CHANGES IN LUTEINIZING-HORMONE AND PROLACTIN CONTROL MECHANISMS PRODUCED BY GLUTAMATE LESIONS OF ARCUATE NUCLEUS

Lesions of the arcuate nucleus and retina were produced by ip administration of 4 g/kg monosodium glutamate to rats on days 2, 4, 6, and 10 after birth, and all experimental work was continued at about 3–5 months of age. In agreement with earlier studies, we noted a striking reduction in the number of cell bodies in the arcuate nucleus, a marked degeneration of the visual system, and smaller anterior pituitaries, ovaries, uteri, testes, and seminal vesicles in adult rats that had been treated with glutamate during the neonatal period. A 60% reduction in the concentration of dopamine in the medial-basal hypothalamus and irregular estrous cycles also were observed in glutamate-treated groups. In two of six groups of glutamate-treated rats, basal serum LH levels were lower than in controls, whereas in one of six groups, PRL was elevated. The remainder of glutamate-treated groups showed no significant change in basal serum PRL or LH levels. After ovariectomy, serum LH levels were lower in glutamate-treated rats than in controls, and glutamate treatment greatly attenuated the surges of LH and PRL seen in ovariectomized rats after treatment with estradiol benzoate. Although glutamate treatment markedly attenuated the release of PRL in ovariectomized rats treated with estrogen, the opposite was true after 5- hydroxytryptophan (5-HTP). In both male and female rats, a marked enhancement of PRL release in response to 30 mg/kg 5-HTP was observed in glutamate-treated groups. The release of PRL after 5-HTP treatment in glutamate rats was significantly greater than the release of PRL after blockade of dopamine receptors. These results suggest that glutamate-induced lesions of the arcuate nucleus result in an impaired release mechanism for LH and PRL when estrogen is the “inducer,”but produce a condition where serotonergic stimuli are much more effective in releasing PRL. The data also suggest that serotonin releases PRL through a PRLreleasing factor. © 1978 by The Endocrine Society.