The pharmacology of synaptically evoked extracellular alkaline shifts was studied in the CA1 area of rat hippocampal slices. 2. Stimulus-evoked alkalinizations were unaffected by 2-amino-5-phosphonovalerate (APV) (20 microM). 3. 6-Cyano-7-nitro-nitroquinoxaline-2,3-dione (CNQX) (10 microM) inhibited the alkalinizations. In the continued presence of CNQX, an APV-sensitive, picrotoxin-insensitive, alkaline shift was elicited in low Mg2+ media. 4. Antidromic stimulation produced small alkaline shifts in comparison with orthodromic activation. 5. Our results demonstrate that in the hippocampal CA1 region, synaptically evoked alkalinizations can arise through both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors. These responses cannot be explained by cell firing per se.
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Chen et al. (1992) studied this question.