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

Abstract

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.

• Authors: J H Skerritt, G A Johnston
• Journal: Clinical and experimental pharmacology & physiology (Clin Exp Pharmacol Physiol) 1983 Sep-Oct Vol. 10 Issue 5 Pg. 527-33 ISSN: 0305-1870 [Print] Australia
• PMID: 6139193 (Publication Type: Journal Article)

Chemical References

• Anticonvulsants
• Neurotransmitter Agents
• Aspartic Acid
• gamma-Aminobutyric Acid
• Phenytoin
• Sodium
• Potassium
• Calcium

Topics

• Animals
• Anticonvulsants (pharmacology)
• Aspartic Acid (metabolism)
• Brain (drug effects, metabolism)
• Calcium (metabolism)
• In Vitro Techniques
• Male
• Neurotransmitter Agents (metabolism)
• Phenytoin (pharmacology)
• Potassium (pharmacology)
• Rats
• Sodium (metabolism)
• gamma-Aminobutyric Acid (metabolism)