Contactin Associates with Na+ Channels and Increases Their Functional Expression
- Katie Kazarinova-Noyes1,
- Jyoti Dhar Malhotra2,
- Dyke P. McEwen2,
- Laura N. Mattei2,
- Erik O. Berglund3,
- Barbara Ranscht3,
- S. Rock Levinson4,
- Melitta Schachner5,
- Peter Shrager1,
- Lori L. Isom2, and
- Zhi-Cheng Xiao1
- 1Departments of Neurobiology/Anatomy and Biochemistry/Biophysics, University of Rochester Medical Center, Rochester, New York 14642,
- 2Department of Pharmacology, University of Michigan, Ann Arbor, Michigan 48109-0632,
- 3Neuroscience Program, The Burnham Institute, La Jolla, California 92037,
- 4Department of Physiology, University of Colorado Health Sciences Center, Denver, Colorado 80262, and
- 5Zentrum fuer Molekulare Neurobiologie, Universitat Hamburg, D-20246 Hamburg, Germany
Abstract
Contactin (also known as F3, F11) is a surface glycoprotein that has significant homology with the β2 subunit of voltage-gated Na+ channels. Contactin and Na+channels can be reciprocally coimmunoprecipitated from brain homogenates, indicating association within a complex. Cells cotransfected with Na+ channel Nav1.2α and β1 subunits and contactin have threefold to fourfold higher peak Na+ currents than cells with Nav1.2α alone, Nav1.2/β1, Nav1.2/contactin, or Nav1.2/β1/β2. These cells also have a correspondingly higher saxitoxin binding, suggesting an increased Na+ channel surface membrane density. Coimmunoprecipitation of different subunits from cell lines shows that contactin interacts specifically with the β1 subunit. In the PNS, immunocytochemical studies show a transient colocalization of contactin and Na+ channels at new nodes of Ranvier forming during remyelination. In the CNS, there is a particularly high level of colocalization of Na+ channels and contactin at nodes both during development and in the adult. Contactin may thus significantly influence the functional expression and distribution of Na+ channels in neurons.
- Received May 24, 2001.
- Revision received June 29, 2001.
- Accepted July 6, 2001.
- Copyright © 2001 Society for Neuroscience





