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Perineuronal nets decrease membrane capacitance of peritumoral fast spiking interneurons in a model of epilepsy.

Bhanu P Tewari1, Lata Chaunsali1, Susan L Campbell1,2

  • 1Glial Biology in Health, Disease, and Cancer Center, Virginia Tech Carilion Research Institute, 2 Riverside Cir., Roanoke, VA, 24016, USA.

Nature Communications
|November 11, 2018
PubMed
Summary
This summary is machine-generated.

Brain tumors cause seizures by damaging fast spiking interneurons (FSNs). This damage, caused by perineuronal nets (PNNs) degrading, impairs GABAergic inhibition, leading to epilepsy.

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Area of Science:

  • Neuroscience
  • Epileptology
  • Oncology

Background:

  • Epileptic seizures are a common symptom in brain tumor patients.
  • The underlying mechanisms of tumor-associated epilepsy are not fully understood.

Purpose of the Study:

  • To elucidate the role of GABAergic inhibition and interneuron function in tumor-associated seizures.
  • To investigate the contribution of perineuronal nets (PNNs) to interneuron dysfunction in the context of brain tumors.

Main Methods:

  • Analysis of peritumoral tissue from brain tumor patients.
  • Electrophysiological recordings from fast spiking interneurons (FSNs).
  • Assessment of perineuronal net (PNN) integrity and composition.

Main Results:

  • Tumor-associated epilepsy is linked to impaired GABAergic inhibition due to loss and dysfunction of peritumoral fast spiking interneurons (FSNs).
  • Degradation of perineuronal nets (PNNs) surrounding FSNs reduces their firing rate by increasing membrane capacitance.
  • Tumor-derived proteolytic enzymes are responsible for PNN degradation, leading to decreased GABA release and hyperexcitability.

Conclusions:

  • Perineuronal nets (PNNs) act as crucial electrostatic insulators for FSNs, enabling high firing rates necessary for proper inhibition.
  • PNN disruption by tumor proteases contributes to the excitation-inhibition imbalance seen in tumor-associated epilepsy.
  • Targeting PNN degradation may offer a novel therapeutic strategy for epilepsy.