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在强迫游泳试验中,快速眼动睡眠剥夺增强了丙咪嗪和地昔帕明的作用,但未增强氯米帕明的作用。

REM sleep deprivation potentiates the effects of imipramine and desipramine but not that of clomipramine in the forced swimming test.

作者信息

Asakura W, Matsumoto K, Ohta H, Watanabe H

机构信息

Section of Pharmacology, Research Institute for Wakan-Yaku (Oriental Medicines), Toyama Medical and Pharmaceutical University, Japan.

出版信息

Jpn J Pharmacol. 1993 Dec;63(4):455-60. doi: 10.1254/jjp.63.455.

Abstract

Effects of REM sleep (REMs) deprivation on the basal swimming activity and the tricyclic anti-depressants-induced increase in swimming activity in the forced swimming test were investigated. Immediately after a 48-hr period of REMs deprivation, the basal swimming activity in REMs-deprived mice was significantly higher than those in group-housed and socially isolated animals used as the control groups. The REMs deprivation-induced increase in the swimming activity was not changed by adrenoceptor antagonists and it returned to the control levels 3 hr after the REMs deprivation treatment. Moreover, imipramine and desipramine but not clomipramine further increased the swimming activity enhanced by REMs deprivation at doses that did not affect the activity in the control groups. The enhancing effect of REMs deprivation on the sensitivity to imipramine and desipramine remained unchanged even at 3 hr after the REMs deprivation treatment, and it was blocked by the alpha 2-adrenoceptor antagonist yohimbine. These results suggest that the REMs deprivation-induced increase in basal swimming activity in the forced swimming test is not mediated by adrenoceptor mechanisms, whereas the enhancing effect of REMs deprivation on the sensitivity to imipramine and desipramine may be mediated by the functional changes in alpha 2-adrenoceptors in the brain.

摘要

研究了快速眼动睡眠(REMs)剥夺对基础游泳活动以及在强迫游泳试验中三环类抗抑郁药诱导的游泳活动增加的影响。在48小时的REMs剥夺期结束后,立即发现REMs剥夺小鼠的基础游泳活动显著高于作为对照组的群居和社会隔离动物。REMs剥夺诱导的游泳活动增加不受肾上腺素能受体拮抗剂的影响,并且在REMs剥夺处理后3小时恢复到对照水平。此外,丙咪嗪和地昔帕明而非氯米帕明在不影响对照组活动的剂量下进一步增加了由REMs剥夺增强的游泳活动。即使在REMs剥夺处理后3小时,REMs剥夺对丙咪嗪和地昔帕明敏感性的增强作用仍然不变,并且被α2-肾上腺素能受体拮抗剂育亨宾阻断。这些结果表明,在强迫游泳试验中,REMs剥夺诱导的基础游泳活动增加不是由肾上腺素能受体机制介导的,而REMs剥夺对丙咪嗪和地昔帕明敏感性的增强作用可能是由大脑中α2-肾上腺素能受体的功能变化介导的。

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