Activation of the ventral medial prefrontal cortex during an uncontrollable stressor reproduces both the immediate and long-term protective effects of behavioral control
Activation of the ventral medial prefrontal cortex during an uncontrollable stressor reproduces both the immediate and long-term protective effects of behavioral control
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DOI：
10.1016/j.neuroscience.2008.04.005
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发表时间：
2008-07-17
期刊：
影响因子：
3.3
通讯作者：
Maier, S. F.
中科院分区：
文献类型：
--
作者：
Amat, J.;Paul, E.;Maier, S. F.
生物体对压力源的行为控制程度决定了压力源的行为和神经化学后遗症，控制的存在可以防止压力源不可控制时发生的典型结果（例如学习失败，夸大恐惧，中背核（DRN） 5-羟色胺激活）。此外，可控压力源的经历会阻止后来不可控压力源的后果（“免疫”）。这些控制效应被认为是由控制诱导的腹侧内侧前额叶皮层（mPFCv）向DRN输出的激活介导的。导致这一解释的实验都涉及到用muscimol使mPFCv失活，表明在压力源期间失活消除了由控制产生的压力源抵抗，而可控的压力源现在表现得好像是不可控的。目前在大鼠身上的实验采用了相反的策略，在应激源时激活mPFCv。在应激源期间mPFCv微注射微小毒素消除了通常在不可控应激源期间发生的DRN 5-HT激活，以及通常在不可控应激后出现的逃避学习缺陷和夸大恐惧。此外，在初始暴露于不可控应激源时，mPFCv激活导致不可控应激源在随后暴露于不可控应激源时产生行为免疫和神经化学免疫。也就是说，mPFCv的联合激活和暴露于一个不可控的压力源导致不可控的压力源表现得好像它是可控的。这些结果有力地支持了行为控制通过激活mPFCv产生应激抵抗的观点。(c) 2008 ibro。Elsevier Ltd.出版。版权所有。
The degree of behavioral control that an organism has over a stressor determines the behavioral and neurochemical sequelae of the stressor, with the presence of control preventing the typical outcomes that occur when the stressor is uncontrollable (e.g. failure to learn, exaggerated fear, dorsal raphe nucleus (DRN) 5-HT activation). Furthermore, an experience with a controllable stressor blocks the consequences of later uncontrollable stressors ("immunization"). These effects of control have been argued to be mediated by control-induced activation of ventral medial prefrontal cortex (mPFCv) output to the DRN. The experiments that have led to this interpretation have all involved the inactivation of the mPFCv with muscimol, showing that inactivation during the stressor eliminates the stressor-resistance produced by control, with the controllable stressor now acting as if it were uncontrollable. The present experiments in rats employed the opposite strategy, activating the mPFCv during the stressor. mPFCv microinjection of picrotoxin during the stressor eliminated the DRN 5-HT activation that normally occurs during the uncontrollable stressor, as well as the escape learning deficit and exaggerated fear that normally follows uncontrollable stress. Furthermore, mPFCv activation during an initial exposure to an uncontrollable stressor led the uncontrollable stressor to produce behavioral and neurochemical immunization when the subjects were later exposed to an uncontrollable stressor. That is, the conjoint activation of the mPFCv and exposure to an uncontrollable stressor led the uncontrollable stressor to act as if it were controllable. These results provide strong support for the argument that behavioral control produced stress-resistance by activating the mPFCv. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.