We examined the effects of the thiol agent cysteamine (CSH), which is known to deplete the hypothalamus of immunoreactive somatostatin, on physiological TSH and β-endorphin secretion in the adult male rat. CSH at doses of 90 and 300 mg/kg CSH produced a rapid decline in plasma TSH, whereas a dose of 30 mg/kg did not alter plasma TSH levels. After the higher doses of CSH, TSH levels in the blood remained lower than control values on day 2, but returned to normal by 1 week. This decrease in TSH within the plasma was not associated with a reduction in hypothalamic TRH concentrations. The TSH response to 500 ng/kg TRH was normal in CSH-treated animals. Blockade of norepinephrine synthesis with diethyldithiocarbamate (500 mg/kg) or fusaric acid (100 mg/kg) inhibited TSH secretion in a manner similar to that of CSH. β-Endorphin-like immunoreactivity (β-End-LI) was elevated in the plasma immediately after CSH (300 mg/kg) administration. This was associated with a 58% reduction in anterior pituitary β-End-LI and no change in hypothalmic β-End-LI. Plasma β-End-LI returned to normal on day 2. The increase in plasma β-End-LI induced by immobilization stress was not compromised by CSH treatment. The observed effects of CSH on both TSH and β-End-LI are consistent with a reduction in central norepinephrine neurotransmission through the known action of CSH to inhibit dopamine-β -hydroxylase. Acute stress may play a role as well in the observed changes in TSH and β-End-LI secretion.
ASJC Scopus subject areas