Presynaptic actions of adenosine are magnesium-dependent.

Reducing the extracellular magnesium concentration of medium bathing a rat hippocampal slice preparation greatly reduced the ability of adenosine to inhibit the synaptically evoked population potential. This loss of potency does not appear to be mediated by increased NMDA receptor activity or increased calcium influx. The results suggest that magnesium is required at the A1 adenosine receptor for its interaction with adenosine.