Adenosine inhibits the NMDA receptor-mediated excitatory postsynaptic potential in the hippocampus.

The effect of the stable adenosine analogue 2-chloroadenosine (CADO) on the component of the field excitatory postsynaptic potential (fepsp) mediated by the N-methyl-D-aspartate (NMDA) type of glutamate receptor was studied in the hippocampal CA1 area of the rat. CADO inhibited the NMDA receptor-mediated component of the fepsp (EC50 = 0.10 +/- 0.02 microM), more efficiently than it inhibited the fepsp (EC50 = 0.40 +/- 0.08 microM). The results suggest that adenosine may modulate phenomena associated with the NMDA receptor, such as synaptic plasticity and excitotoxicity.