Role of the hypothalamic paraventricular nucleus in the secretion of thyrotropin under adrenergic and cold-stimulated conditions in the rat.

Abstract

To investigate the role of central noradrenergic systems in the regulation of TSH secretion, clonidine (an alpha 2-adrenergic agonist) and an electrolytic procedure were used. The administration of a small dose (50 micrograms/kg, iv) of clonidine induced a significant rise in immunoreactive TSH levels in the plasma with a short time lag in unanesthetized, unrestrained rats. The TSH-stimulating effect of clonidine was significantly reduced by passive immunization with rabbit antiserum to TRH. In rats with midbrain transection, the plasma TSH elevation in response to clonidine did not differ from that of sham-operated controls, whereas bilateral lesions in the paraventricular nucleus (PVN) markedly diminished the TSH secretory response. In contrast, the placement of electrolytic lesions in the dorsal raphe nucleus caused a significant increase in the basal TSH concentrations within 3 days, and magnified the TSH response to alpha 2-adrenergic stimulation. Acute exposure to cold (2-3 C) induced a prompt increase in the plasma TSH concentrations in normal rats. Bilateral lesions in the medial preoptic/anterior hypothalamus had no effect on the TSH response to cold exposure. In rats with the dorsal raphe nucleus lesions no significant effect was observed on the responsiveness to cold. In rats bearing PVN lesions, however, plasma TSH levels decreased significantly compared with sham-operated controls within 4 days, and also remained at basal levels during the whole period of cold exposure. The results of the present study provide evidence supporting the hypothesis that the PVN is essential for the process of TRH-TSH secretion, which is accelerated under cold-stimulated conditions, presumably via the central noradrenergic system(s).