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The Journal of Neuroscience, June 1, 1999, 19(11):4245-4262

Mice Deficient for Tenascin-R Display Alterations of the Extracellular Matrix and Decreased Axonal Conduction Velocities in the CNS

Philipp Weber¹, Udo Bartsch^{1, 3}, Matthew N. Rasband², Reiner Czaniera³, Yolande Lang⁴, Horst Bluethmann⁴, Richard U. Margolis⁵, S. Rock Levinson⁶, Peter Shrager², Dirk Montag¹, and Melitta Schachner³

¹ Department of Neurobiology, Swiss Federal Institute of Technology, Hönggerberg, CH 8093 Zürich, Switzerland, ² Department of Neurobiology and Anatomy, University of Rochester Medical Center, Rochester, New York 14642, ³ Zentrum für Molekulare Neurobiologie, Universität Hamburg, D 20246 Hamburg, Germany, ⁴ Department Roche Genetics, F. Hoffmann-LaRoche, CH 4070 Basel, Switzerland, ⁵ Department of Pharmacology, New York University Medical Center, New York, New York 10016, and ⁶ Department of Physiology, University of Colorado Medical School, Denver, Colorado 80262

Tenascin-R (TN-R), an extracellular matrix glycoprotein of the CNS, localizes to nodes of Ranvier and perineuronal nets and interacts in vitro with other extracellular matrix components and recognition molecules of the immunoglobulin superfamily. To characterize the functional roles of TN-R in vivo, we have generated mice deficient for TN-R by homologous recombination using embryonic stem cells. TN-R-deficient mice are viable and fertile. The anatomy of all major brain areas and the formation and structure of myelin appear normal. However, immunostaining for the chondroitin sulfate proteoglycan phosphacan, a high-affinity ligand for TN-R, is weak and diffuse in the mutant when compared with wild-type mice. Compound action potential recordings from optic nerves of mutant mice show a significant decrease in conduction velocity as compared with controls. However, at nodes of Ranvier there is no apparent change in expression and distribution of Na⁺ channels, which are thought to bind to TN-R via their 2 subunit. The distribution of carbohydrate epitopes of perineuronal nets recognized by the lectin Wisteria floribunda or antibodies to the HNK-1 carbohydrate on somata and dendrites of cortical and hippocampal interneurons is abnormal. These observations indicate an essential role for TN-R in the formation of perineuronal nets and in normal conduction velocity of optic nerve.

Key words: extracellular matrix glycoprotein; HNK-1 carbohydrate; inhibitory interneurons; knock-out mutation; node of Ranvier; parvalbumin; phosphacan; sodium channel

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Copyright © 1999 Society for Neuroscience  0270-6474/99/19114245-18$05.00/0

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