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Steroid-monoamine feedback interactions in discrete brain regions using as a model the monosodium glutamate
Abstract:
The present studies examine the effects of neonatal treatment with monosodium glutamate (MSG) on dopamine (DA), 5-hydroxytryptamine (5-HT) and norepinephrine (NE) metabolism in discrete brain regions and correlate them with steroid receptor kinetics in the anterior pituitary (PIT), preoptic hypothalamus (POA) and caudal hypothalamus (HYP), and with steroid negative and positive feedback effects on luteinizing hormone (LH) secretion. Substantial decreases in the neuronal activity of all three amines in the arcuate nucleus, decreased DA and 5-HT metabolism in the suprachiasmatic nucleus and, surprisingly, increased metabolism of 5-HT and NE in the median eminence was observed in adult ovariectomized (OVX), MSG-treated versus OVX, vehicle-treated litter mate controls. Measurement of estradiol receptors in the nuclear and cytosolic fractions of the POA, HYP and PIT from MSG- and vehicle-treated rats killed during diestrus or 2 weeks after OVX revealed no differences. Similarly, no differences in cytosolic progestin receptors between control and MSG unprimed or estradiol-primed, OVX rats or on progestin receptor translocation induced by progesterone in Eb-primed rats were observed. Negative and positive feedback effects of estradiol or the positive feedback of progesterone on LH secretion were not significantly impaired in MSG rats, and indeed, MSG animals actually were hyper-responsive to the administration of the steroids or of luteinizing hormone-releasing hormone. These results indicate that the MSG-induced damage to DA, 5-HT and NE elements observed within several preoptic and hypothalamic nuclei does not impair estrogen and progestin receptor kinetics, nor does it prevent adequate negative or positive steroid feedback responses, if appropriate steroid regimens are employed, and that the impaired gonadal function reported in these animals does not result primarily from inadequate steroid feedback mechanisms.