Modulation of neuronal excitability by endogenous adenosine in the absence of synaptic transmission.

Rat hippocampal slices were superfused with low calcium, high magnesium medium. Reductions in flow rate were associated with a marked depression of antidromically elicited afterpotentials with little change in the initial antidromic population spike recorded from CA1 pyramidal neurons. The depression of the afterpotential at the lower flow rates was largely reversed by the adenosine antagonist, theophylline (100 microM), by adenosine deaminase (10 micrograms/ml) and was mimicked by the application of the adenosine reuptake blocker, dipyridamole (100 microM). Since synaptic transmission was blocked, it is concluded that sufficient endogenous adenosine exists in the absence of synaptic function to alter neuronal excitability.