REGULATION OF D-ASPARTATE RELEASE BY GLUTAMATE AND GABA RECEPTORS IN CEREBRAL CORTICAL SLICES FROM DEVELOPING AND AGING MICE

The basal release of D-[H-3]aspartate, an unmetabolized analogue of gl utamate, from cerebral cortical slices remained at the same level from three-day-old to 24-month-old mice, but the response to K+ stimulatio n (50 mM) was smaller in young than in adult or aged mice. Kainate, N- methyl-D-aspartate and quisqualate (0.1 mM) stimulated the basal relea se of D-aspartate in the cerebral cortex of seven-day-old mice, the ef fects of kainate and N-methyl-D-aspartate being reduced by their antag onists 6-cyano-7-nitroquinoxaline- 2,3-dione (CNQX) and dizocilpine ma leate, respectively, indicating that in the immature cerebral cortex t he kainate and N-methyl-D-aspartate types of the glutamate receptor ar e involved in the basal release. The K+-stimulated release was not aff ected by glutamate agonists in developing mice, though they markedly a ttenuated the evoked release in adults. The inhibitory amino acids GAB A, taurine and glycine depressed the K+-stimulated release only in the adult cerebral cortex. The action of GABA was abolished by bicucullin e, demonstrating the involvement of presynaptic GABA(A) receptors. The glycine effect was strychnine-insensitive, characteristic of the glyc ine modulatory site in the N-methyl-D-aspartate receptor. This kind of regulation by both kainate and N-methyl-D-aspartate receptors could b e of physiological significance, particularly in the immature cerebral cortex.