title: Hydration state controls stress responsiveness and social behavior.
abstract: Life stress frequently occurs within the context of homeostatic challenge, requiring integration of physiological and psychological need into appropriate hormonal, cardiovascular, and behavioral responses. To test neural mechanisms underlying stress integration within the context of homeostatic adversity, we evaluated the impact of a pronounced physiological (hypernatremia) challenge on hypothalamic-pituitary-adrenal (HPA), cardiovascular, and behavioral responses to an acute psychogenic stress. Relative to normonatremic controls, rats rendered mildly hypernatremic had decreased HPA activation in response to physical restraint, a commonly used rodent model of psychogenic stress. In addition, acute hypernatremia attenuated the cardiovascular response to restraint and promoted faster recovery to prestress levels. Subsequent to restraint, hypernatremic rats had significantly more c-Fos expression in oxytocin- and vasopressin-containing neurons within the supraoptic and paraventricular nuclei of the hypothalamus. Hypernatremia also completely eliminated the increased plasma renin activity that accompanied restraint in controls, but greatly elevated circulating levels of oxytocin. The endocrine and cardiovascular profile of hypernatremic rats was predictive of decreased anxiety-like behavior in the social interaction test. Collectively, the results indicate that acute hypernatremia is a potent inhibitor of the HPA, cardiovascular, and behavioral limbs of the stress response. The implications are that the compensatory responses that promote renal-sodium excretion when faced with hypernatremia also act on the nervous system to decrease reactivity to psychogenic stressors and facilitate social behavior, which may suppress the anxiety associated with approaching a communal water source and support the social interactions that may be encountered when engaging in drinking behavior.
authors.affiliation: Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, College of Medicine, Cincinnati, Ohio 45219, USA.
authors.forename: Eric G
authors.initials: EG
authors.lastname: Krause
authors.forename: Annette D
authors.initials: AD
authors.lastname: de Kloet
authors.forename: Jonathan N
authors.initials: JN
authors.lastname: Flak
authors.forename: Michael D
authors.initials: MD
authors.lastname: Smeltzer
authors.forename: Matia B
authors.initials: MB
authors.lastname: Solomon
authors.forename: Nathan K
authors.initials: NK
authors.lastname: Evanson
authors.forename: Stephen C
authors.initials: SC
authors.lastname: Woods
authors.forename: Randall R
authors.initials: RR
authors.lastname: Sakai
authors.forename: James P
authors.initials: JP
authors.lastname: Herman
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D003345:Corticosterone / Q000097:blood; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D006339:Heart Rate / Q000502:physiology; D055103:Hypodermoclysis; D008297:Male; D009995:Osmosis; D010121:Oxytocin / Q000097:blood; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000378:metabolism; D011863:Radioimmunoassay / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D012919:Social Behavior; D012965:Sodium Chloride / Q000494:pharmacology; D013315:Stress, Psychological / Q000097:blood / Q000503:physiopathology*; D013495:Supraoptic Nucleus / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors; D014660:Vasoactive Intestinal Peptide / Q000097:blood
chemical_list: D014660:Vasoactive Intestinal Peptide; D012965:Sodium Chloride; D010121:Oxytocin; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone