Wang Y, Lee H K
Department of Pharmacology, National Defense Medical Center, Taipei, Taiwan, Republic of China.
Neuropharmacology. 1989 Apr;28(4):343-50. doi: 10.1016/0028-3908(89)90028-2.
The purpose of this experiment was to investigate the interaction of GABA (gamma aminobutyric acid) with PCP (phencyclidine) and sigma receptor agonists in the cerebellum. Drugs were applied directly to a single cerebellar Purkinje neuron of urethane-anesthetized rats, through a multibarrel pipette. The PCP receptor agonist, (+)PCMP [1-(-1-phenylcyclohexyl)-3-methyl piperidine], significantly enhanced GABA-induced inhibition. On the other hand, its stereoisomer, (-)PCMP, had no such modulatory effect. Dexoxadrol, a sigma receptor agonist, similar to (+)PCMP, potentiated GABA-induced depression. Its stereoisomer, levoxadrol, although inhibiting the spontaneous firings of Purkinje neurons, did not alter the effect of GABA. In conclusion, the findings indicate that the electrophysiological mechanisms of PCP-induced facilitation of GABA-induced reactions are similar to those triggered by sigma agonists in the cerebellum.
本实验的目的是研究γ-氨基丁酸（GABA）与苯环利定（PCP）及σ受体激动剂在小脑的相互作用。通过多管移液管将药物直接施加于经乌拉坦麻醉大鼠的单个小脑浦肯野神经元。PCP受体激动剂(+)PCMP [1-(-1-苯基环己基)-3-甲基哌啶]可显著增强GABA诱导的抑制作用。另一方面，其立体异构体(-)PCMP则无此调节作用。σ受体激动剂右吗拉胺与(+)PCMP类似，可增强GABA诱导的抑制作用。其立体异构体左吗拉胺虽然可抑制浦肯野神经元的自发放电，但并不改变GABA的作用。总之，研究结果表明，PCP诱导促进GABA诱导反应的电生理机制与小脑σ激动剂触发的机制相似。
