Herberg L J, Stephens D N
Pharmacol Biochem Behav. 1975 Mar-Apr;3(2):263-9. doi: 10.1016/0091-3057(75)90156-2.
The antiparkinsonian drug amantadine HCl caused a dose-dependent depression of electrical self-stimulation, followed by a dose-dependent enhancement. Neither action was correlated with the differential effects of d- and l-amphetamine at different implantation sites. The initial depression was not prevented by pretreatment with anticholinergic or antiserotonergic agents nor by depression of catecholamine (CA) synthesis. The stimulant effects of amantadine and d-amphetamine summated but did not interact, response rates after d-amphetamine being augmented by pretreatment with amantadine except at intervals at which amantadine was by itself depressant. It is concluded that the initial effect of amantadien is caused by impulse-independent release of a pool of intraneuronal CA, causing dissociation between reinforcement signals and the rat's responses. This is followed by amphetamine-like facilitation of impulse-dependent release; the first action depresses performance, the second enhances it.
抗帕金森病药物盐酸金刚烷胺会引起剂量依赖性的电刺激自我兴奋抑制，随后是剂量依赖性的增强。这两种作用均与不同植入部位的右旋和左旋苯丙胺的差异效应无关。抗胆碱能或抗血清素能药物预处理，或儿茶酚胺（CA）合成抑制均不能预防最初的抑制作用。金刚烷胺和右旋苯丙胺的兴奋作用相加但不相互作用，除了在金刚烷胺自身具有抑制作用的间隔外，右旋苯丙胺预处理会增强其反应率。结论是，金刚烷胺的初始作用是由神经元内CA池的冲动非依赖性释放引起的，导致强化信号与大鼠反应之间的分离。随后是类似苯丙胺的对冲动依赖性释放的促进作用；第一种作用抑制表现，第二种作用增强表现。
