Mereu G, Casu M, Gessa G L
Brain Res. 1983 Mar 28;264(1):105-10. doi: 10.1016/0006-8993(83)91125-3.
The effect of i.v. sulpiride on the firing rate of dopaminergic neurons in the substantia nigra, pars compacta (SN-DA cells) and tyrosine hydroxylase (TH) activity in the caudate nucleus was studied. In rats, paralyzed with succinylcholine and artificially respirated, (-)-sulpiride (10-50 mg/kg) produced a dose-related increase in the firing rate of SN-DA cells and in TH activity. On the contrary, in rats anesthetized with halothane, (-)-sulpiride (up to 50 mg/kg) activated neither dopaminergic firing nor TH activity. However, (-)-sulpiride (10-25 mg/kg) readily reversed the inhibitory effect of i.v. apomorphine (25 micrograms/kg) on dopaminergic firing in both anesthetized and unanesthetized rats. Since sulpiride fails to inhibit DA-sensitive adenylate cyclase, it may be concluded that DA receptors, whose blockade results in increased dopaminergic firing and TH activation, are not coupled with this enzyme. Moreover, the results indicate that the mechanism responsible for firing and TH stimulation is inhibited by halothane anesthesia. The latter significantly decreased also the stimulant effect of i.v. haloperidol on striatal TH activity.
研究了静脉注射舒必利对黑质致密部多巴胺能神经元（SN-DA细胞）放电率以及尾状核中酪氨酸羟化酶（TH）活性的影响。在使用琥珀酰胆碱使其麻痹并进行人工呼吸的大鼠中，（-）-舒必利（10 - 50毫克/千克）可使SN-DA细胞的放电率和TH活性呈剂量依赖性增加。相反，在使用氟烷麻醉的大鼠中，（-）-舒必利（高达50毫克/千克）既不激活多巴胺能放电，也不激活TH活性。然而，（-）-舒必利（10 - 25毫克/千克）能轻易逆转静脉注射阿扑吗啡（25微克/千克）对麻醉和未麻醉大鼠多巴胺能放电的抑制作用。由于舒必利不能抑制对多巴胺敏感的腺苷酸环化酶，因此可以得出结论，其阻断作用导致多巴胺能放电增加和TH激活的多巴胺受体与该酶不偶联。此外，结果表明，负责放电和TH刺激的机制受到氟烷麻醉的抑制。后者也显著降低了静脉注射氟哌啶醇对纹状体TH活性的刺激作用。
