Freedman R
Biol Psychiatry. 1977 Apr;12(2):181-97.
Using the rat cerebellar Purkinje cell as a model neuronal system, the effects of norepinephrine and fluphenazine, an antipsychotic drug, are examined. Fluphenazine is shown to be a potent, specific antagonist of the norepinephrine-mediated inhibition of Purkinje cell discharge. Norepinephrine, despite its inhibitory action on spontaneous firing of the Purkinje cell, increases its responsiveness to afferent synaptic pathways. These data thus imply that norepinephrine may increase the brain's sensitivity to incoming information, and that antipsychotic drugs interfere with this effect. A role for norepinephrine, as well as dopamine, in the genesis of psychosis is suggested on the basis of their mutual antagonism by anti-psychotic drugs. The facilatory effects of NE on neuronal information-processing are used to predict a possible participation of NE in the perceptual difficulties noted in psychosis.
以大鼠小脑浦肯野细胞作为模型神经元系统，研究了去甲肾上腺素和抗精神病药物氟奋乃静的作用。结果表明，氟奋乃静是去甲肾上腺素介导的浦肯野细胞放电抑制的强效、特异性拮抗剂。去甲肾上腺素尽管对浦肯野细胞的自发放电有抑制作用，但会增加其对传入突触通路的反应性。因此，这些数据表明去甲肾上腺素可能会增加大脑对传入信息的敏感性，而抗精神病药物会干扰这种作用。基于抗精神病药物对去甲肾上腺素和多巴胺的相互拮抗作用，提示去甲肾上腺素以及多巴胺在精神病的发生中起作用。去甲肾上腺素对神经元信息处理的促进作用被用于预测去甲肾上腺素可能参与了精神病中所观察到的感知障碍。
