Inhibition of amino acid transmitter release from rat brain slices by phenytoin and related anticonvulsants.

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. At 100 mumol/l, 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. In contrast, several other anticonvulsants, namely ethosuximide, methsuximide, carbamazepine, sulthiame and dipropylacetate failed to alter potassium-evoked release of either amino acid. 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.
AuthorsJ H Skerritt, G A Johnston
JournalClinical and experimental pharmacology & physiology (Clin Exp Pharmacol Physiol) 1983 Sep-Oct Vol. 10 Issue 5 Pg. 527-33 ISSN: 0305-1870 [Print] ENGLAND
PMID6139193 (Publication Type: Journal Article)
Chemical References
  • Anticonvulsants
  • Neurotransmitter Agents
  • Aspartic Acid
  • gamma-Aminobutyric Acid
  • Phenytoin
  • Sodium
  • Potassium
  • Calcium
  • Animals
  • Anticonvulsants (pharmacology)
  • Aspartic Acid (secretion)
  • Brain (drug effects, secretion)
  • Calcium (metabolism)
  • In Vitro Techniques
  • Male
  • Neurotransmitter Agents (secretion)
  • Phenytoin (pharmacology)
  • Potassium (pharmacology)
  • Rats
  • Sodium (metabolism)
  • gamma-Aminobutyric Acid (secretion)

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