Abstract
CRH seems to be of fundamental importance in depressive illness. Melancholic depressed patients, with a syndrome of hyperarousal, have increased activity of CRH-producing neurones. Conversely, there is evidence to support the notion that patients with atypical depression, a syndrome of hypoarousal, have decreased activity of CRH-producing neurones. CRH-induced kindling is a possible model for the natural history of depressive illness. Finally, effective treatments for depressive illness, such as tricyclic antidepressants, decrease CRH production, and drugs, such as carbamazepine, effective in preventing the recurrence of affective disorder, also decrease CRH production. Interestingly, these drugs are not particularly effective in the treatment of atypical depression, which seems to be related not to an activation of CRH-producing neurones, but rather to a decrease of CRH secretion.
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