Dissociation of Systemic and Central Effects of Neurotensin on the Secretion of Growth Hormone, Prolactin, and Thyrotropin*

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Abstract
Neurotensin (NT), a tridecapeptide originally isolated from the hypothalamus, exhibits a wide variety of biological effects which depend on the site of peptide administration. The systemic and central effects of NT on GH, PRL, and TSH secretion were compared in urethane anesthetized, estrogen-primed male rats.ntravenous NT (30 /xg/kg or 7.5–9.0 /xg/rat) produced a marked rise in plasma GH and PRL, which peaked at 5 rnin, and in plasma TSH, which peaked at 15 min. In contrast, intraventricular (ivt) NT (2 and 5 /ig) significantly decreased plasma levels of all three hormones. The PRL and TSH rises after systemic TRH (0.4 /ig/ kg) were inhibited by the ivt injection of NT (0.2 and 2.0 jug). The GH rise after chlorpromazine (200 jug/kg, iv) was completely suppressed by NT (0.5 and 0.2 jug, ivt), whereas that of PRL was partially suppressed. To evaluate the possible mediation of NT effects by substance P, somatostatin, and histamine, the pituitary hormon responses to these compounds were measured. The injection of substance P (5 tig, ivt) was without effect on pituitary hormone secretion, and the injection of somatostatin (5 /ig, ivt) was followed by a decrease in plasma TSH only. Intravenous histamine (5 mg/kg) increased plasma levels of all three hormones, whereas ivt histamine (25 /ig) resulted in a slight increase in PRL levels only. Simultaneous administration of diphenhydramine (5 mg/kg) blocked the hormonal responses to the systemic injection of histamine but not of NT. The results 1) demonstrate the discordant effects of central vs. systemic NT on pituitary hormone secretion; 2) indicate that the NT effects on the pituitary, in contrast to those reported on the endocrine pancreas, are not mediated by histamine; and 3) are consistent with a peptidergic neurotransmitter role for NT in the central nervous system.

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