Przegaliński E, Siwanowicz J, Bigajska K, Baran L
J Pharm Pharmacol. 1984 Sep;36(9):626-8. doi: 10.1111/j.2042-7158.1984.tb04913.x.
Several lines of evidence (binding studies, reduced responsiveness of brain adenylate cyclase to noradrenergic stimulation) indicate that chronic treatment with electroconvulsive shock (ECS) induces down-regulation of central beta-adrenoceptors. The effect of acute and chronic (10 days) treatment with ECS on salbutamol-induced suppression of exploratory activity in rats has been examined. This effect was prevented by chronic but not by acute treatment with ECS. Chronic treatment with ECS did not affect exploratory activity. The salbutamol-induced hypoactivity is mediated through central beta-adrenoceptors (antagonistic effect of (-)-propranolol but not (+)-propranolol or practolol), so the results may be regarded as functional evidence at the behavioral level for the down-regulation of beta-adrenoceptors produced by chronic treatment with ECS.
多条证据线索（结合研究、脑腺苷酸环化酶对去甲肾上腺素能刺激的反应性降低）表明，电惊厥休克（ECS）的长期治疗会导致中枢β-肾上腺素能受体下调。研究了ECS急性和慢性（10天）治疗对沙丁胺醇诱导的大鼠探索活动抑制的影响。这种作用可被ECS的慢性治疗而非急性治疗所阻断。ECS的慢性治疗不影响探索活动。沙丁胺醇诱导的活动减少是通过中枢β-肾上腺素能受体介导的（（-）-普萘洛尔有拮抗作用，而（+）-普萘洛尔或普拉洛尔则无），因此这些结果可被视为在行为水平上支持ECS长期治疗导致β-肾上腺素能受体下调的功能证据。
