Conditional deletion of TrkC does not modify limbic epileptogenesis

Epilepsy Res. 2012 Nov;102(1-2):126-30. doi: 10.1016/j.eplepsyres.2012.07.019. Epub 2012 Sep 12.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Disease Models, Animal
  • Epilepsy / genetics*
  • Epilepsy / physiopathology
  • Gene Deletion
  • Integrases / genetics
  • Kindling, Neurologic / genetics
  • Limbic System / physiopathology*
  • Membrane Glycoproteins / genetics*
  • Mice
  • Mice, Knockout
  • Protein-Tyrosine Kinases / genetics*
  • RNA, Messenger / genetics
  • Receptor, trkC / genetics*

Substances

  • Membrane Glycoproteins
  • RNA, Messenger
  • Ntrk2 protein, mouse
  • Protein-Tyrosine Kinases
  • Receptor, trkC
  • Cre recombinase
  • Integrases