Abstract
Exposure to stressful stimuli causes activation of the hypothalamic-pituitary-adrenal axis which rapidly releases high concentrations of glucocorticoid stress hormones, resulting in increased cellular metabolism and spontaneous oxygen and nitrogen radical formation. High concentrations of nitrogen radicals, including nitric oxide, cause damage to cellular proteins in addition to inhibiting components of the mitochondrial transport chain, leading to cellular energy deficiency. During stress exposure, pharmacological inhibition of nitric oxide production reduces indicators of anxiety- and depressive-like behavior in animal models. Therefore, the purpose of this review is to present an overview of the current literature on stress-evoked changes in the nitrergic system, particularly within neural tissue.
Highlights
An acute stress response is mediated by the tripartite activation of the sympatho-adrenal-medullary (SAM), hypothalamic-spinaladrenal (HSA), and hypothalamic-pituitary-adrenal (HPA) axes
The locus ceruleus is the primary source of central noradrenergic signaling, functioning via the ascending noradrenergic bundle and descending through preganglionic neurons in the intermediolateral cell column (IML) of the spinal cord to innervate the adrenal medulla (Sara, 2009; Ulrich-Lai and Herman, 2009)
The paraventricular nucleus (PVN) of the hypothalamus is considered the apex of the HPA stress response as release of corticotropin-releasing hormone from the parvocellular neurosecretory neurons triggers anterior pituitary corticotrophs to release the pro-opiomelanocortin fragment, adrenocorticotropic hormone (ACTH), into the circulation
Summary
An acute stress response is mediated by the tripartite activation of the sympatho-adrenal-medullary (SAM), hypothalamic-spinaladrenal (HSA), and hypothalamic-pituitary-adrenal (HPA) axes. The PVN facilitates corticosterone release directly through the HSA stress axis via adrenocortical innervation from the IML, and indirectly via an alternative stress pathway involving prolactin release (Buijs et al, 1999; Lowry, 2002; Ulrich-Lai et al, 2006; Jaroenporn et al, 2009) This sensitizes the adrenal gland to ACTH, resulting in corticosterone release from the zona fasciculata of the adrenal cortex thereby exerting the characteristics downstream cellular and metabolic effects of stress (Buijs et al, 1999; Lowry, 2002; Weiser et al, 2011). Since dysfunction of the nitrergic system has been implicated in the neuropathogenesis of several stress-related disease states, the present review summarizes our current understanding and advances relating to the impact of stress on the nitrergic system
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