Ono N, Saito R, Abiru T, Kamiya H, Furukawa T
Pharmacol Biochem Behav. 1986 Aug;25(2):463-7. doi: 10.1016/0091-3057(86)90024-9.
Involvement of prostaglandin (PG) in cataleptic behavior was investigated by a high bar test method in rats. PG F2 alpha (F2a) and E2 administered intracerebroventricularly (ICV) elicited cataleptic behavior in a dose-dependent manner. The cataleptic behaviors produced by PGs were markedly inhibited by ICV pretreatment with propranolol. The cataleptic behaviors induced by haloperidol were also inhibited by propranolol. The PG F2a- and haloperidol-induced cataleptic behaviors were almost abolished by the thermal coagulation of bilateral striatum where the dopaminergic and cholinergic link is found. The pilocarpine-induced cataleptic behavior was potentiated by ICV treatment with PG F2a. On the other hand, the cataleptic behavior elicited by haloperidol was reduced after oral treatment with aspirin, a PG synthesis inhibitor. These results suggest that PGs seem to be participated in incidence of cataleptic behavior, which might involve alteration of brain beta-adrenoceptor activity.
采用高架试验法在大鼠中研究前列腺素（PG）与僵住行为的关系。脑室内（ICV）注射PG F2α（F2a）和E2可剂量依赖性地引发僵住行为。普萘洛尔脑室内预处理可显著抑制PGs产生的僵住行为。普萘洛尔也可抑制氟哌啶醇诱导的僵住行为。双侧纹状体热凝术几乎消除了PG F2a和氟哌啶醇诱导的僵住行为，而双侧纹状体存在多巴胺能和胆碱能联系。PG F2a脑室内注射可增强毛果芸香碱诱导的僵住行为。另一方面，氟哌啶醇诱导的僵住行为在口服PG合成抑制剂阿司匹林后减弱。这些结果表明，PGs似乎参与了僵住行为的发生，这可能涉及脑β-肾上腺素能受体活性的改变。
