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催产素对大鼠避水应激诱导的结肠运动加速的抑制作用。

Inhibitory effect of oxytocin on accelerated colonic motility induced by water-avoidance stress in rats.

作者信息

Matsunaga M, Konagaya T, Nogimori T, Yoneda M, Kasugai K, Ohira H, Kaneko H

机构信息

Department of Neurology, Ban Buntane Hotokukai Hospital, Fujita Health University, Aichi, Japan.

出版信息

Neurogastroenterol Motil. 2009 Aug;21(8):856-e59. doi: 10.1111/j.1365-2982.2009.01286.x. Epub 2009 Mar 9.

Abstract

Recent studies have indicated that brain and gut activities are interrelated and exposure to several stressors, such as water-avoidance stress, stimulates the motor function of the gut through corticotropin-releasing factor (CRF)-signalling pathways in the brain. Central oxytocin is known to attenuate stress responses, including CRF expression in the brain. Here, we examined whether central oxytocin attenuated the acceleration of colonic motility induced by water-avoidance stress. A force transducer was attached to the distal colon of male rat, and the colonic motility and faecal pellet output were recorded while the rats were exposed to water-avoidance stress. Intracerebroventricular (i.c.v.) injections of oxytocin (5, 50 and 500 pmol) and the oxytocin receptor antagonist tocinoic acid (25 microg) were administered before exposure to water-avoidance stress, and the effect of oxytocin on colonic motor function was determined. Centrally administered oxytocin inhibited the accelerated colonic motility induced by water-avoidance stress. The effective dose ranged between 5 and 50 pmol on i.c.v. injection. Oxytocin also decreased the number of CRF-positive cells in the paraventricular nucleus and corticosterone release. The inhibitory effect of oxytocin on accelerated colonic motility was blocked by pretreatment with oxytocin receptor antagonist. Furthermore, centrally administered tocinoic acid enhanced the acceleration of colonic motility. These results suggested that endogenous central oxytocin may contribute to the regulation of colonic function and inhibit the brain CRF-signalling pathways targeting the gut, resulting in the inhibition of stress-induced colonic contractions.

摘要

近期研究表明,大脑与肠道活动相互关联,暴露于多种应激源(如禁水应激)会通过大脑中的促肾上腺皮质激素释放因子(CRF)信号通路刺激肠道运动功能。已知中枢催产素可减弱应激反应,包括大脑中CRF的表达。在此,我们研究了中枢催产素是否能减弱禁水应激诱导的结肠运动加速。将力传感器连接到雄性大鼠的远端结肠,在大鼠暴露于禁水应激时记录结肠运动和粪便颗粒排出情况。在暴露于禁水应激之前,脑室内(i.c.v.)注射催产素(5、50和500 pmol)以及催产素受体拮抗剂托西酸(25 μg),并测定催产素对结肠运动功能的影响。中枢给予的催产素抑制了禁水应激诱导的结肠运动加速。脑室内注射的有效剂量范围为5至50 pmol。催产素还减少了室旁核中CRF阳性细胞的数量以及皮质酮的释放。催产素受体拮抗剂预处理可阻断催产素对结肠运动加速的抑制作用。此外,中枢给予托西酸可增强结肠运动的加速。这些结果表明,内源性中枢催产素可能有助于调节结肠功能,并抑制靶向肠道的大脑CRF信号通路,从而抑制应激诱导的结肠收缩。

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