PREPUBERTAL DYSFUNCTION OF THE LHRH LH AXIS IN MONOSODIUM GLUTAMATE-TREATED RATS REVEALED BY THE LH RESPONSE TO N-METHYL-D-ASPARTATE/

Hypogonadism is a remarkable effect of the neurotoxic lesion of the hy pothalamus caused by neonatal administration of monosodium glutamate ( MSG) in the rat. We investigated the effect of MSG treatment on pre- a nd peripubertal development of hypothalamic-pituitary axis by evaluati ng the release of luteinizing hormone (LH) evoked by the glutamate ago nist N-methyl-D-aspartate (NMDA) which is apparently mediated by LHRH release. NMDA (30 mg/kg i.p.) lacked effect on LH release in 30-day-ol d MSG-treated male rats. In the 40 day-old MSG male rats only the 30 m g/kg doses of NMDA were able to induce low LH surges. In the young adu lt males, MSG did not alter the pituitary responsiveness to NMDA. The 30 and 40-day-old MSG OVX-E(2) rats exhibited low responses to NMDA ev en at the highest doses. In 40-day-old OVX-E(2) rats injected neonatal ly 4 times with MSG, NMDA (30 mg/kg) was unable to increase LH release . These results make evident that-the neonatal administration of MSG i mpairs the hypothalamic-pituitary responsiveness to NMDA in pre- and p eripubertal rats in relation with the grade of depletion of neurons in the mediobasal hypothalamus. It seems possible that hypogonadism caus ed by MSG is due in part to a prepubertal failure in the excitatory tr ansmission controlling LHRH/LH secretion.