The effect of isoflurane on excitatory synaptic transmission in the rat hippocampus

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Abstract
The purpose of this investigation was to study the effect of isoflurane on excitatory synaptic transmission. Rat hippocampal slices maintainedin vitrowere used as a model. Isoflurane caused a dose‐dependent reduction of the excitatory postsynaptic potential (EPSP); 1.5% isoflurane reduced the EPSP by 35 ± 9% (mean ± s.d.) and 3% by 57 ± 11%. Neither spontaneous nor potassium‐stimulated efflux of the glutamate analogue D‐(3H) aspartate was changed, but the content of D‐(3H) aspartate in slices loaded during isoflurane was reduced to 83 ± 12% of control (P<0.05). The intracellularly recorded response to direct application of glutamate increased by 37 ± 20% during isoflurane (3%) and 50 ± 5% during halothane (2%). Isoflurane (3%) enhanced the response to the glutamate receptor agonist quisqualate by 44 ± 19%, whereas the N‐methyl‐D‐aspartate response was unchanged. Isoflurane enhanced the tetanic depression of the population spike. The present results suggest that isoflurane reduces excitatory synaptic transmission by a presynaptic mechanism.