Preface The survival and well-being of all species requires appropriate physiological responses to environmental and homeostatic challenges. The reestablishment and maintenance of homeostasis entails the coordinate activation and control of neuroendocrine and autonomic stress systems. These collective stress responses are mediated via largely overlapping circuits in the limbic forebrain, hypothalamus and brainstem, so that the respective contribution of the neuroendocrine and autonomic systems is tuned in accordance with stressor modality or intensity. Limbic regions that are responsible for regulating stress responses intersect with circuits that are responsible for memory and reward, providing a means to tailor the stress response with respect to prior experience and anticipated outcomes.

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The adrenal gland is an essential stress-responsive organ that is part of both the hypothalamic-pituitary-adrenal axis and the sympatho-adrenomedullary system. Chronic stress exposure commonly increases adrenal weight, but it is not known to what extent this growth is due to cellular hyperplasia or hypertrophy and whether it is subregion specific. Moreover, it is not clear whether increased production of adrenal glucocorticoid after chronic stress is due to increased sensitivity to adrenocorticotropic hormone (ACTH) vs. increased maximal output. The present studies use a 14-day chronic variable stress (CVS) paradigm in adult male rats to assess the effects of chronic stress on adrenal growth and corticosterone steroidogenesis. Exogenous ACTH administration (0-895 ng/100 g body wt) to dexamethasone-blocked rats demonstrated that CVS increased maximal plasma and adrenal corticosterone responses to ACTH without affecting sensitivity. This enhanced function was associated with increased adrenal weight, DNA and RNA content, and RNA/DNA ratio after CVS, suggesting that both cellular hyperplasia and hypertrophy occurred. Unbiased stereological counting of cells labeled for Ki67 (cell division marker) or 4,6-diamidino-2-phenylindole (nuclear marker), combined with zone specific markers, showed that CVS induced hyperplasia in the outer zona fasciculata, hypertrophy in the inner zona fasciculata and medulla, and reduced cell size in the zona glomerulosa. Collectively, these results demonstrate that increased adrenal weight after CVS is due to hyperplasia and hypertrophy that occur in specific adrenal subregions and is associated with increased maximal corticosterone responses to ACTH. These chronic stress-induced changes in adrenal growth and function may have implications for patients with stress-related disorders.

Individuals often eat calorically dense, highly palatable "comfort" foods during stress for stress relief. This article demonstrates that palatable food intake (limited intake of sucrose drink) reduces neuroendocrine, cardiovascular, and behavioral responses to stress in rats. Artificially sweetened (saccharin) drink reproduces the stress dampening, whereas oral intragastric gavage of sucrose is without effect. Together, these results suggest that the palatable/rewarding properties of sucrose are necessary and sufficient for stress dampening. In support of this finding, another type of natural reward (sexual activity) similarly reduces stress responses. Ibotenate lesions of the basolateral amygdala (BLA) prevent stress dampening by sucrose, suggesting that neural activity in the BLA is necessary for the effect. Moreover, sucrose intake increases mRNA and protein expression in the BLA for numerous genes linked with functional and/or structural plasticity. Lastly, stress dampening by sucrose is persistent, which is consistent with long-term changes in neural activity after synaptic remodeling. Thus, natural rewards, such as palatable foods, provide a general means of stress reduction, likely via structural and/or functional plasticity in the BLA. These findings provide a clearer understanding of the motivation for consuming palatable foods during times of stress and influence therapeutic strategies for the prevention and/or treatment of obesity and other stress-related disorders.corticosterone | anxiety-related behavior | synaptophysin | cAMP response element-binding protein | calcium/calmodulin-dependent protein kinase T he obesity epidemic is fueled by the easy availability of palatable, calorically dense foods amid an ever-escalating level of daily stress (1-3). Humans and rodents increase palatable food consumption when stressed (3-6), and the term "comfort food" is commonly used to signify possible stress-dampening properties of certain foods (particularly calorically dense foods containing high amounts of carbohydrates and/or fats). Indeed, comfort food intake in humans is linked with improved emotional states (7), and a high-carbohydrate diet is associated with reduced resting and stress-evoked cortisol levels (8-11).Stress (a real or perceived threat to homeostasis or well-being) typically evokes both physiological and emotional responses (reviewed in ref. 12). The physiological responses include activation of the hypothalamic-pituitary-adrenocortical (HPA) axis and the sympathetic branch of the autonomic nervous system. Activation of the sympathetic nervous system has numerous effects, including increases in heart rate and blood pressure. Activation of the HPA axis results in elevations in circulating adrenocorticotropic hormone (ACTH) and glucocorticoids (e.g., cortisol in humans and corticosterone in rats). Glucocorticoids have widespread action on numerous physiological processes, including mobilization of stored energy and maintenance of vascular tone. Perceived stressors also engage emotional respons...