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“ The synaptic effects of novel antiepileptic drugs in the dentate gyrus ”

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June 22, 2010 10:30 - 10:30


Temporal lobe epilepsy is the most common epilepsy syndrome with medical refractory characteristics. It is caused by the imbalance between excitatory and inhibitory synaptic transmission in hippocampus which cause hyperexcitabilities of the neuronal circuits and recruit spontaneous recurrent seizures. Dentate gyrus (DG), the gate of hippocampus, filters high-frequency activities spreading from entorhinal cortex into hippocampus and plays a critical role in regulating the neuronal activities of hippocampus. During seizure propagation, most abnormal activities overcome the dentate gate and spread to the residual areas of the brain. It is considered that reducing the excitabilities in DG will be helpful to reduce seizure activities and clinically-used drugs possibly act on this area to exert their anticonvulsive effects. Our aim is to investigate whether antiepileptic drugs show effects on the synaptic transmission in DG since most studies on these drugs place emphasis on the io notropic effects while few on the synaptic ones. In our present study, we investigated the action of antiepileptic drugs on the glutamate transmission system in DG by whole-cell patch-clamp recording performed on acute brain slices. By testing several novel antiepileptic drugs, we found that (1) lamotrigine inhibited postsynaptic AMPA receptor and reduced glutamate release; (2) levetiracetam inhibited glutamate transmission through presynaptic P/Q-type Ca2+ channel; and (3) carisbamate reduced glutamate transmission possibly through presynaptic Na+ channels in the DG. These results not only propose the mechanisms to interpret why these drugs are “antiepileptic”, but also suggest that inhibiting the glutamate transmission in the DG is another potential way to treat epilepsy.

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BSI Private Event
Hokto Kazama