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Related Experiment Video

Updated: Apr 20, 2026

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Decrease of neocortical paired-pulse depression in GAERS and possible implication of gap junctions.

Sylvain Gigout1, Jacques Louvel1, René Pumain1

  • 1INSERM U1129 "Infantile Epilepsies and Brain Plasticity", Paris, France; University Paris Descartes, Sorbonne Paris Cité; CEA, Gif sur Yvette, France.

Neuroscience Letters
|December 3, 2014
PubMed
Summary
This summary is machine-generated.

Neocortical paired-pulse depression (PPD) is maintained in thalamocortical slices from epilepsy models, but is reduced in Genetic Absence Epilepsy Rats from Strasbourg (GAERS), suggesting altered NMDA receptor or gap junction function.

Keywords:
Absence epilepsyCarbenoxoloneGap junctionsPaired-pulse protocolQuinidineThalamocortical slices

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Area of Science:

  • Neuroscience
  • Epilepsy Research
  • Synaptic Transmission

Background:

  • Thalamocortical slices are crucial for studying thalamocortical interactions and absence epilepsy.
  • The maintenance and alterations of intracortical synaptic transmission, specifically paired-pulse depression (PPD), in epilepsy models remain unclear.
  • The role of gap junctions (GJs) in intracortical transmission, distinct from their role in epileptiform discharges, is largely unknown.

Purpose of the Study:

  • To determine if intracortical synaptic transmission and PPD are preserved in thalamocortical slices from Genetic Absence Epilepsy Rat from Strasbourg (GAERS) and non-epileptic rats (NER).
  • To investigate whether PPD is altered in GAERS, a genetic model of absence epilepsy.
  • To examine the effects of gap junction blockers on intracortical transmission.

Main Methods:

  • Electrophysiological recordings of intracortical connection efficacy and PPD in thalamocortical slices from GAERS and NER.
  • Application of N-methyl-D-aspartate (NMDA) receptor antagonist to assess its effect on PPD.
  • Administration of GJ blockers (carbenoxolone, quinidine) to coronal slices from Wistar rats to evaluate effects on intracortical responses and PPD.

Main Results:

  • Intracortical connection efficacy was not impaired in GAERS compared to NER.
  • Neocortical PPD was preserved in NER but significantly decreased in GAERS.
  • NMDA receptor blockade reduced PPD in NER but had no effect in GAERS; GJ blockers did not affect cortical responses to white matter stimulation but decreased PPD in Wistar rat slices.

Conclusions:

  • Neocortical PPD is maintained in thalamocortical slices and is altered in the GAERS model.
  • The decreased PPD in GAERS suggests a potential reduction in NMDA receptor function and/or astrocytic gap junction activity.
  • Gap junction blockers have differential effects on PPD, indicating a complex role in intracortical transmission.