Increased stress vulnerability after a prefrontal cortex lesion in female rats
Increased stress vulnerability after a prefrontal cortex lesion in female rats
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DOI：
10.1016/j.brainresbull.2003.08.004
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发表时间：
2003-10-15
影响因子：
3.8
通讯作者：
Ter Horst, GJ
中科院分区：
文献类型：
--
作者：
Gerrits, M;Westenbroek, C;Ter Horst, GJ
对情感性精神障碍患者的神经影像学研究表明，前额叶皮层的多个区域（包括内侧前额叶皮层和眶额皮层）的体积减少和局部脑血流量减少。这种异常的大脑活动是由慢性压力引起的。女性比男性更容易出现情感障碍。在当前的实验中，雌性mPFC损伤和非损伤大鼠进行3周的慢性不可预测的压力，以确定在处理慢性压力的mPFC的作用;和mPFC损伤的后果，以应对连续的压力事件。雌性大鼠mPFC损伤后，应激诱导的下丘脑背内侧核和室旁核Fos表达变化增强，血浆儿茶酚胺水平显著升高。此外，mPFC病变显着减少的时间出现的压力引起的行为变化，在开放领域。总而言之，mPFC功能障碍影响雌性大鼠对慢性应激的反应方式，它不仅增加了参与神经内分泌和自主神经应激反应的脑区的激活，而且还显着减少了行为变化的发生时间。(C)2003年爱思唯尔公司All rights reserved.
Neuroimaging studies in patients suffering from affective disorders have shown decreased volume and reduced regional cerebral blood flow in multiple areas of the prefrontal cortex, including the medial prefrontal cortex and the orbitofrontal cortex. This aberrant brain activity is among other things attributed to chronic stress. Affective disorders occur more often in women than in men. In the current experiment, female mPFC-lesioned and non-lesioned rats were subjected to 3 weeks of chronic unpredictable stress in order to determine the role of the mPFC in dealing with chronic stress; and the consequences of mPFC damage for coping with consecutive stressful events. mPFC damage in female rats intensified the stress-induced activation of the dorsomedial nucleus of the hypothalamus and the paraventricular nucleus of the hypothalamus as measured with Fos expression changes and markedly increased plasma catecholamine levels after 3 weeks of unpredictable stress. Additionally, an mPFC lesion significantly reduced the time of appearance of stress-induced behavioral changes in the open field. Altogether, mPFC dysfunction affects the way female rats react to chronic stress, it not only increased the activation of brain regions involved in neuroendocrine and autonomic responses to stress but it also significantly reduced the time of onset of behavioral changes. (C) 2003 Elsevier Inc. All rights reserved.