Thalamic-hypothalamic interrelationships and stress-induced rebounding adrenocortical response in the pigeon.
Plasma corticosterone levels were determined by protein-binding assay at 2- and 5-min intervals after systemic or neurogenic stress. The same corticosterone (B) profile was observed after hemispherectomy as in intact pigeons, exhibiting episodic increase including several successive peaks after stress application. Hypothalamic stimulation of ACTH injection resulted in a simpler adrenocortical response, analogous to the first peak of the response to stress. Postero-lateral deafferentation of the hypothalamus unabled neurogenic stress to promote any plasma B increase and significantly altered the response to systemic stress since only the first peak of B occurred. Such a single peak response to both systemic and neurogenic stresses was observed after surgical interruption of neural connections between hypothalamic and thalamic structures without interferring with posterior afferents to the basal hypothalamus. The role of thalamic-hypothalamic interrelationships in modulating the stress-induced adrenocorticotropic activity is discussed.
D000302:Adrenal Cortex / Q000187:drug effects / Q000503:physiopathology*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000344:Afferent Pathways / Q000503:physiopathology; D000818:Animals; D010856:Columbidae; D003345:Corticosterone / Q000097:blood; D004597:Electroshock; D007031:Hypothalamus / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D013312:Stress, Physiological / Q000503:physiopathology*; D013788:Thalamus / Q000187:drug effects / Q000503:physiopathology*
D000324:Adrenocorticotropic Hormone; D003345:Corticosterone