Associative somatodendritic interaction in layer V pyramidal neurons is not affected by the antiepileptic drug lamotrigine

The European Journal of Neuroscience
Thomas Berger, Hans-R Lüscher

Abstract

The antiepileptic drug lamotrigine was described to exert its effects on neuronal excitability via voltage-gated sodium and calcium, as well as hyperpolarization-activated conductances. In order to define the effects of lamotrigine on the excitability of layer V pyramidal cells of the rat somatosensory cortex we performed patch-clamp recordings from the soma and dendrite of this major cortical output cell type in acute slices. Voltage-clamp experiments revealed the blockade of the persistent sodium current by 50-100 micro m lamotrigine as well as by 50 micro m of the anticonvulsant drug phenytoin. In somatic current-clamp studies lamotrigine, in a therapeutic concentration range, depolarizes the membrane potential reflecting the activation of the hyperpolarization-activated current. This depolarization reduces the rheobase and increases the spiking frequency at the onset of the spike train. For long depolarizing current pulses under lamotrigine, however, a use-dependent block of sodium channels reduces spiking frequency and spike amplitude. The depolarization due to 50-100 micro m lamotrigine reduces additionally the critical frequency of back-propagating spikes necessary to elicit a dendritic calcium action potential. Ten to t...Continue Reading

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Citations

Jul 8, 2005·Psychopharmacology·Charles H LargeDonald C Goff
Feb 17, 2007·Epilepsy Currents·Carl E Stafstrom
Jun 3, 2008·Progress in Neuro-psychopharmacology & Biological Psychiatry·Mark J HuntStefan Kasicki

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