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INHIBITION OF AMINO ACID TRANSMITTER RELEASE FROM RAT BRAIN SLICES BY PHENYTOIN AND RELATED ANTICONVULSANTS
Author(s) -
Skerritt John H.,
Johnston Graham A. R.
Publication year - 1983
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1983.tb00221.x
Subject(s) - phenytoin , anticonvulsant , pharmacology , chemistry , epilepsy , medicine , neuroscience , biology
SUMMARY 1. The in vitro effects of the major non‐benzodiazepine anticonvulsants were studied upon potassium‐stimulated release of radiolabelled GABA and D‐aspartate from minislices of rat cerebral cortex. 2. At 100 μmol/1, some anticonvulsants effective in grand mal seizures (phenytoin, phenobarbitone, mephobarbitone and beclamide) selectively inhibited K + ‐evoked release of the excitant amino acid D‐aspartate, consistent with an anticonvulsant action. 3. In contrast, several other anticonvulsants, namely ethosuximide, methsuximide, carbamazepine, sulthiame and dipropylacetate failed to alter potassium‐evoked release of either amino acid. 4. The ionic basis of phenytoin action on release was further studied; interactions with both neuronal calcium and sodium ion channels appear necessary for the drug's inhibitory action.