Effects of phenytoin on the amygdala neurons in vitro

Li Ling Cheng; Su Jane Wang; Jing Jane Tsai; Po Wu Geana

doi:10.1159/000139532

Effects of phenytoin on the amygdala neurons in vitro

Li Ling Cheng, Su Jane Wang, Jing Jane Tsai, Po Wu Geana

Department of Pharmacology

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

Abstract

The present study was aimed at elucidating the possible mechanisms underlying the anticonvulsant efficacy of phenytoin using intracellular recording techniques in the in vitro amygdalar slice preparation. Synaptic response mediated by the N-methyl-D-aspartate (NMDA) receptor (EPSPnmda) was isolated pharmacologically by application of a solution containing non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (10 μmol/l) and γ-aminobutyric acid_A receptor antagonist bicuculline (20 μmol/l). Phenytoin inhibits the amplitude of EPSPnmda without affecting the postsynaptic depolarization induced by exogenous application of NMDA. In addition, phenytoin increases the magnitude of paired-pulse facilitation which is consistent with a presynaptic mode of action. These results suggest that inhibition of transmitter release due to presynaptic blockade of Na⁺ and/or Ca²⁺ channels may account largely for the anticonvulsant efficacy of phenytoin.

Original language	English
Pages (from-to)	228-234
Number of pages	7
Journal	Pharmacology
Volume	55
Issue number	5
DOIs	https://doi.org/10.1159/000139532
Publication status	Published - 1997 Jan 1

All Science Journal Classification (ASJC) codes

Pharmacology

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title = "Effects of phenytoin on the amygdala neurons in vitro",

abstract = "The present study was aimed at elucidating the possible mechanisms underlying the anticonvulsant efficacy of phenytoin using intracellular recording techniques in the in vitro amygdalar slice preparation. Synaptic response mediated by the N-methyl-D-aspartate (NMDA) receptor (EPSPnmda) was isolated pharmacologically by application of a solution containing non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (10 μmol/l) and γ-aminobutyric acidA receptor antagonist bicuculline (20 μmol/l). Phenytoin inhibits the amplitude of EPSPnmda without affecting the postsynaptic depolarization induced by exogenous application of NMDA. In addition, phenytoin increases the magnitude of paired-pulse facilitation which is consistent with a presynaptic mode of action. These results suggest that inhibition of transmitter release due to presynaptic blockade of Na+ and/or Ca2+ channels may account largely for the anticonvulsant efficacy of phenytoin.",

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AU - Cheng, Li Ling

AU - Wang, Su Jane

AU - Tsai, Jing Jane

AU - Geana, Po Wu

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N2 - The present study was aimed at elucidating the possible mechanisms underlying the anticonvulsant efficacy of phenytoin using intracellular recording techniques in the in vitro amygdalar slice preparation. Synaptic response mediated by the N-methyl-D-aspartate (NMDA) receptor (EPSPnmda) was isolated pharmacologically by application of a solution containing non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (10 μmol/l) and γ-aminobutyric acidA receptor antagonist bicuculline (20 μmol/l). Phenytoin inhibits the amplitude of EPSPnmda without affecting the postsynaptic depolarization induced by exogenous application of NMDA. In addition, phenytoin increases the magnitude of paired-pulse facilitation which is consistent with a presynaptic mode of action. These results suggest that inhibition of transmitter release due to presynaptic blockade of Na+ and/or Ca2+ channels may account largely for the anticonvulsant efficacy of phenytoin.

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Effects of phenytoin on the amygdala neurons in vitro

Abstract

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