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Regulation of Thalamic and Cortical Network Synchrony by Scn8a.

Neuron | Mar 8, 2017

Voltage-gated sodium channel (VGSC) mutations cause severe epilepsies marked by intermittent, pathological hypersynchronous brain states. Here we present two mechanisms that help to explain how mutations in one VGSC gene, Scn8a, contribute to two distinct seizure phenotypes: (1) hypoexcitation of cortical circuits leading to convulsive seizure resistance, and (2) hyperexcitation of thalamocortical circuits leading to non-convulsive absence epilepsy. We found that loss of Scn8a leads to altered RT cell intrinsic excitability and a failure in recurrent RT synaptic inhibition. We propose that these deficits cooperate to enhance thalamocortical network synchrony and generate pathological oscillations. To our knowledge, this finding is the first clear demonstration of a pathological state tied to disruption of the RT-RT synapse. Our observation that loss of a single gene in the thalamus of an adult wild-type animal is sufficient to cause spike-wave discharges is striking and represents an example of absence epilepsy of thalamic origin.

Pubmed ID: 28238546 RIS Download

Mesh terms: Animals | Disease Models, Animal | Electroencephalography | Epilepsy, Absence | Mice | NAV1.6 Voltage-Gated Sodium Channel | Nerve Net | Phenotype | Seizures | Synapses | Thalamus

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Data used in this publication

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Associated grants

  • Agency: NINDS NIH HHS, Id: R01 NS034774
  • Agency: NINDS NIH HHS, Id: R01 NS072221
  • Agency: NINDS NIH HHS, Id: R01 NS048336
  • Agency: NINDS NIH HHS, Id: T32 NS007280
  • Agency: NINDS NIH HHS, Id: R01 NS065187
  • Agency: NINDS NIH HHS, Id: R01 NS090911

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