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Saransaari P, Oja SS: Regulation of D-aspartate release by glutamate and GABA receptors in cerebral cortical slices from developing and ageing mice. Neuroscience. 1994 May;60(1):191-8.
The basal release of D-[3H] aspartate, an unmetabolized analogue of glutamate, from cerebral cortical slices remained at the same level from three-day-old to 24-month-old mice, but the response to K+ stimulation (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 release of D-aspartate in the cerebral cortex of seven-day-old mice, the effects of kainate and N-methyl-D-aspartate being reduced by their antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and dizocilpine maleate, respectively, indicating that in the immature cerebral cortex the kainate and N-methyl-D-aspartate types of the glutamate receptor are involved in the basal release. The K (+)-stimulated release was not affected by glutamate agonists in developing mice, though they markedly attenuated the evoked release in adults. The inhibitory amino acids GABA, taurine and glycine depressed the K (+)-stimulated release only in the adult cerebral cortex. The action of GABA was abolished by bicuculline, demonstrating the involvement of presynaptic GABAA receptors. The glycine effect was strychnine-insensitive, characteristic of the glycine modulatory site in the N-methyl-D-aspartate receptor. This kind of regulation by both kainate and N-methyl-D-aspartate receptors could be of physiological significance, particularly in the immature cerebral cortex. |
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