Abstract

Experiments were conducted to determine the effects of neonatal administration of L-monosodium glutamate (MSG) on behavioral and endocrine function in the female rat. Administration of MSG (4 mg/kg body weight) at days 1, 3, 5, 7 and 9 in neonates results in a delay of vaginal opening (VO) and the absence of ovulation at the time of VO. However, some rats were observed to ovulate after VO if they were subjected to sequential laparotomies. MSG-treated rats also fail to exhibit compensatory ovarian hypertrophy. Ovariectomized MSG-treated rats injected with estradiol benzoate (EB) followed by a progesterone injected 2 days later did not exhibit sexual beahvior to male rats, while all the control rats displayed lordosis. Chronic treatment with EB for 12 days, followed by a progesterone injection on the 12th day, resulted in a marked improvement of the sexual receptivity of the MSG-treated rats. The body weight of the MSG-treated animals was lower than that of the controls during development although the MSG animals looked obese. Food intake is normal in the MSG-treated rats, but when expressed as intake/100 g body weight, the MSG-treated rats appeared slightly hyperphagic, MSG-treated rats respond with increased food intake after ovariectomy and EB treatment suppresses the increased food intake. Thus, the control of food intake by estrogen does not seem to be affected by the MSG treatment; in fact, these animals seem to be more sensitive than control rats to the anorectic effects of EB. Neonatal MSG treatment appears to affect the neural control for the tonic secretion of gonadotropins by destroying arcuate nuclei. This undoubtedly reduces the reproductive capacity of the animals by impeding the growth and secretions of their ovaries. The findings that chronic estrogen followed by progesterone treatment can reinstate sexual receptivity in MSG-treated animals suggests that the arcuate nuclei are not needed for the expression of sexual behavior and that estrogens might remedy the fertility problems of MSG-treated animals.

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