Tzschentke T M, Schmidt W J
Department of Neuropharmacology, Zoological Institute, University of Tübingen, Germany.
Neurosci Lett. 1998 Feb 13;242(2):114-6. doi: 10.1016/s0304-3940(98)00023-8.
Previous studies have shown that antagonists at glutamatergic N-methyl-D-aspartate (NMDA) or alpha-amino-3-hydroxy-5-methyl-4-isoxazolpropionic acid (AMPA) receptors can disrupt the development or expression, respectively, of conditioned place preference (CPP) induced by drugs of abuse. The present study examined the effects of inhibition of presynaptic glutamate release by riluzole on the development of morphine- and amphetamine-induced CPP. Morphine (10 mg/kg), D,L-amphetamine (4 mg/kg) and riluzole (4 mg/kg) itself each produced a significant CPP; however, when riluzole was co-administered with morphine or amphetamine during the conditioning sessions, no CPP developed. It is concluded that non-specific disruption of glutamatergic neurotransmission prevents the development of morphine- and amphetamine-induced CPP.
先前的研究表明,谷氨酸能N-甲基-D-天冬氨酸(NMDA)受体或α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体的拮抗剂可分别破坏由滥用药物诱导的条件性位置偏爱(CPP)的形成或表达。本研究检测了利鲁唑抑制突触前谷氨酸释放对吗啡和苯丙胺诱导的CPP形成的影响。吗啡(10毫克/千克)、D,L-苯丙胺(4毫克/千克)和利鲁唑(4毫克/千克)本身均可产生显著的CPP;然而,在条件训练期间,当利鲁唑与吗啡或苯丙胺联合给药时,并未形成CPP。得出的结论是,谷氨酸能神经传递的非特异性破坏可阻止吗啡和苯丙胺诱导的CPP的形成。