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Conditional deletion of TrkC does not modify limbic epileptogenesis.


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.

SUBMITTER: Soren Leonard A 

PROVIDER: S-EPMC3489989 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature

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Conditional deletion of TrkC does not modify limbic epileptogenesis.

Soren Leonard A A   Puranam Ram S RS   Helgager Jeffrey J   Liu Gumei G   McNamara James O JO  

Epilepsy research 20120912 1-2


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 wi  ...[more]

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