Dexmedetomidine improves excessive extracellular glutamate-induced synaptic depression (BRAINRES-D-21-00941)

[Display omitted] •Excessive glutamate depresses glutamatergic excitatory synaptic transmissions.•The depression is mainly mediated by NMDA receptors.•The depressed transmissions are improved by α2-adrenoceptor stimulation.•Dexmedetomidine, α2-agonist and a sedative, improves glutamate-excitotoxicity.•β1-agonistic action deteriorates glutamate-excitotoxicity. We investigated the effects of dexmedetomidine, a selective α2-adrenergic agonist and a sedative, on excessive glutamate-induced depressions of central excitatory synaptic transmissions in vitro. From the CA1 in rat hippocampal slices, orthodromically elicited population spikes (PSs) and field excitatory postsynaptic potentials (fEPSPs) at 0.1 Hz were simultaneously recorded. ANOVA was used for statistics, and p