Journal
NEUROSCIENCE
Volume 141, Issue 1, Pages 515-520Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2006.03.020
Keywords
BDNF; NT3; seizures; neurotrophins; hippocampus; phosphorylation
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Funding
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P01NS017771, R01NS056217] Funding Source: NIH RePORTER
- NINDS NIH HHS [NS17771, R01 NS056217] Funding Source: Medline
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The kindling model of epilepsy is a form of neuronal plasticity induced by repeated induction of pathological activity in the form of focal seizures. A causal role for the neurotrophin receptor, tyrosine receptor kinase B, in epileptogenesis is supported by multiple studies of the kindling model. Not only is tyrosine receptor kinase B required for epileptogenesis in this model but enhanced activation of tyrosine receptor kinase B has been identified in the hippocampus in multiple models of limbic epileptogenesis. The neurotrophin ligand mediating tyrosine receptor kinase B activation during limbic epileptogenesis is unknown. We hypothesized that neurotrophin-4 (NT4) activates tyrosine receptor kinase B in the hippocampus during epileptogenesis and that NT4-mediated activation of tyrosine receptor kinase B promotes limbic epileptogenesis. We tested these hypotheses in NT4-deficient mice with a targeted deletion of NT4 gene using the kindling model. The development and persistence of amygdala kindling were examined in wild type (+/+) and NT4 null mutant (-/-) mice. No differences were found between +/+ and -/- mice with respect to any facet of the development or persistence of kindling. Despite the absence of NT4, activation of the tyrosine receptor kinase B receptor in the mossy fiber pathway as assessed by phospho-trk immunohistochernistry was equivalent to that of +/+ mice. Together these findings demonstrate that NT4 is not required for limbic epileptogenesis nor is it required for activation of tyrosine receptor kinase B in hippocampus during limbic epileptogenesis. (c) 2006 Published by Elsevier Ltd on behalf of IBRO.
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