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

Brain Res. 1993 Mar 26;606(2):351-6. doi: 10.1016/0006-8993(93)91007-f.

Abstract

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.

MeSH terms

  • 2-Chloroadenosine / pharmacology
  • 6-Cyano-7-nitroquinoxaline-2,3-dione
  • Acetylcholine / pharmacology
  • Adenosine / pharmacology*
  • Animals
  • Dose-Response Relationship, Drug
  • Electrophysiology
  • Hippocampus / drug effects
  • Hippocampus / physiology*
  • Magnesium / pharmacology
  • Male
  • Osmolar Concentration
  • Picrotoxin / pharmacology
  • Quinoxalines / pharmacology
  • Rats
  • Rats, Wistar
  • Receptors, N-Methyl-D-Aspartate / physiology*
  • Synapses / drug effects
  • Synapses / physiology*

Substances

  • Quinoxalines
  • Receptors, N-Methyl-D-Aspartate
  • Picrotoxin
  • 2-Chloroadenosine
  • 6-Cyano-7-nitroquinoxaline-2,3-dione
  • Magnesium
  • Adenosine
  • Acetylcholine