Pituitary Responsiveness to LHRH Stimulation in Hamsters Treated Neonatally with Monosodium Glutamate

Abstract

Previous studies have shown that neonatal administration of monosodium glutamate (MSG) results in a clearly defined lesion of the arcuate nucleus which disrupts mechanisms regulating normal FSH but not LH secretion in the adult female hamster. The present study was designed to investigate the effects of neonatally administered MSG or hypertonic saline (control) on the in vivo and in vitro responses to LHRH in adult animals. In order to evaluate these responses under a comparable hormonal background, all animals were ovariectomized at 2-3 months of age and given 50 micrograms of estradiol benzoate 3 weeks later. 24 h later, animals were anesthetized with sodium pentobarbital and a blood sample taken for baseline levels of gonadotropins; they were immediately given 5 or 25 ng LHRH intravenously, and LH and FSH responses to LHRH were determined by sampling at 15-min intervals over a 1-hour period. Pituitary content of LH and FSH was determined in a similar group of control and MSG-treated animals which did not receive the hypothalamic hormone. Basal LH secretion, the dose-response of LH to LHRH, and the pituitary concentration or content were similar in control and MSG-treated hamsters. In contrast to LH, basal FSH levels were significantly lower, the FSH responses to LHRH were greatly attenuated, and a dose response to LHRH was absent in MSG-treated animals when compared to control values. Pituitary FSH concentration and content did not differ between control and MSG-treated animals. However, when pituitaries were removed, hemidissected, preincubated for 1 h, and incubated in the presence or absence of 8.5 x 10(-9) or 8.5 x 10(-10) M LHRH for 3 consecutive 1-hour periods, no differences were noted between control and experimental animals regarding basal (no LHRH) or LHRH-stimulated release of LH and FSH. These results suggest that the decreased basal FSH levels and the attenuated FSH response to LHRH observed in vivo in MSG-treated animals may be due to an alteration in a neural or extraneural component which is involved in regulating the release of FSH by LHRH and which is evident in the absence of a functional arcuate nucleus and/or develops directly as the result of the neonatal administration of MSG.