Zhang J, Chiodo L A, Freeman A S
Department of Psychiatry, Wayne State University School of Medicine, Detroit, MI.
Eur J Pharmacol. 1993 Jan 19;230(3):371-4. doi: 10.1016/0014-2999(93)90576-4.
The effects of i.v. administration of the noncompetitive NMDA receptor antagonists, phencyclidine and MK-801, and the sigma receptor ligand, 1,3-di(2-tolyl)guanidine (DTG), on the firing rates of non-dopaminergic mid brain neurons were evaluated in chloral hydrate-anesthetized rats. Phencyclidine and MK-801 inhibited the activity of putative gamma-aminobutyric acid (GABA)-containing interneurons identified by their response to foot-pinch. DTG did not significantly alter neuronal activity. These results suggest that the reported excitatory effects of non-competitive NMDA receptor antagonists on dopamine neuronal activity are due, in part, to disinhibition secondary to the inhibition of interneuron activity.
在水合氯醛麻醉的大鼠中,评估了静脉注射非竞争性N-甲基-D-天冬氨酸(NMDA)受体拮抗剂苯环己哌啶和MK-801以及σ受体配体1,3-二(2-甲苯基)胍(DTG)对非多巴胺能中脑神经元放电率的影响。苯环己哌啶和MK-801抑制了通过对夹足反应鉴定的假定含γ-氨基丁酸(GABA)的中间神经元的活性。DTG没有显著改变神经元活性。这些结果表明,报道的非竞争性NMDA受体拮抗剂对多巴胺神经元活性的兴奋作用部分是由于中间神经元活性抑制继发的去抑制作用。