Rebec G V, Gelman J, Alloway K D, Bashore T R
Pharmacol Biochem Behav. 1983 Nov;19(5):759-63. doi: 10.1016/0091-3057(83)90076-x.
At doses known to elicit catalepsy in rats, haloperidol (1.0 and 2.0 mg/kg) and pimozide (4.0 mg/kg), injected intraperitoneally, failed to alter the spontaneous activity of neurons in the amygdaloid complex of locally anesthetized, immobilized rats. In contrast, clozapine and thioridazine, which are devoid of cataleptic effects even at high doses (10.0 and 20.0 mg/kg), caused a dramatic and prolonged increase in firing rate, whereas chlorpromazine, which produces relatively mild catalepsy at doses of 5.0 and 10.0 mg/kg, produced an intermediate response. These results, which were obtained throughout the amygdaloid complex, indicate that the cataleptogenic potency of the antipsychotic drugs is inversely correlated with their ability to accelerate neuronal activity. This finding is discussed in relation to the known mechanisms of action of these drugs on various neurotransmitter systems in the amygdaloid complex.
在已知能诱发大鼠僵住症的剂量下,腹腔注射氟哌啶醇(1.0和2.0毫克/千克)和匹莫齐特(4.0毫克/千克),未能改变局部麻醉、固定的大鼠杏仁核复合体中神经元的自发活动。相比之下,氯氮平和硫利达嗪即使在高剂量(10.0和20.0毫克/千克)时也没有僵住症效应,它们会导致放电率急剧且持续增加,而氯丙嗪在5.0和10.0毫克/千克剂量时会产生相对轻微的僵住症,其反应介于两者之间。这些在整个杏仁核复合体中获得的结果表明,抗精神病药物的致僵住症效力与其加速神经元活动的能力呈负相关。结合这些药物对杏仁核复合体中各种神经递质系统的已知作用机制对这一发现进行了讨论。