Prevention by 5-HT1A receptor agonists of restraint stress- and yohimbine-induced release of cholecystokinin in the frontal cortex of the freely moving rat
Prevention by 5-HT1A receptor agonists of restraint stress- and yohimbine-induced release of cholecystokinin in the frontal cortex of the freely moving rat
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DOI：
10.1016/s0028-3908(98)00209-3
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发表时间：
1999-04-01
影响因子：
4.7
通讯作者：
Benoliel, JJ
中科院分区：
文献类型：
--
作者：
Becker, C;Hamon, M;Benoliel, JJ
与胆囊收缩素（CCK）参与焦虑相关行为的想法一致，以前的研究表明，应激条件和一种“致焦虑”药物育亨宾增加了清醒大鼠皮质释放CCK样物质（CCKLM），这种影响可以被地西泮阻止。在这里，我们调查是否其他抗焦虑药物，如5-HT 1A受体激动剂也可以影响皮质CCKLM的释放。事实上，丁螺环酮（1 mg/kg i. p.），阿奈螺酮（1 mg/kg i. p.）去甲来索匹隆（3 mg/kg i. p.）受影响，对自己，CCKLM释放。然而，用后一种药物预处理完全取消了束缚应激对肽流出的刺激作用。正如5-HT 1A受体参与的预期，特他洛尔（10 mg/kg i.p）显著降低丁螺环酮对束缚应激诱发的CCKLM溢出的抑制作用。另一方面，用丁螺环酮、阿奈螺环酮或来索匹隆预处理也抑制育亨宾（5 mg/kg i. p.）皮质CCKLM流出。这些数据支持的想法，5-HT 1A受体激动剂的抗焦虑作用可以介导的，至少部分地，通过他们的抑制影响皮质CCK能系统。(C)1999 Elsevier Science Ltd.保留所有权利。
In line with the idea that cholecystokinin (CCK) is involved in anxiety-related behaviours, previous investigations showed that stressful conditions and an 'anxiogenic' drug, yohimbine, increased the cortical release of CCK like-material (CCKLM) in awake rats, and that this effect could be prevented by diazepam. Here, we investigated whether other anxiolytic drugs such as 5-HT1A receptor agonists could also affect cortical CCKLM release. Indeed, neither buspirone (1 mg/kg i.p.), alnespirone (1 mg/kg i.p.) nor lesopitron (3 mg/kg i.p.) affected, on their own, CCKLM release. However, pretreatment with the latter drugs completely abolished the stimulatory effect of restraint stress on the peptide outflow. As expected of the involvement of 5-HT1A receptors, tertatolol (10 mg/kg i.p) markedly reduced the inhibitory effect of buspirone on restraint stress-evoked CCKLM overflow. On the other hand, pretreatment with buspirone, alnespirone or lesopitron also inhibited the stimulatory effect of yohimbine (5 mg/kg i.p.) on cortical CCKLM outflow. These data support the idea that the anxiolytic action of 5-HT1A receptor agonists could be mediated, at least partly, through their inhibitory influence on cortical CCK-ergic systems. (C) 1999 Elsevier Science Ltd. All rights reserved.