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. Posterolateral 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.

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Thalamic and intact pigeons were equipped with a chronic arterial catheter and with a miniature electronic device for hypothalamic telestimulation. Chronic catheterization allowed for repetitive blood sampling in freely moving birds subjected to either systemic (ether inhalation) or neurogenic (electrical foot shocks) stress and to electrical stimulation of the hypothalamic corticotropic area. Corticosterone levels were determined by protein binding assay at 2-, then 5- and 10-min intervals, for 100 min. Basal and experimentally modified plasma corticosterone concentrations were not different in thalamic and intact pigeons. Corticosterone profile exhibited episodic increase including three peaks at 12, 35 and 60 min after stress application. Only the first peak of plasma corticosterone appeared after hypothalamic stimulation. It is suggested that extrahypothalamic neuronal networks are responsible for the long-lasting repetitive adrenocorticotropic response to stress, which are not involved in the single response to hypothalamic stimulation itself. Furthermore, such extrahypothalamic neuronal networks should be located at the diencephalic or rhombencephalic level since hemispherectomized pigeons exhibited the same profile of stress-induced episodic hypercorticosteronemia as seen in intact birds.

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