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神经肽Y会损害叙利亚仓鼠条件性战败行为的习得。

Neuropeptide Y impairs the acquisition of conditioned defeat in Syrian hamsters.

作者信息

Lacey Tiara, Sweeting Josiah, Kingston Rody, Smith Michael, Markham Chris M

机构信息

Department of Biology, Spelman College, Atlanta, GA, 30314, USA.

Department of Psychology, Morehouse College, Atlanta, GA, 30314, USA.

出版信息

Neurosci Lett. 2019 Jan 18;690:214-218. doi: 10.1016/j.neulet.2018.09.049. Epub 2018 Oct 9.

Abstract

Recent evidence indicates that Neuropeptide Y (NPY) may function as a potent anxiolytic as well as a resilience factor that can insulate the brain from the effects of stress. However, most of these studies have utilized physical stressors such as shock or restraint. In the present study, we use an ethologically-based model in Syrian hamsters (Mesocricetus auratus) called Conditioned Defeat (CD) to investigate whether NPY can ameliorate the effect of social defeat stress. In the CD model, a male Syrian hamster is socially defeated by a larger, more aggressive conspecific. Subsequently, when paired with a smaller, non-aggressive intruder (NAI) in its own home cage, changes in its behavioral repertoire occur, including a reduction in aggression and chemosensory (social) investigation, and a concomitant increase in submissive behaviors. In Experiment 1, hamsters were infused intracerebroventricularly (icv) with NPY prior to social defeat, and 24-hours later, hamsters were exposed to a NAI. Results indicate that NPY significantly reduced submissive/defensive behaviors in socially defeated hamsters compared to control animals. In Experiment 2, we examined whether this effect was mediated by the NPY Y1 receptor. Subjects were first pre-treated with the Y1 receptor antagonist BIBP 3226 or vehicle, followed by NPY and then socially defeated. Upon testing with a NAI 24-hours later, pretreatment with BIBP 3226 failed to block the NPY effect compared to controls. These results demonstrate that NPY may function as an important resilience factor in socially defeated hamsters, but that these effects are not mediated by the Y1 receptor.

摘要

最近的证据表明,神经肽Y(NPY)可能作为一种有效的抗焦虑因子以及一种恢复力因子发挥作用,能够使大脑免受压力的影响。然而,这些研究大多使用了电击或束缚等身体应激源。在本研究中,我们使用一种基于行为学的叙利亚仓鼠(金仓鼠)条件性挫败(CD)模型,来研究NPY是否能改善社会挫败应激的影响。在CD模型中,一只雄性叙利亚仓鼠会被一只体型更大、更具攻击性的同种动物在社交中击败。随后,当它在自己的笼子里与一只体型较小、没有攻击性的入侵者(NAI)配对时,其行为模式会发生变化,包括攻击性和化学感觉(社交)探究行为减少,同时顺从行为增加。在实验1中,仓鼠在遭受社会挫败之前通过脑室内(icv)注射NPY,24小时后,让仓鼠接触NAI。结果表明,与对照动物相比,NPY显著减少了遭受社会挫败的仓鼠的顺从/防御行为。在实验2中,我们研究了这种效应是否由NPY Y1受体介导。首先用Y1受体拮抗剂BIBP 3226或溶剂对实验对象进行预处理,然后注射NPY,接着使其遭受社会挫败。24小时后用NAI进行测试时,与对照组相比,用BIBP 3226预处理未能阻断NPY的作用。这些结果表明,NPY可能作为遭受社会挫败的仓鼠的一种重要恢复力因子发挥作用,但这些效应不是由Y1受体介导的。

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