Conditional deletion of TrkC does not modify limbic epileptogenesis.

Journal Article (Journal Article)

The neurotrophin receptor, tropomyosin-related kinase B (TrkB), is required for epileptogenesis in the kindling model. The role of a closely related neurotrophin receptor, TrkC, in limbic epileptogenesis is unknown. We examined limbic epileptogenesis in the kindling model in TrkC conditional null mice, using a strategy that previously established a critical role of TrkB. Despite elimination of TrkC mRNA, no differences in development of kindling were detected between TrkC conditional null and wild type control mice. These findings reinforce the central role of TrkB as the principal neurotrophin receptor involved in limbic epileptogenesis.

Full Text

Duke Authors

Cited Authors

  • Soren Leonard, A; Puranam, RS; Helgager, J; Liu, G; McNamara, JO

Published Date

  • November 2012

Published In

Volume / Issue

  • 102 / 1-2

Start / End Page

  • 126 - 130

PubMed ID

  • 22980123

Pubmed Central ID

  • PMC3489989

Electronic International Standard Serial Number (EISSN)

  • 1872-6844

Digital Object Identifier (DOI)

  • 10.1016/j.eplepsyres.2012.07.019


  • eng

Conference Location

  • Netherlands