Depolarization-induced release of [3H]d-aspartate from GABAergic neurons caused by reversal of glutamate transporters

摘要: Abstract Cultured neocortical neurons, which predominantly consist of GABAergic neurons exhibit a pronounced stimulus-coupled GABA release. Since the cultures may contain small population glutamatergic and have high content glutamate it was interest to examine if in addition γ-aminobutyric acid (GABA) could be released from these cultures. The were preloaded with [ 3 H] d -aspartate subsequently its release followed during depolarization induced by potassium concentration or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPA) receptor agonists, AMPA kainate. Depolarization 55 mM increased more than 10-fold. When non-specific calcium-channel blockers cobalt lanthanum included stimulation buffer potassium, decreased about 40%. These results indicated that some might originate vesicular pool. applied 2-fold not prevented cobalt. has rapid desensitizing effect on receptors, examined whether under non-desensitizing conditions able induce an as compared applying alone. desensitization receptors blocked 6-chloro-3,4-dihydro-3-(2-norbornen-5-yl)-2H-1,2,4-benzothiadiazine-7-sulphonamide-1,1-dioxide (cyclothiazide). Under conditions, AMPA-induced highly enhanced showing 10-fold increase over basal Addition did decrease amount released, indicating originated cytoplasmic Kainate, induces almost showed similar observed for conditions. NMDA antagonist (5 R ,10  S )-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801) had only minor effects Thus, depolarization-induced cultured appears caused mainly reversal transporters.