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The medial amygdala modulates body weight but not neuroendocrine responses to chronic stress.
J Neuroendocrinol 2010; 22(1):13-23JN

Abstract

Stress pathologies such as depression and eating disorders (i.e. anorexia nervosa) are associated with amygdalar dysfunction, which are linked with hypothalamic-pituitary-adrenal axis (HPA) axis hyperactivity. The medial amygdaloid nucleus (MeA), a key output nucleus of the amygdaloid complex, promotes HPA axis activation to acute psychogenic stress and is in a prime position to mediate the deleterious effects of chronic stress on physiology and behaviour. The present study tests the hypothesis that the MeA is necessary for the development of maladaptive physiological changes caused by prolonged stress exposure. Male rats received bilateral ibotenate or sham lesions targeting the MeA and one half underwent 2 weeks of chronic variable stress (CVS) or served as home cage controls. Sixteen hours post CVS, all animals were exposed to an acute restraint challenge. CVS induced thymic involution, adrenal hypertrophy, and attenuated body weight gain and up-regulation of hypothalamic corticotrophin-releasing hormone mRNA expression. Consistent with previous literature, lesions of the MeA dampened stress-induced increases in corticosterone after 30 min of exposure to acute restraint stress. However, this effect was independent of CVS exposure, suggesting that the MeA may not be critical for modulating neuroendocrine responses after chronic HPA axis drive. Interestingly, lesion of the MeA modestly exaggerated the stress-induced attenuation of weight gain. Overall, the data obtained suggest that the MeA modulates the neuroendocrine responses to acute but not chronic stress. In addition, the data suggest that the MeA may be an important neural component for the control of body weight in the face of chronic stress.

Authors+Show Affiliations

Department of Psychiatry, University of Cincinnati, Cincinnati, OH 45237, USA. matia.solomon@uc.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

19912476

Citation

Solomon, M B., et al. "The Medial Amygdala Modulates Body Weight but Not Neuroendocrine Responses to Chronic Stress." Journal of Neuroendocrinology, vol. 22, no. 1, 2010, pp. 13-23.
Solomon MB, Jones K, Packard BA, et al. The medial amygdala modulates body weight but not neuroendocrine responses to chronic stress. J Neuroendocrinol. 2010;22(1):13-23.
Solomon, M. B., Jones, K., Packard, B. A., & Herman, J. P. (2010). The medial amygdala modulates body weight but not neuroendocrine responses to chronic stress. Journal of Neuroendocrinology, 22(1), pp. 13-23. doi:10.1111/j.1365-2826.2009.01933.x.
Solomon MB, et al. The Medial Amygdala Modulates Body Weight but Not Neuroendocrine Responses to Chronic Stress. J Neuroendocrinol. 2010;22(1):13-23. PubMed PMID: 19912476.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The medial amygdala modulates body weight but not neuroendocrine responses to chronic stress. AU - Solomon,M B, AU - Jones,K, AU - Packard,B A, AU - Herman,J P, Y1 - 2009/11/14/ PY - 2009/11/17/entrez PY - 2009/11/17/pubmed PY - 2010/3/3/medline SP - 13 EP - 23 JF - Journal of neuroendocrinology JO - J. Neuroendocrinol. VL - 22 IS - 1 N2 - Stress pathologies such as depression and eating disorders (i.e. anorexia nervosa) are associated with amygdalar dysfunction, which are linked with hypothalamic-pituitary-adrenal axis (HPA) axis hyperactivity. The medial amygdaloid nucleus (MeA), a key output nucleus of the amygdaloid complex, promotes HPA axis activation to acute psychogenic stress and is in a prime position to mediate the deleterious effects of chronic stress on physiology and behaviour. The present study tests the hypothesis that the MeA is necessary for the development of maladaptive physiological changes caused by prolonged stress exposure. Male rats received bilateral ibotenate or sham lesions targeting the MeA and one half underwent 2 weeks of chronic variable stress (CVS) or served as home cage controls. Sixteen hours post CVS, all animals were exposed to an acute restraint challenge. CVS induced thymic involution, adrenal hypertrophy, and attenuated body weight gain and up-regulation of hypothalamic corticotrophin-releasing hormone mRNA expression. Consistent with previous literature, lesions of the MeA dampened stress-induced increases in corticosterone after 30 min of exposure to acute restraint stress. However, this effect was independent of CVS exposure, suggesting that the MeA may not be critical for modulating neuroendocrine responses after chronic HPA axis drive. Interestingly, lesion of the MeA modestly exaggerated the stress-induced attenuation of weight gain. Overall, the data obtained suggest that the MeA modulates the neuroendocrine responses to acute but not chronic stress. In addition, the data suggest that the MeA may be an important neural component for the control of body weight in the face of chronic stress. SN - 1365-2826 UR - https://www.unboundmedicine.com/medline/citation/19912476/The_medial_amygdala_modulates_body_weight_but_not_neuroendocrine_responses_to_chronic_stress_ L2 - https://doi.org/10.1111/j.1365-2826.2009.01933.x DB - PRIME DP - Unbound Medicine ER -