Dextromethorphan attenuates hypoxia-induced neuronal dysfunction in rat neocortical slices.
We investigated the effects of the antitussive dextromethorphan (DM; 100 microM) on the extracellular DC potential, extracellular calcium concentration ([Ca2+]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 [Ca2+]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 Ca2+ influx.
Luhmann
H J
HJ
Institute of Neurophysiology, University of Cologne, Germany.
Scheid
M
M
D000818:Animals; D015687:Cell Hypoxia; D002540:Cerebral Cortex / Q000187:drug effects / Q000502:physiology*; D003915:Dextromethorphan / Q000494:pharmacology*; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
D003915:Dextromethorphan