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Effects of intrathecal (i.t.) administration of TRH and the TRH analogue, DN1417, on plasma catecholamines and glucose levels were studied in conscious male rats. The i.t. administration of TRH (0.6 and 3 nmol) at the T8–10 vertebral level resulted in a dose-related increase in epinephrine (E), norepinephrine (NE), and glucose levels, which was suppressed by prior administration of the ganglionic blocker, hexamethonium (1.5 mg/100 g b. wt.). I.t. administration of TRH (3 nmol) caused small increases in plasma E and glucose at the C7-T1 vertebral level, but it did not change plasma E, NE and glucose levels at the sacral level. DN1417 (3 nmol) administered i.t. at the T8–10 or C7-T1 vertebral level had a more potent and long-lasting effect in stimulating the release of E than TRH. These findings suggest that TRH may act on sympathetic preganglionic neurons at the T7–10 spinal levels and stimulate the release of cathecholamines from the adrenal medulla.

The mechanism by which galanin (GAL) stimulates prolactin (PRL) secretion was investigated in urethane-anesthetized male rats. The PRL release induced by intracerebroventricular (i.c.v.) injection of porcine GAL (pGAL) was similar to that induced by rat GAL. The PRL release induced by pGAL was partially blocked by alpha-adrenergic antagonists, phentolamine (1 microgram/rat, i.c.v.; 29.1 +/- 4.5 ng/ml vs control 66.9 +/- 10.2 ng/ml, P less than 0.01) and tolazoline (1 microgram/rat, i.c.v.; 25.9 +/- 4.4 ng/ml vs control 59.6 +/- 10.9 ng/ml, P less than 0.05). Neither propranolol (1 microgram/rat, i.c.v.), a beta-adrenergic antagonist, nor prazosin (1 microgram/rat, i.c.v.), an alpha 1-adrenergic antagonist, inhibited pGAL-induced PRL release. Naloxone (125 micrograms/100 g body wt., i.v. 30 min before), an opiate antagonist, also inhibited pGAL-induced PRL release (25.9 +/- 4.0 ng/ml vs 59.1 +/- 7.2 ng/ml, P less than 0.01). Combined treatment with naloxone and phentolamine caused greater inhibition of pGAL-induced PRL release than did phentolamine alone (10.3 +/- 1.5 ng/ml vs 23.2 +/- 4.7 ng/ml, P less than 0.05), but the inhibition was similar to that induced by naloxone alone. These findings suggest that alpha 2-adrenergic and opioidergic mechanisms are involved in PRL release induced by GAL.

Brain opiatergic, alpha-adrenergic and GABAergic mechanisms are known to play a stimulating role in growth hormone (GH) secretion in the rat. Plasma GH levels were increased by intracerebroventricular (i.c.v.) injection of somatostatin-14 (SRIF-14, 5 micrograms/rat) in conscious rats. GH release induced by i.c.v. SRIF-14 was blunted by either intravenous (i.v.) injection of phenoxybenzamine (500 micrograms/100 g b. wt.), an alpha-adrenergic blocker, or picrotoxin (150 micrograms/100 g b. wt.), a GABA antagonist, in the rat. On the other hand, i.v. injection of naloxone (125 micrograms/100 g b. wt.), an opiate antagonist, did not affect GH release induced by i.c.v. SRIF-14. These findings suggest that alpha-adrenergic and GABAergic mechanisms but not opiatergic mechanisms are involved in central SRIF-induced GH secretion in the rat.