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The Journal of Neuroscience, June 1, 2003, 23(11):4509-4518
Previous Article | Next Article 
Kv3.1b Is a Novel Component of CNS Nodes
Jérôme Devaux,1,6
Gisèle Alcaraz,2
Judith Grinspan,3
Vann Bennett,4
Rolf Joho,5
Marcel Crest,6 and
Steven S. Scherer1
1 Department of Neurology, The University of Pennsylvania Medical Center,
Philadelphia, Pennsylvania 19104-6077,
2 Institut National de la Santé et de la Recherche Médicale
Unité 464, Institut Jean Roche, Faculté de Médecine Nord,
Université de la Méditerranée, 13916 Marseille Cedex 20,
France,
3 Division of Neurology Research, Children's Hospital of Philadelphia,
Philadelphia, Pennsylvania 19104-6077,
4 Howard Hughes Medical Institute and Departments of Biochemistry and Cell
Biology, Duke University Medical Center, Durham, North Carolina 27710,
5 Center for Basic Neuroscience, The University of Texas Southwestern Medical
Center, Dallas, Texas 75390-9111, and
6 Laboratoire Intégration des Informations Sensorielles, Centre National
de la Recherche Scientifique, 13402 Marseille Cedex 20, France
We herein demonstrate that Kv3.1b subunits are present at nodes of Ranvier
in the CNS of both rats and mice. Kv3.1b colocalizes with voltage-gated
Na+ channels in a subset of nodes in the spinal cord, particularly
those of large myelinated axons. Kv3.1b is abundantly expressed in the gray
matter of the spinal cord, but does not colocalize with Na+
channels in initial segments. In the PNS, few nodes are Kv3.1b-positive.
During the development of the CNS, Kv3.1b clustering at nodes occurs later
than that of Na+ channels, but precedes the juxtaparanodal
clustering of Kv1.2. Moreover, in myelin-deficient rats, which have severe CNS
dysmyelination, node-like clusters of Kv3.1b and Na+ channels are
observed even in regions devoid of oligodendrocytes. Ankyrin G
coimmunoprecipitates Kv3.1b in vivo, indicating that these two
proteins may interact in the CNS at nodes. 4-Aminopyridine, a K+
channel blocker, broadened the compound action potential recorded from adult
rat optic nerve and spinal cord, but not from the sciatic nerve. These effects
were also observed in Kv3.1-deficient mice. In conclusion, Kv3.1b is the first
K+ channel subunit to be identified in CNS nodes; but Kv3.1b does
not account for the effects of 4-aminopyridine on central myelinated
tracts.
Key words: Shaw; potassium channels; oligodendrocyte; Schwann cells; myelin; multiple sclerosis
Received Aug. 22, 2002;
revised Feb. 21, 2003;
accepted Mar. 12, 2003.
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