Behavioral, neuroendocrine and serotonergic consequences of single social defeat and repeated fluoxetine pretreatment in the Lewis rat strain
Behavioral, neuroendocrine and serotonergic consequences of single social defeat and repeated fluoxetine pretreatment in the Lewis rat strain
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DOI：
10.1016/s0306-4522(98)00742-8
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发表时间：
1999-01-01
期刊：
影响因子：
3.3
通讯作者：
Chaouloff, F
中科院分区：
文献类型：
--
作者：
Berton, O;Durand, M;Chaouloff, F
我们分析了刘易斯大鼠（一种对慢性社会应激高度敏感的近交系）中，单次（30分钟）社交失败，随后与攻击者进行14-18小时的感觉接触的一些行为、神经内分泌和肾上腺素能的后果[Berton O.等人（1998）Neuroscience 82，147-159]。此外，我们还研究了选择性5-羟色胺再摄取抑制剂氟西汀（7.5 mg/kg/天，持续21天）预处理对上述结果的影响。一个单一的社会失败引发食欲减退和体重减轻，并增加了高架十字迷宫的焦虑。它不影响基线血浆促肾上腺皮质激素水平和肾素活性，但降低血浆皮质酮水平。另一方面，后者的变量随后急性强迫游泳应激的反应钝化（皮质酮）或放大（促肾上腺皮质激素，肾素活性）之前的失败。海马5-羟色胺转运体的密度，但不是海马5-羟色胺-1A和皮质5-羟色胺-2A受体的密度，减少了一个单一的社会失败;此外，既不色氨酸的可用性和5-羟色胺合成/代谢，也不5-羟色胺-1A自身受体介导的功能（抑制5-羟色胺合成，暴食症）受到影响。氟西汀预处理减少了社交失败引起的食欲减退、体重减轻和焦虑，而不影响对照动物的这些变量。这种预处理增加血浆皮质酮水平在休息和急性应激大鼠，但取消社会失败引起的皮质酮低反应急性强迫游泳应激。除了中脑5-羟色胺转运体密度降低外，氟西汀不影响本文分析的其他神经元能指标，即5-羟色胺-1A和5-羟色胺-2A受体密度、5-羟色胺合成/代谢。刘易斯大鼠的单一社交失败产生行为和内分泌改变，这可能模拟人类焦虑症的某些方面。在该范例中，既往氟西汀治疗具有适应性行为和可能的神经内分泌效应，而不影响本文分析的中枢神经系统的关键要素。(C)1999年IBRO。出版社：Elsevier Science Ltd
We have analysed some behavioral, neuroendocrine and serotonergic consequences of a single (30-min) social defeat followed by 14-18 h of sensory contact with the aggressor, in Lewis rats, an inbred strain highly sensitive to chronic social stressors [Berton O. et al. (1998) Neuroscience 82, 147-159]. In addition, we have investigated how the aforementioned consequences are affected by pretreatment with the selective serotonin reuptake inhibitor, fluoxetine (7.5 mg/kg/day for 21 days). A single social defeat triggered hypophagia and body weight loss, and increased anxiety in the elevated plus-maze. It did not affect baseline plasma adrenocorticotropic hormone levels and renin activity, but decreased plasma corticosterone levels. On the other hand, the responses of the latter variables to subsequent acute forced swim stress were blunted (corticosterone) or amplified (adrenocorticotropic hormone, renin activity) by prior defeat. The density of hippocampal serotonin transporters, but not that of hippocampal serotonin-1A and cortical serotonin-2A receptors, was decreased by a single social defeat; in addition, neither tryptophan availability and serotonin synthesis/metabolism, nor serotonin-1A autoreceptor-mediated functions (inhibition of serotonin synthesis, hyperphagia) were affected. Fluoxetine pretreatment diminished social defeat-induced hypophagia, body weight loss and anxiety without affecting these variables in control animals. This pretreatment increased plasma corticosterone levels in resting and acutely stressed rats, but abolished social defeat-elicited corticosterone hyporesponsiveness to acute forced swim stress. Except for a decrease in midbrain serotonin transporter density, fluoxetine did not affect the other serotonergic indices analysed herein, i.e. serotonin-1A and serotonin-2A receptor densities, serotonin synthesis/metabolism.A single social defeat in Lewis rats produces behavioral and endocrine alterations that may model some aspects of human anxiety disorders. In this paradigm, prior fluoxetine treatment is endowed with adaptive behavioral, and possibly neuroendocrine, effects without affecting the key elements of central serotonergic systems analysed herein. (C) 1999 IBRO. Published by Elsevier Science Ltd.