Abstract
In the CA1 region of rat hippocampal slices, the antiepileptic drug 2-phenyl-1,3-propanediol dicarbamate (felbamate; 100–1300 μM) concentration-dependently decreased extracellularly recorded synaptic potentials. The effect was significant at 200 μM, and became maximal at 700 μM felbamate, with a 70% decrease in population spike amplitude and 25% reduction of dendritic field excitatory postsynaptic potential (fEPSP) slope. Both α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl- d-aspartate (NMDA) receptor-mediated components of the fEPSP were decreased by 700 μM felbamate. Up to 300 μM felbamate did not affect long-term potentiation (LTP), whereas 500 μM decreased the magnitude of LTP. Higher concentrations of felbamate (700–1300 μM) blocked induction of somatic and dendritic LTP completely, but reversibly. It appears that the concentrations of felbamate which affect LTP are higher than those needed for its antiepileptic action.
Published Version
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