A decrease of cytosol estrogen receptors in the hypothalamus as a result of treatment of neonatal rats with glutamate.

Experiments were performed to determine whether the neuroendocrine dysfunctions of rats treated neonatally with monosodium glutamate (MSG) could be related to a loss of cytoplasmic estrogen receptors. Female rats treated with MSG as neonates were ovariectomized as adults and killed by decapitation 2 or 3 weeks after ovariectomy. Body, gonadal and anterior pituitary gland weights in MSG-treated rats were depressed when compared to that seen in their littermate controls. Serum prolactin concentration was elevated in the MSG-treated rats. Serum luteinizing hormone (LH) concentration was significantly lower in MSG-treated rats than in controls at 2 weeks, but not at 3 weeks after ovariectomy, suggesting a sluggish postovariectomy rise of serum LH concentration. Serum follicle-stimulating hormone (FSH) concentration was not altered by the MSG treatment. The concentration of cytosol estrogen receptors in the anterior pituitary gland was similar to that of controls, but hypothalamic concentration of estrogen receptors decreased as a result of the MSG treatment. After dissection of different hypothalamic regions, it was found that the greatest depletion of the cytosol estrogen receptors occurred in the arcuate-median eminence region. The results raise the possibility that some reproductive impairments of MSG-treated rats could stem from a decrease in cytosol estrogen receptors in the arcuate-median eminence region.