Forebrain pathways mediating stress-induced hormone secretion

Exposure to hostile conditions initiates the secretion of several hormones, including corticosterone/cortisol, catecholamines, prolactin, oxytocin, an d renin, as part of the survival mechanism. Such conditions are often refer red to as "stressors" and can be divided into three categories: external co nditions resulting in pain or discomfort, internal homeostatic disturbances , and learned or associative responses to the perception of impending endan germent, pain, or discomfort ("psychological stress"). The hormones release d in response to stressors often are referred to as "stress hormones" and t heir secretion is regulated by neural circuits impinging on hypothalamic ne urons that are the final output toward the pituitary gland and the kidneys. This review discusses the forebrain circuits that mediate the neuroendocri ne responses to stressors and emphasizes those neuroendocrine systems that have previously received little attention as stress-sensitive hormones: ren in, oxytocin, and prolactin. Anxiolytic drugs of the benzodiazepine class a nd other drugs that affect catecholamine, GABAA, histamine, and serotonin r eceptors alter the neuroendocrine stress response. The effects of these dru gs are discussed in relation to their effects on forebrain neural circuits that regulate stress hormone secretion. For psychological stressors such as conditioned fear, the neural circuits mediating neuroendocrine responses i nvolve cortical activation of the basolateral amygdala, which in turn activ ates the central nucleus of the amygdala. The central amygdala then activat es hypothalamic neurons directly, indirectly through the bed nucleus of the stria terminalis, and/or possibly via circuits involving brainstem seroton ergic and catecholaminergic neurons. The renin response to psychological st ress, in contrast to those of ACTH and prolactin, is not mediated by the be d nucleus of the stria terminalis and is not suppressed by benzodiazepine a nxiolytics. Stressors that challenge cardiovascular homeostasis, such as he morrhage, trigger a pattern of neuroendocrine responses that is similar to that observed in response to psychological stressors. These neuroendocrine responses are initiated by afferent signals from cardiovascular receptors w hich synapse in the medulla oblongata and are relayed either directly or in directly to hypothalamic neurons controlling ACTH, prolactin, and oxytocin release. In contrast, forebrain pathways may not be essential for the renin response to hemorrhage. Thus current evidence indicates that although a di verse group of stressors initiate similar increases in ACTH, renin, prolact in, and oxytocin, the specific neural circuits and neurotransmitter systems involved in these responses differ for each neuroendocrine system and stre ssor category.