EXTRACELLULAR ALKALINE TRANSIENTS MEDIATED BY GLUTAMATE RECEPTORS IN THE RAT HIPPOCAMPAL SLICE ARE NOT DUE TO A PROTON CONDUCTANCE

1. The ionic mechanism of extracellular alkaline transients mediated by alpha-amino-3-hydroxy-5-methylisoxazolate-4 pionic acid(AMPA) receptor channels was studied in the rat hippocampal slice (area CA1) by means of H+-, Ca2+- and Na+-selective microelectrodes. 2. Alkaline transients mediated by selective synaptic activation of AMPA receptors were coupled to a transient fall in extracellular Ca2+ ([Ca2+](o)). 3. Removal of [Ca2+](o) blocked the alkaline transient evoked by microinjection of AMPA, but had little effect on the simultaneous tetrodotoxin-resistant fall in extracellular Na+ ([Na+](o)). 4. Alkaline transients evoked by microinjection of gamma-aminobutyric acid (GABA) were not affected by removal of [Ca2+](o). GABA had no effect on [Na+](o). 5. The present results indicate that activity-induced glutamatergic alkaline transients in the hippocampal slice are due to an influx of Ca2+, and not to a conductive movement of H+ ions across glutamate-gated cation channels.