Loading

Commentary Open Access
Volume 2 | Issue 2 | DOI: https://doi.org/10.46439/Neuroscience.2.013

Oligodendrocyte regulation of synaptogenesis may contribute to epilepsy development both in multiple sclerosis and polymicrogyria

  • 1Postgraduate Program in Biosciences and Biotechnology, North Fluminense State University Darcy Ribeiro, Campos, Brazil
  • 2Institute of Biodiversity and Sustainability NUPEM, The Federal University of Rio de Janeiro, Campus Macaé, Brazil
  • 3Faculty of Medicine, Department of Pathological Anatomy, The Federal University of Rio de Janeiro, Brazil
+ Affiliations - Affiliations

Corresponding Author

Sheila Espírito Santo Araújo, espiritosanto.sheila@uenf.br, Henrique Rocha Mendonca,  hrmendonca@macae.ufrj.br

Received Date: July 27, 2021

Accepted Date: August 25, 2021

Abstract

CNS myelination is a well-known biological phenomenon related to increase in action potential conduction speed and synaptic integration. Demyelination or abnormal myelination has been related to seizures and epilepsy either in patients or animal models. Although its role in fastening action potential propagation has been confirmed, few additional biological functions of CNS myelin has been described. Among these, myelin proteins such as NogoA were demonstrated to block axon elongation and synaptic potentiation. In light of our novel data on NogoA role in synaptogenesis, we propose a mechanism by which CNS myelin might regulate epileptogenesis both in multiple sclerosis and polymicrogyria.

Author Information X