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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Chronic ethanol intoxication enhances (3H)CCPA binding and does not reduce A1 adenosine receptor function in rat cerebellum.
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Chronic ethanol intoxication enhances (3H)CCPA binding and does not reduce A1 adenosine receptor function in rat cerebellum.

机译：慢性乙醇中毒可增强（3H）CCPA结合，并且不会降低大鼠小脑的A1腺苷受体功能。

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摘要

The effects of acute and chronic treatment with ethanol on the function of A1 adenosine receptor in the rat cerebellar cortex were investigated. Acute administration of ethanol (0.5-5 g/kg) had no effect on the binding of the A1-receptor agonist [3H]2-chloro-N6-cyclopentyladenosine ([3H]CCPA) or that the antagonist [3H]8-cyclopentyl-1-3-dipropylxanthine ([3H]DPCPX) in rat cerebellar cortical membranes. Rats were rendered ethanol dependent by repeated forced oral administration of ethanol (12-18 g/kg per day) for 6 days. [3H]CCPA binding was increased by 23% in cerebellar cortical membranes prepared from rats killed 3 h after ethanol withdrawal compared with saline-treated animals. The increase in [3H]CCPA binding was still apparent 12-24 h after the last ethanol administration, but was no longer detectable 3-6 days after ethanol withdrawal. In contrast, the binding of [3H]DPCPX was not modified in the cerebellar cortex of rats killed at various times after ethanol withdrawal. The acute administration of CCPA [0.25-1 mg/kg, intraperitoneally (IP)] suppressed the tremors and audiogenic seizures apparent 24 h after ethanol withdrawal. Moreover, repeated coadministration of CCPA (0.5 mg/kg, IP, four times daily) and ethanol did not prevent the generation of audiogenic seizures during withdrawal but completely prevented mortality. Finally, CCPA antagonized with similar potencies and efficacies the isoniazid-induced convulsions observed in control and ethanol-withdrawn rats. These results indicate that long-term treatment with intoxicating doses of ethanol enhances [3H]CCPA binding but does not reduce the anticonvulsant efficacy of CCPA or the function of A1 adenosine receptors.
机译：研究了乙醇急慢性治疗对大鼠小脑皮层A1腺苷受体功能的影响。急性给予乙醇（0.5-5 g / kg）对A1受体激动剂[3H] 2-氯-N6-环戊基腺苷（[3H] CCPA）或拮抗剂[3H] 8-环戊基的结合没有影响大鼠小脑皮质膜中的-1-3-二丙基黄嘌呤（[3H] DPCPX）。通过重复强制口服乙醇（每天12-18 g / kg）6天，使大鼠具有乙醇依赖性。与用盐水处理的动物相比，在撤除乙醇3小时后杀死的大鼠制备的小脑皮质膜中，[3H] CCPA结合增加了23％。在最后一次乙醇施用后12-24小时，[3H] CCPA结合的增加仍然很明显，但是在撤除乙醇后3-6天不再可检测到。相反，在撤除乙醇后的不同时间处死的大鼠小脑皮质中，[3H] DPCPX的结合没有改变。 CCPA的急性给药[0.25-1 mg / kg，腹膜内（IP）]抑制了停药24小时后的震颤和听觉性癫痫发作。而且，CCPA（0.5 mg / kg，IP，每天四次）和乙醇的重复共同给药不能阻止停药期间听源性癫痫发作的发生，但可以完全防止死亡。最后，CCPA拮抗了在对照组和撤回乙醇的大鼠中观察到的异烟肼诱发的惊厥，其作用和功效相似。这些结果表明，长期使用中毒剂量的乙醇治疗可增强[3H] CCPA的结合，但不会降低CCPA的抗惊厥功效或A1腺苷受体的功能。

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