Electroshock seizures in mice: effect on brain adenosine and its metabolites.
Adenosine and its immediate metabolites, inosine and hypoxanthine, were measured in mouse brain following the induction of electroshock seizures and after a subconvulsive series of electric shocks. Electroshock seizures resulted in a marked and prolonged rise in inosine, with maximal values at 5 min. Hypoxanthine increased more slowly but reached high levels by 10 min. Adenosine was unchanged. Phenytoin and to a lesser extent phenobarbital reduced these effects. Following the subconvulsive stimulus, 15 single shocks over an interval of 5 sec, inosine increased rapidly, adenosine rose slightly, and hypoxanthine did not change. Both phenytoin and phenobarbital blocked these increases in adenosine and inosine. Early elevations in inosine may play some role in seizure generation and propagation. The high levels of inosine and hypoxanthine found after recovery may be involved in the termination of epileptic activity, possibly by interacting with the benzodiazepine receptor for which they are ligands.[1]References
- Electroshock seizures in mice: effect on brain adenosine and its metabolites. Lewin, E., Bleck, V. Epilepsia (1981) [Pubmed]
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