Adenosine influences the high-affinity uptake of transmitter glutamate and aspartate under conditions of hepatic encephalopathy.

The high-affinity uptake of transmitter glutamate and aspartate in hippocampal slices incubated in sera from patients with hepatic encephalopathy was dramatically reduced in neuropil areas by more than 50% compared with the control level. Adenosine compensates for these reduction in reuptake capacity in a concentration-dependent fashion reaching normal values at 500 microM adenosine. The renormalization of glutamate and aspartate uptake caused by adenosine might reasonably be expected to have potential therapeutic implications for the treatment of hepatic encephalopathy.