Nicotinic activation of CRH neurons in extrahypothalamic regions of the rat brain
Abstract
Nicotine is known to have multiple effects on neuroendocrine, autonomic, and behavioral responses. Its neuroendocrine effect on the stress-responsive hormone, ACTH, depends on central pathways that act on corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus of the hypothalamus (PVN). Other CRH neurons throughout the brain also are involved in coordinating aspects of the stress response, but very little is known about the effect of nicotine on CRH neurons in extrahypothalamic regions that are involved in the autonomic and behavioral responses to stress. The current study sought to determine the extent of nicotinic activation of extrahypothalamic CRH neurons, since these neurons may be involved in mediating the central effects of nicotine. Freely moving rats were pretreated with a low dose of colchicine, infused with nicotine (0.045 mg/kg/30 s or 0.135 mg/kg/90 s, i.v.), and cardiac perfused 1 h later. Double-label immunocytochemistry identified the activated (positive for cFos protein) CRH neurons in limbic structures (bed nucleus of the stria terminalis [BNST] and central nucleus of the amygdala [CNA]), the dorsal raphe (DR), and Barrington's nucleus (BN); comparisons were made to the PVN. In all of thes...Continue Reading
Associated Clinical Trials
References
The role of limbic and hypothalamic corticotropin-releasing factor in behavioral responses to stress
Nicotine activates NPY and catecholaminergic neurons in brainstem regions involved in ACTH secretion
Citations
Hypothalamic-pituitary-adrenocortical responses to psychological stress and risk for smoking relapse
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