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Alterations in baseline and challenged pituitary-adrenocortical function constitute the most extensively studied abnormalities in affective disorders. The recent availability of corticotropin-releasing hormone (CRH) for clinical studies opened the possibility to further investigate pathophysiology underlying aberrant ACTH and cortisol secretion. When injected to depressives CRH induces a blunted ACTH but normal cortisol release. Similar response patterns were observed among patients with panic disorder and alcoholism. In these diseases, enhanced baseline pituitary adrenocortical activity appears to be driven by a CNS disturbance resulting in overactive CRH secreting neurons. In addition to these endocrine findings we observed among normal controls suppressed nocturnal slow-wave sleep and growth hormone surges during infusions of CRH. Our clinical investigations with CRH support that this neuropeptide is involved in mediation of several neuroendocrine and behavioral changes frequently observed in depressive syndromes.
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