The Role of the Hippocampus in Feedback Regulation of the Hypothalamic-Pituitary-Adrenocortical Axis*

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Abstract
Introduction THE hippocampus has received considerable attention as a potential regulator of the hypothalamic-pituitary-adrenocortical (HPA) axis. After the demonstration by Harris' laboratory (1) that the hypothalamus could affect adrenocortical function, investigation extended to identifying other brain areas that might influence hypothalamic activity. Early evidence for hippocampal projections to the hypothalamus and the role of the limbic system in emotions made the hippocampus a likely component of a stress-activated system such as the adrenocortical axis (2,3). This hypothesis has been borne out not only by physiological studies but also by pharmacological evidence that the hippocampus contains corticosteroid receptors. This review will focus solely on the physiological data for, and the possible mechanisms underlying, the hippocampal regulation of HPA sensitivity to corticosteroid feedback. This subject has been addressed by McEwen et al. (4) and more recently by Canny (5). However, the literature has expanded since the former review, and considerable controversy remains regarding the role of hippocampal corticosteroid receptors following the latter review; we believe these issues merit further attention. In focusing on the hippocampus, we do not intend to imply that it is the only brain corticosteroid feedback site, nor that it plays a more important role than the hypothalamus. However, the hippocampus is one of the regions most susceptible to damage by insults such as ischemia, hypoglycemia, and seizure (6). Consequently, the hippocampus is of particular interest among potential glucocorticoid feedback sites not only because of the considerable and varied evidence for its influence on HPA activity, but also because that influence may be so easily disrupted.

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