EFFECT OF NEONATAL EXPOSURE TO MONOSODIUM L-GLUTAMATE ON REGIONAL GABA RELEASE DURING POSTNATAL-DEVELOPMENT

Monosodium L-glutamate (MSG) causes neuronal lesions in certain brain regions when systemically given to young animals. Also, when glutamate (Glu) builds up in the intersynaptic space, it induces neuroexcitator y and neurocytotoxic effects, events mediated by several Glu receptors . Some of these receptors such as NMDA and AMPA receptors are present in the very earliest developmental stages of the central nervous syste m and play a major role in neuronal plasticity during synaptogenesis. In this paper, the GABAergic system vulnerability was determined in te rms of [H-3]-GABA release during postnatal development. [H-3]-GABA rel ease on days 14, 21, 30, and 60 days after birth was assessed for the cerebral cortex (CC), hippocampus (Hp) and striatum (S) in rats perina tally treated at days 1, 3, 5, and 7 after birth with MSG. The results show a major decrease in baseline [H-3]-GABA release in the CC (30 an d 60 days after birth) and the Hp (beginning day 21 after birth) vs th e control groups [intact rats and rats given a NaCl solution equimolar to that of MSG (eqNaCl)] while in the S baseline release remained unc hanged. Stimulated [H-3]-GABA release was decreased in the CC on days 14 and 21 after birth and significantly increased on day 60 after birt h vs the controls. In the Hp, a decrease was seen on days 14, 21, and 60 after birth vs the controls while stimulated [3H]-GABA release was decreased in the S vs the controls at all ages studied. No significant differences in stimulated [H-3]-GABA release were found between the i ntact group and the group treated with eqNaCl on days 30 and 60 after birth. Results show that CC, Hp and S GABAergic neurones are a major t arget for the effect of perinatally given MSG and suggest a possible d ecrease in the number of Hp GABAergic neurones while these results in CC and S suggest a modified neuronal plasticity. NMDA receptor and cal cium involvement are discussed as significant mediators of these event s. (C) 1998 Elsevier Science Ltd. All rights reserved.