title: The medial amygdala modulates body weight but not neuroendocrine responses to chronic stress.
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.affiliation: Department of Psychiatry, University of Cincinnati, Cincinnati, OH 45237, USA. matia.solomon@uc.edu
authors.forename: M B
authors.initials: MB
authors.lastname: Solomon
authors.forename: K
authors.initials: K
authors.lastname: Jones
authors.forename: B A
authors.initials: BA
authors.lastname: Packard
authors.forename: J P
authors.initials: JP
authors.lastname: Herman
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism / Q000503:physiopathology; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000679:Amygdala / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D000704:Analysis of Variance; D000818:Animals; D034961:Antigens, Nuclear / Q000378:metabolism; D001835:Body Weight / Q000502:physiology*; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D007051:Ibotenic Acid / Q000633:toxicity; D007091:Image Processing, Computer-Assisted; D017403:In Situ Hybridization; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009478:Neuropeptide Y / Q000235:genetics / Q000378:metabolism; D009929:Organ Size / Q000502:physiology; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D011333:Pro-Opiomelanocortin / Q000235:genetics / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011863:Radioimmunoassay; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000502:physiology*; D013315:Stress, Psychological / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D013950:Thymus Gland / Q000378:metabolism / Q000503:physiopathology
chemical_list: D034961:Antigens, Nuclear; D009419:Nerve Tissue Proteins; D009478:Neuropeptide Y; D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger; C546339:Rbfox3 protein, rat; D007051:Ibotenic Acid; D011333:Pro-Opiomelanocortin; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone