Modulation of BNST 5-HT responses by corticosterone

描述(由Candient提供)：终纹床核(BNST)被认为是由于暴露在不可控制的、不可预测的和/或慢性压力下而产生的焦虑样状态的中介。这些应激源与5-羟色胺(5-羟色胺)和皮质酮释放的长期升高有关。许多BNST神经元在外源性5-羟色胺的作用下表现出5-HT1A介导的抗焦虑超极化和5-HT2介导的焦虑性去极化。因此，每个细胞的净反应取决于这两个反应的平衡。已有研究表明，慢性皮质酮可降低几个脑区的5-HT1a功能，增加5-HT2功能。BNST内的这种作用应该会改变5-羟色胺反应的平衡，有利于更多的5-羟色胺介导的去极化，当与增加的5-羟色胺释放相结合时，可以调节焦虑。这一建议的具体目的是确定慢性皮质酮是否使BNST神经元的电生理反应倾向于5-HT2介导的功能，以及慢性皮质酮是否对BNST 5-羟色胺产生更多的焦虑行为特征。

DESCRIPTION (provided by candidate): The bed nucleus of the stria terminalis (BNST) is believed to mediate anxiety-like states produced by exposure to uncontrollable, unpredictable, and/or chronic stress. These stressors are associated with long-term elevations in serotonergic (5-HT) and corticosterone release. Many individual BNST neurons exhibit both a 5-HT1A-mediated, anxiolytic, hyperpolarization and a 5-HT2-mediated, anxiogenic, depolarization in response to exogenous 5-HT application. The net response of each cell thus depends on the balance of these two responses. Chronic corticosterone has been shown to decrease 5-HT1A function and increase 5- HT2 function in several brain areas. This action within the BNST should shift the balance of 5-HT responses to favor more 5-HT2-mediated depolarizations, which, when combined with increased 5-HT release, could mediate anxiety. The specific aims in this proposal are designed to determine whether chronic corticosterone shifts the electrophysiological response of BNST neurons to favor 5-HT2-mediated function, and whether chronic corticosterone produces a more anxiogenic behavioral profile to BNST 5-HT.