Whitlock B B, Liu Y, Chang S, Saini P, Ha B K, Barrett T W, Wolfe S A
Department of Medical Microbiology and Immunology, Ohio State University College of Medicine, Columbus 43210, USA.
J Neuroimmunol. 1996 Jul;67(2):83-96. doi: 10.1016/0165-5728(96)00041-0.
High concentrations of novel, haloperidol- and DTG-inaccessible (+)-[3H]-3-PPP binding sites were found in human peripheral blood leukocytes rat spleen and splenocytes, but not in rat brain. Splenic sites were localized in a course punctate pattern in the marginal zones and red pulp. The pharmacology of the splenic sites was: (-)-SKF 10,047 > or = naltrexone = (-)-pentazocine > (+)-pentazocine = (-)-3-PPP = (+)-SKF 10,047 > or = (+)-3-PPP > or = dextrorphan > dextromethorphan > PCP > clorgyline. DTG, haloperidol, TCP, (-)-deprenyl and SKF 525-A did not complete. Binding activity was destroyed by heating and phospholipase C, but not by proteases or glycosidases. These sites may be involved in immunomodulation by opiate and sigma receptor agonists.
在人外周血白细胞、大鼠脾脏和脾细胞中发现了高浓度的新型、对氟哌啶醇和二硫代甘油(DTG)不可及的(+)-[3H]-3-苯基哌嗪(3-PPP)结合位点,但在大鼠脑中未发现。脾脏中的位点以粗大的点状模式定位于边缘区和红髓。脾脏位点的药理学特性为:(-)-司可巴比妥10,047≥纳曲酮=(-)-喷他佐辛>(+)-喷他佐辛=(-)-3-PPP=(+)-司可巴比妥10,047≥(+)-3-PPP≥右啡烷>右美沙芬>苯环己哌啶>氯吉兰。DTG、氟哌啶醇、三氯丙嗪、(-)-丙炔苯丙胺和SKF 525-A无作用。加热和磷脂酶C可破坏结合活性,但蛋白酶或糖苷酶无此作用。这些位点可能参与阿片和σ受体激动剂的免疫调节。