Balsara J J, Muley M P, Vaidya A S, Chandorkar A G
Psychopharmacology (Berl). 1981;75(4):396-9. doi: 10.1007/BF00435861.
Baclofen, the parachlorophenyl analog of GABA, was found to induce catalepsy and to inhibit the traction response in mice. However, baclofen pretreatment, instead of antagonizing methamphetamine stereotypy and apomorphine-induced cage climbing behavior, was found to potentiate these behaviors, thereby ruling out the possibility of its possessing postsynaptic dopamine (DA) receptor blocking activity. The possible mechanism involved in the induction of catalepsy and in the inhibition of the traction response by baclofen is discussed on the basis that baclofen, by inhibiting the firing of the nigrostriatal and mesolimbic DA neurons, reduces the release of DA and thereby produces a functional lack of DA at postsynaptic DA receptor sites with resultant induction of catalepsy and inhibition of the traction response. Further, the hyper-responsiveness to methamphetamine and apomorphine is explained on the basis that, as the postsynaptic DA receptors are acutely deprived of their transmitter, following baclofen pretreatment, they become supersensitive to the DA agonists.
巴氯芬是γ-氨基丁酸（GABA）的对氯苯基类似物，已发现它可诱发小鼠僵住症并抑制其牵张反应。然而，研究发现，巴氯芬预处理非但不能拮抗甲基苯丙胺刻板行为和阿扑吗啡诱导的笼内攀爬行为，反而会增强这些行为，从而排除了其具有突触后多巴胺（DA）受体阻断活性的可能性。基于巴氯芬通过抑制黑质纹状体和中脑边缘多巴胺能神经元的放电，减少多巴胺释放，从而在突触后多巴胺受体部位产生功能性多巴胺缺乏，进而导致僵住症的诱发和牵张反应的抑制，讨论了巴氯芬诱发僵住症和抑制牵张反应的可能机制。此外，对甲基苯丙胺和阿扑吗啡的高反应性可解释为，在巴氯芬预处理后，由于突触后多巴胺受体突然失去其递质，它们对多巴胺激动剂变得超敏感。
