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• W1910362049 startingPage "7069" @default.
• W1910362049 abstract "Topiramate is a widely used antiepileptic agent whose mechanism of action is poorly understood. The drug has been reported to interact with various ion channel types, including AMPA/kainate receptors. In whole-cell voltage-clamp recordings from principal neurons of the rat basolateral amygdala, topiramate at low concentrations (IC50, approximately 0.5 microm) selectively inhibited pharmacologically isolated excitatory synaptic currents mediated by kainate receptors containing the GluR5 subunit. Topiramate also partially depressed predominantly AMPA-receptor-mediated EPSCs, but with lower efficacy. Topiramate did not alter the degree of facilitation in paired-pulse experiments, and it reduced the amplitude of miniature EPSCs without affecting their frequency, demonstrating that the block of synaptic responses occurs postsynaptically. Inhibition of GluR5 kainate receptors could represent a key mechanism underlying the anticonvulsant activity of topiramate. Moreover, these results support the concept that GluR5 kainate receptors represent a novel target for antiepileptic drug development." @default.
• W1910362049 created "2016-06-24" @default.
• W1910362049 creator A5004551722 @default.
• W1910362049 creator A5018569584 @default.
• W1910362049 date "2003-08-06" @default.
• W1910362049 modified "2023-10-13" @default.
• W1910362049 title "Selective Antagonism of GluR5 Kainate-Receptor-Mediated Synaptic Currents by Topiramate in Rat Basolateral Amygdala Neurons" @default.
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• W1910362049 doi "https://doi.org/10.1523/jneurosci.23-18-07069.2003" @default.
• W1910362049 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6740668" @default.
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