Skip to main content

Immunohistochemical evidence of seizure-induced activation of trkB receptors in the mossy fiber pathway of adult mouse hippocampus.

Publication ,  Journal Article
He, X-P; Minichiello, L; Klein, R; McNamara, JO
Published in: J Neurosci
September 1, 2002

Genetic and pharmacological perturbations suggest that tyrosine receptor kinase B (trkB) receptor activation promotes limbic epileptogenesis, but whether or where trkB activation occurs during epileptogenesis is uncertain. Because activation of trk receptors involves phosphorylation of specific tyrosine residues (Segal et al., 1996), the availability of antibodies that selectively recognize the phosphorylated form of trk receptors at the Shc site permits an immunohistochemical assessment of trk receptor activation. We reported previously increased phospho-specific trk (p-trk) immunoreactivity in the mossy fiber pathway of the hippocampus during epileptogenesis in rats (Binder et al., 1999b). Because the p-trk antibody does not distinguish among trkA, trkB, and trkC, the identity of the neurotrophin receptor(s) undergoing phosphorylation was uncertain. The development of mice carrying a point mutation of the Shc binding site (Y515F) in the trkB gene (trkB(shc)) provided an opportunity to test the hypothesis that trkB is the neurotrophin receptor undergoing phosphorylation. Epileptogenesis in wild-type (WT) mice was associated with increased p-trk immunoreactivity in both the mossy fiber pathway and CA3 stratum oriens of hippocampus. In contrast, the epileptogenesis-associated increase of p-trk immunoreactivity was reduced in trkB(shc) mutant mice. The development of epileptogenesis as measured by electrophysiological and behavioral indices did not differ between trkB(shc) mutant and WT mice. These data demonstrate that the neurotrophin receptor trkB undergoes phosphorylation in the mossy fiber pathway and CA3 stratum oriens of the hippocampus during limbic epileptogenesis. In addition, the signaling pathways activated by the Shc site of trkB exert no detectable regulatory effects on limbic epileptogenesis.

Duke Scholars

Altmetric Attention Stats
Dimensions Citation Stats

Published In

J Neurosci

DOI

EISSN

1529-2401

Publication Date

September 1, 2002

Volume

22

Issue

17

Start / End Page

7502 / 7508

Location

United States

Related Subject Headings

  • Signal Transduction
  • Seizures
  • Receptor, trkB
  • Phosphorylation
  • Neurology & Neurosurgery
  • Mutagenesis, Site-Directed
  • Mossy Fibers, Hippocampal
  • Mice, Mutant Strains
  • Mice
  • Kindling, Neurologic
 

Citation

APA
Chicago
ICMJE
MLA
NLM
He, X.-P., Minichiello, L., Klein, R., & McNamara, J. O. (2002). Immunohistochemical evidence of seizure-induced activation of trkB receptors in the mossy fiber pathway of adult mouse hippocampus. J Neurosci, 22(17), 7502–7508. https://doi.org/10.1523/JNEUROSCI.22-17-07502.2002
He, Xiao-Ping, Liliana Minichiello, Rüdiger Klein, and James O. McNamara. “Immunohistochemical evidence of seizure-induced activation of trkB receptors in the mossy fiber pathway of adult mouse hippocampus.J Neurosci 22, no. 17 (September 1, 2002): 7502–8. https://doi.org/10.1523/JNEUROSCI.22-17-07502.2002.
He, Xiao-Ping, et al. “Immunohistochemical evidence of seizure-induced activation of trkB receptors in the mossy fiber pathway of adult mouse hippocampus.J Neurosci, vol. 22, no. 17, Sept. 2002, pp. 7502–08. Pubmed, doi:10.1523/JNEUROSCI.22-17-07502.2002.
He X-P, Minichiello L, Klein R, McNamara JO. Immunohistochemical evidence of seizure-induced activation of trkB receptors in the mossy fiber pathway of adult mouse hippocampus. J Neurosci. 2002 Sep 1;22(17):7502–7508.

Published In

J Neurosci

DOI

EISSN

1529-2401

Publication Date

September 1, 2002

Volume

22

Issue

17

Start / End Page

7502 / 7508

Location

United States

Related Subject Headings

  • Signal Transduction
  • Seizures
  • Receptor, trkB
  • Phosphorylation
  • Neurology & Neurosurgery
  • Mutagenesis, Site-Directed
  • Mossy Fibers, Hippocampal
  • Mice, Mutant Strains
  • Mice
  • Kindling, Neurologic