors.
采用油脂间隙法,在1微摩尔新斯的明存在的情况下,记录大鼠颈上神经节的慢兴奋性突触后电位和慢抑制性突触后电位,使用选择性拮抗剂对其中涉及的毒蕈碱受体进行分类。心脏选择性M2拮抗剂,如AF-DX 116,可抑制慢抑制性突触后电位并增强慢兴奋性突触后电位。M1选择性拮抗剂哌仑西平对两种电位的抑制作用相同。然而,哌仑西平对慢兴奋性突触后电位的高效能表明它是由M1受体介导的。发现慢兴奋性和抑制性突触后电位在药理学上分别类似于该制剂中毒蕈碱激动剂诱导的去极化和超极化。还研究了两种毒蕈碱激动剂对突触后电位的作用。得出的结论是,慢兴奋性突触后电位由M1受体介导,慢抑制性突触后电位由类心脏M2受体介导。