Disruption of the neurotrophin-3 receptor gene trkC eliminates Ia muscle afferents and results in abnormal movements

Rüdiger Klein, Inmaculada Silos-Santiago, Richard J. Smeyne, Sergio A. Lira, Riccardo Brambilla, Sherri Bryant, Li Zhang, William D. Snider, Mariano Barbacid

Research output: Contribution to journalArticlepeer-review

Abstract

THE trkC gene is expressed throughout the mammalian nervous system and encodes a series of tyrosine protein kinase isoforms that serve as receptors for neurotrophin-3 (NT3), a member of the nerve growth factor (NGF) family of neurotrophic factors. One of these isoforms, gp145(trkC)/TrkC K1, mediates the trophic properties of NT3 in cultured cells. Here we show that homozygous mice defective for TrkC tyrosine protein kinase receptors lack Ia muscle afferent projections to spinal motor neurons and have fewer large myelinated axons in the dorsal root and posterior columns of the spinal cord. These mice display abnormal movements and postures, indicating that NT3/TrkC-dependent sensory neurons may play a primary role in proprioception, the sense of position and movement of the limbs.

Original languageEnglish
Pages (from-to)249-251
Number of pages3
JournalNature
Volume368
Issue number6468
DOIs
Publication statusPublished - Mar 17 1994

ASJC Scopus subject areas

  • General

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