Restraint stress stimulation of prolactin and ACTH secretion: Role of brain histamine

Abstract

The possible role of brain histamine in the release of prolactin, ACTH and corticosterone following acute restraint, was pharmacologically evaluated in adult male rats. Fifteen min of restraint caused marked increases in the plasma levels of these hormones. α-Fluoromethyl histidine (FH), a histidine decarboxylase inhibitor which depleted hypothalamic histamine, inhibited the enhancement of plasma prolactin levels. In contrast, plasma ACTH levels were not modified. FH treatment decreased plasma corticosterone concentrations in animals submitted to stress or in rest; this suggests a direct action of FH on the adrenal. Intraventricular (IVT) injection of ranitidine (H 2 antagonist) blunted the prolactin response to restraint stress whereas its systemic administration had no effect. On the contrary, pyrilamine (H 1 antagonist) given systemically decreased slightly, but significantly, the prolactin rise but when injected IVT it was ineffective. Pyrilamine was also unable to affect the ranitidine action. ACTH and corticosterone levels in plasma of restrained rats were not modified by the histamine antagonists. It is concluded that histamine is involved, mainly through central H 2 receptors, in the enhancement of plasma prolactin levels produced by an acute stress. The failure of both antihistaminic compounds and a histamine depletor to alter the ACTH stimulation suggest that histamine has no participation in the hypophysio-corticoadrenal response to acute restraint.