Interactions of the anticonvulsants diphenylhydantoin and carbamazepine with adenosine on cerebral cortical neurons.
Diphenylhydantoin, administered either by iontophoresis from a multibarreled pipette or intraperitoneally, prolonged the duration of adenosine-evoked depressions of the spontaneous firing of rat cerebral cortical neurons. In larger amounts, iontophoretically applied diphenylhydantoin depressed the firing of cortical neurons. The depressant actions of both adenosine and diphenylhydantoin were antagonized by caffeine (20 mg/kg). These results support a previous suggestion that diphenylhydantoin may exert its central effects by inhibiting adenosine uptake, thus potentiating the levels of extracellular adenosine. Carbamazepine failed to potentiate the actions of iontophoretically applied adenosine on cerebral cortical neurons, and at higher doses it reduced the duration of adenosine-elicited depressions. This finding is consistent with suggestions that carbamazepine may act as an antagonist at adenosine receptors.
D000241:Adenosine / Q000378:metabolism*; D000818:Animals; D000927:Anticonvulsants / Q000378:metabolism / Q000494:pharmacology; D002220:Carbamazepine / Q000378:metabolism / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D010672:Phenytoin / Q000378:metabolism / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
D000927:Anticonvulsants; D002220:Carbamazepine; D010672:Phenytoin; D000241:Adenosine