Effects of cysteamine pretreatment and hypothalamic periventricular nucleus lesion on the cold-stimulated thyrotropin responses to intracerebroventricular 5-hydroxytryptamine in male rats.

Abstract The hypothalamic somatostatinergic system was devitalized in male rats by intracerebroventricular (icv) cysteamine (CSH) pretreatment (250 mug/rat/day into the third ventricle) on 4 consecutive days or by a limited lesion of the hypothalamic periventricular nucleus (PeVNx). The acute effect of icv serotonin (5-HT) on the cold-stimulated thyrotropin (TSH) and prolactin responses were studied in these animals. The experiments were performed 24 h after the last saline or CSH infusions and 7 days after the sham- or PeVN-lesions. CSH and PeVNx decreased the hypothalamic somatostatin content by 44% to 57% and 19% to 28%, respectively. PeVNx did not affect hypothalamic thyrotropin-releasing hormone content. 5-HT infusion (9 mug/rat icv) into the anterior third ventricle elevated, although not significantly, TSH levels in both saline- or CSH-pretreated rats. 5-HT infusion into the anterior third ventricle did not affect TSH in sham-operated rats. However, 5-HT augmented the cold-stimulated TSH levels after PeVNx compared to sham-lesion. Inversely, 5-HT infusion (9 mug/rat) into the posterior third ventricle inhibited TSH secretion irrespective of the pretreatment or lesion. The inhibitory action of 5-HT on TSH was significantly suppressed by CSH. 5-HT infusions elevated serum prolactin levels irrespective of the infusion site, pretreatment or lesion. 5-HT infusion into both the anterior and the posterior third ventricle decreased rectal temperature in saline-pretreated, sham- and PeVN-lesioned rats. The hypothermie effect of 5-HT was weakened by CSH. The hypothalamic levels of noradrenaline, dopamine and their metabolites were not significantly affected by CSH and PeVNx. 5-HT infusion into the anterior third ventricle decreased hypothalamic dopamine content in both saline- and CSH-pretreated rats. However, such an effect was not seen in sham- or PeVN-lesioned animals. Although CSH is an inhibitor of dopamine-beta-hydroxylase, this activity was not reflected in serum TSH or prolactin levels. The results support our hypothesis of the site-dependent action of icv 5-HT or TSH secretion. The elevation of TSH levels may arise from the inhibition of somatostatin release from rostral anterior hypothalamus. The inhibition of TSH secretion may result from the inhibition of thyrotropin-releasing hormone release from more caudal periventricular structures of the hypothalamus.