Abstract
We investigated the effects of the antitussive dextromethorphan (DM; 100 μM) on the extracellular DC potential, extracellular calcium concentration ([Ca 2+] o) and on stimulus-evoked field potential (FP) responses in rat neocortical slices during hypoxia. DM significantly reduced the amplitude of the anoxic depolarization (AD) and the associated [Ca 2+] o decrease by 47.6% and 48.5%, respectively, but did not change the onset latency and the duration of the AD. DM did not affect the preservation or recovery of excitatory synaptic transmission and significantly suppressed paired-pulse inhibition in the postanoxic recovery phase. These results indicate that DM exerts its potential neuroprotective action by reducing the hypoxia-induced depolarization and Ca 2+ influx.
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