SeminarPast EventNeuroscience

Targeting aberrant dendritic integration to treat cognitive comorbidities of epilepsy

Schedule
Wednesday, November 18, 2020
16:00 UTC
Heinz Beck

Prof

Institute for Experimental Epileptology and Cognition

Host: Clinical and Experimental Epilepsy

Event Information

Host

Clinical and Experimental Epilepsy

Duration

70 minutes

Abstract

Memory deficits are a debilitating symptom of epilepsy, but little is known about mechanisms underlying cognitive deficits. Here, we describe a Na+ channel-dependent mechanism underlying altered hippocampal dendritic integration, degraded place coding, and deficits in spatial memory. Two-photon glutamate uncaging experiments revealed that the mechanisms constraining the generation of Na+ spikes in hippocampal 1st order pyramidal cell dendrites are profoundly degraded in experimental epilepsy. This phenomenon was reversed by selectively blocking Nav1.3 sodium channels. In-vivo two-photon imaging revealed that hippocampal spatial representations were less precise in epileptic mice. Blocking Nav1.3 channels significantly improved the precision of spatial coding, and reversed hippocampal memory deficits. Thus, a dendritic channelopathy may underlie cognitive deficits in epilepsy and targeting it pharmacologically may constitute a new avenue to enhance cognition.

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