Hori T, Suzuki T, Baba A, Abe S, Yamamoto T, Moroji T, Shiraishi H
Department of Psychiatry, University of Tsukuba, Ibarak, Japan.
Neurosci Lett. 1996 May 17;209(3):153-6. doi: 10.1016/0304-3940(96)11617-7.
The effects of phencyclidine (PCP) and its metabolites on serotonin (5-hydroxytryptamine, 5-HT) receptors were studied. PCP and its metabolites inhibited the uptake of [3H]5-HT and the binding of [3H]paroxetine in rat brain, while they failed to inhibit either [3H]5-HT binding to 5-HT1 receptors or [3H]ketanserin binding to 5-HT2 receptors. The trans-isomer of 4-phenyl-4-(I-piperidinyl)cyclo-hexanol (trans-4-PPC), the major metabolite of PCP, rather than PCP itself, inhibited [3H]5-HT uptake most potently. These results suggest that the serotonergic effects of PCP, in part, may be based on the effects of PCP metabolites on 5-HT uptake.
研究了苯环己哌啶(PCP)及其代谢产物对5-羟色胺(5-HT)受体的影响。PCP及其代谢产物抑制大鼠脑内[3H]5-HT的摄取和[3H]帕罗西汀的结合,但它们既不抑制[3H]5-HT与5-HT1受体的结合,也不抑制[3H]酮色林与5-HT2受体的结合。PCP的主要代谢产物4-苯基-4-(1-哌啶基)环己醇(反式-4-PPC)的反式异构体,而非PCP本身,最有效地抑制了[3H]5-HT的摄取。这些结果表明,PCP的5-羟色胺能效应部分可能基于PCP代谢产物对5-HT摄取的影响。