Modulation of behavioral inhibition in appetitive extinction following manipulation of adrenal steroids in rats: Implications for involvement of the hippocampus.

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Abstract
Corticosterone, the principal glucocorticoid in the rat, binds selectively to the CA1 [commissura anterior] pyramidal neurons of the hippocampus where the hormone has been demonstrated to exert a moderate chronic suppression of spontaneous activity. In the 1st experiment, the functional behavioral significance of this hormone-brain interaction was investigated in the extinction of an appetitive runway response in normal rats and those with lesions of the hippocampus. During extinction, half of the animals in each group were given daily s.c. injections of corticosterone. While the classical retardation effect of hippocampal lesions on appetitive extinction was replicated, hormone treatment was without effect in normal or hippocampally damaged subjects. The absence of a hormone effect in normals was primarily attributed to a saturated limited-binding system operating in the normal animal. Experiment 2 tested this notion, repeating the 1st experiment, with adrenalectomized (ADX), ADX + corticosterone replacement, and normal groups of animals. Adrenalectomy produced a striking facilitation of extinction which was speculated to be the result of a hyperactive inhibitory neural organ free from an inhibitory endocrine feedback. Corticosterone treatment normalized the progress of extinction in ADX animals, providing support for the aforementioned speculation. In the normal animal, a stress-induced surge in hormone level may interact with a limited-capacity neural binding to produce a transient dynamic range of behavioral disinhibition, perhaps promoting persistence during initial stages of frustrative nonreward in moderate stress tasks.