GLUTAMATE receptor activation induces an extracellular alkalinization in rodent hippocampus. We studied its Ca2+ dependence and pharmacology in hippocampal slices. Glutamate-evoked alkaline shifts were blocked by 0 Ca2+ saline. Alkalinizations induced by AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) and NMDA (N-methyl-D-aspartate) were abolished by 20 μM CNQX (6-cyano-7-nitro-nitroquinoxaline-2,3-dione) and 50 μM APV (DL-2-amino-5-phosphonovaIerate), respectively. The AMPA-and NMDA-evoked alkaline shifts were blocked by 0 Ca2+, however, AMPA-induced [K+]o elevation was unaffected. These data suggest that the glutamate receptor-channel does not mediate H+ influx, and support a role for Ca2+-H+ exchange.
- Excitatory synaptic transmission
- Extracellular pH
- Glutamate uptake
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