In rats anesthetized with pentobarbital, increments in corticosterone concentration were elicited upon electrical stimulation through chronically implanted electrodes. Prestimulation steroid levels were low. Poststimulation levels varied according to the site stimulated. These sites, ranging in order of responsiveness from greatest to least, were amygdala, mammillary hypothalamus, tuberal hypothalamus, and preoptic area. The corticosterone increments obtained under anesthesia were similar in magnitude to those obtained in the absence of anesthesia. Placement of the electrodes in the median eminence itself did not enhance the responsiveness. Hind leg shock evoked a steroid increment comparable to that produced by tuberal stimulation ; and ketamine, a centrally acting drug, provided an estimate of the maximal centrally elicited response. The evidence is consistent with the view that excitatory afferent paths to corticotropin releasing factor (CRF) neurons and the CRF neurons themselves lie distributed in the tissue stimulated.

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The effect of ketamine, a centrally-acting, nonbarbiturate anesthetic, on plasma corticosterone was studied in male rats. Ketamine administered intraperitoneally (i.p.) at anesthetic and subanesthetic doses (120–15 mg/kg) elicited corticosterone responses of the same magnitude as a pharmacological dose of ACTH. The plasma corticosterone response to ketamine was abolished in 24 h hypophysectomized rats and was blocked by dexamethasone (4 mg/kg i.p., 10 h prior to ketamine). The steroid response to ketamine was not significantly changed by prior systemic treatment with atropine or phentolamine. Pretreatment with propranolol or haloperidol, either singly or in combination, resulted in significant decreases in the corticosterone response to ketamine. These results suggest that the corticosterone response to ketamine is mediated through a facilitatory β-adrenergic and/or dopaminergic pathway or some hybrid thereof, and that ketamine is a convenient and useful agent for testing pituitary adrenal responsiveness in the rat.

A non stressful environment was established for awake unrestrained cats to test the excitability of infundibular area sites mediating ACTH release. Each subject was chronically implanted with bilateral electrodes and catheterized in the superior vena cava. Plasma corticosterone and cortisol concentration were determined by fluorometry after chromatographic separation. Samples were taken during both sham and electrical stimulation while the subjects, of their own volition, reclined in a tray. Control samples collected early in the 3-month experimental period showed cortisol values as high as the cortisol response to ACTH. Repetition of the control sampling procedure produced low cortisol levels. No discernible change in the cats’ overt behavior accompanied this decrease in cortisol. Electrical stimulation, which produced a rise in plasma cortisol, did not necessarily result in an overt behavioral reaction. When control cortisol values were high, stimulation was followed by no change or a decrease in cortisol concentration; when cortisol values were low it resulted in increased cortisol concentration. The excitatory influence of infundibular stimulation on cortisol was confirmed under barbiturate anesthesia. It is concluded that electrical stimulation of the infundibular area maximally elevates cortisol when control values are low. Repeated training lowers initially high cortisol levels.

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