首页> 美国卫生研究院文献>The Journal of Neuroscience >Role of the Amygdala in the Coordination of Behavioral Neuroendocrine and Prefrontal Cortical Monoamine Responses to Psychological Stress in the Rat
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Role of the Amygdala in the Coordination of Behavioral Neuroendocrine and Prefrontal Cortical Monoamine Responses to Psychological Stress in the Rat

机译:杏仁核在行为神经内分泌和前额叶皮质单胺反应对大鼠心理应激的协调作用。

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摘要

Exposure to mild stress is known to activate dopamine (DA), serotonin (5-HT), and norepinephrine (NE) metabolism in the anteromedial prefrontal cortex (m-PFC). Neuroanatomical site(s) providing afferent control of the stress activation of the m-PFC monoaminergic systems is at present unknown. The present study used a conditioned stress model in which rats were trained to fear a substartle-threshold tone paired previously with footshock and assessed for behavioral, neuroendocrine, and neurochemical stress responses. Bilateral NMDA-induced excitotoxic lesioning of the basolateral and central nuclei of the amygdala was performed before or after training. Pretraining amygdala lesions blocked stress-induced freezing behavior, ultrasonic vocalizations, adrenocortical activation, and dopaminergic metabolic activation in the m-PFC. Post-training amygdala lesions blocked stress-induced m-PFC DA, 5-HT, and NE metabolic activation. Post-training amygdala lesions also blocked stress-induced freezing and defecation, and greatly attenuated adrenocortical activation. These data provide evidence of amygdalar control of stress-induced metabolic activation of the monoaminergic systems in the m-PFC, as well as amygdalar integration of behavioral and neuroendocrine components of the rat stress response. These results are discussed in terms of possible relevance to stress-induced exacerbation of schizophrenic symptoms and the pathophysiology of post-traumatic stress disorder.
机译:暴露于轻度压力下会激活前额叶前额叶皮层(m-PFC)中的多巴胺(DA),血清素(5-HT)和去甲肾上腺素(NE)代谢。目前未知提供对m-PFC单胺能系统的应激激活进行控制的神经解剖部位。本研究使用条件应激模型,在该模型中,训练大鼠恐惧与惊吓配对的惊吓阈下音调,并评估其行为,神经内分泌和神经化学应激反应。在训练之前或之后,进行双侧NMDA引起的杏仁核基底外侧和中央核的兴奋性毒性损伤。预先训练的杏仁核病变阻止了m-PFC中的压力诱导的冰冻行为,超声波发声,肾上腺皮质激活和多巴胺能代谢激活。训练后杏仁核病变阻止了应激诱导的m-PFC DA,5-HT和NE代谢激活。训练后的杏仁核病变还阻止了压力诱导的冰冻和排便,并大大减弱了肾上腺皮质的激活。这些数据提供了杏仁核控制应激诱导的m-PFC中单胺能系统代谢代谢的证据,以及大鼠应激反应的行为和神经内分泌成分的杏仁核整合。从可能与精神分裂症症状的应激诱发加重和创伤后应激障碍的病理生理学相关性方面讨论了这些结果。

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