苯环利定结合位点与σ受体之间的体内功能相互作用，导致大鼠出现点头行为。
In vivo functional interaction between phencyclidine binding sites and sigma receptors to produce head-weaving behavior in rats.
作者信息
Kitaichi K, Noda Y, Hasegawa T, Furukawa H, Nabeshima T
机构信息
Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine, Showa-ku, Japan.
出版信息
Eur J Pharmacol. 1996 Dec 30;318(2-3):205-11. doi: 10.1016/s0014-2999(96)00771-6.
To investigate the in vivo functional interaction between phencyclidine (1-(1-phenylcyclohexyl)piperidine; PCP) binding sites and sigma receptors, we examined the effects of sigma receptor ligands on stereotyped head-weaving behavior induced by PCP, a putative PCP/sigma receptor ligand, and (+)-5-methyl-10,11-dihydroxy-5H-dibenzo(a,d)cyclo-hepten-5,10-imin e ((+)-MK-801; dizocilpine), a selective PCP binding site ligand, in rats. PCP (7.5 mg/kg, i.p.)-induced head-weaving behavior was inhibited by both N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)-phenyl]-ethylamine (NE-100; 0.03-1.0 mg/kg, p.o.), a selective sigma1 receptor ligand, and alpha-(4-fluorophenyl)-4-(5-fluoro-2-pyrimidinyl)-1-piperidine butanol (BMY-14802; 3 and 10 mg/kg, p.o.), a prototype sigma receptor ligand, in a dose-dependent manner, whereas NE-100 (0.1-1.0 mg/kg, p.o.) and BMY-14802 (3 and 10 mg/kg, p.o.) did not inhibit dizocilpine (0.25 mg/kg, s.c.)-induced head-weaving behavior. These results suggest that NE-100 and BMY-14802 act via sigma receptors. Dizocilpine-induced head-weaving behavior was potentiated by 1,3-di-o-tolyl-guanidine (DTG; 0.03-0.3 microg/kg, i.v.) and (+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine ((+)-3-PPP; 3 and 6 mg/kg, i.p.), sigma1/sigma2 receptor ligands, as well as by (+)-N-allyl-normetazocine ((+)-SKF-10,047: 8 mg/kg, i.p.), a sigma1 receptor ligand, while DTG (0.3 microg/kg, i.v.), (+)-3-PPP (6 mg/kg, i.p.) and (+)-SKF-10,047 (8 mg/kg, i.p.) did not induce this behavior. Potentiation of dizocilpine-induced head-weaving behavior by DTG (0.3 microg/kg, i.v.), (+)-3-PPP (6 mg/kg, i.p.) and (+)-SKF-10,047 (8 mg/kg, i.p.) was completely blocked by NE-100 (0.1 mg/kg, p.o.) and BMY-14802 (10 mg/kg, p.o.). These results suggest that PCP binding sites and sigma receptors are involved in PCP-induced head weaving behavior, and that sigma1 receptors play an important role in modulation of the head-weaving behavior.
为研究苯环己哌啶（1 - （1 - 苯基环己基）哌啶；PCP）结合位点与σ受体之间的体内功能相互作用，我们检测了σ受体配体对PCP（一种假定的PCP/σ受体配体）以及（+） - 5 - 甲基 - 10,11 - 二羟基 - 5H - 二苯并（a，d）环庚烯 - 5,10 - 亚胺（（+） - MK - 801；地佐环平）（一种选择性PCP结合位点配体）诱导的大鼠刻板摇头行为的影响。PCP（7.5毫克/千克，腹腔注射）诱导的摇头行为受到N，N - 二丙基 - 2 - [4 - 甲氧基 - 3 - （2 - 苯乙氧基） - 苯基]乙胺（NE - 100；0.03 - 1.0毫克/千克，口服）和α - （4 - 氟苯基） - 4 - （5 - 氟 - 2 - 嘧啶基） - 1 - 哌啶丁醇（BMY - 14802；3和10毫克/千克，口服）的抑制作用，这两种分别是选择性σ1受体配体和原型σ受体配体，且呈剂量依赖性，而NE - 100（0.1 - 1.0毫克/千克，口服）和BMY - 14802（3和10毫克/千克，口服）并未抑制地佐环平（0.25毫克/千克，皮下注射）诱导的摇头行为。这些结果表明NE - 100和BMY - 14802通过σ受体发挥作用。地佐环平诱导的摇头行为被1,3 - 二 - o - 甲苯基胍（DTG；0.03 - 0.3微克/千克，静脉注射）、（+） - 3 - （3 - 羟基苯基） - N - （1 - 丙基）哌啶（（+） - PPP；3和6毫克/千克，腹腔注射）（σ1/σ2受体配体）以及（+） - N - 烯丙基去甲美沙酮（（+） - SKF - 10,047：8毫克/千克，腹腔注射）（一种σ1受体配体）增强，而DTG（0.3微克/千克，静脉注射）、（+） - PPP（6毫克/千克，腹腔注射）和（+） - SKF - 10,047（8毫克/千克，腹腔注射）本身并不诱导这种行为。DTG（0.3微克/千克，静脉注射）、（+） - PPP（6毫克/千克，腹腔注射）和（+） - SKF - 10,047（8毫克/千克，腹腔注射）对 地佐环平诱导的摇头行为的增强作用被NE - 100（0.1毫克/千克，口服）和BMY - 14802（10毫克/千克，口服）完全阻断。这些结果表明PCP结合位点和σ受体参与了PCP诱导的摇头行为，且σ1受体在这种摇头行为的调节中起重要作用。
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