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

Journal of Neuroscience - Tập 19 Số 11 - Trang 4245-4262 - 1999
Philipp Weber1, Udo Bartsch1,2, Matthew N. Rasband3, R Czaniera4, Yolande Lang5, Horst Bluethmann5, Richard U. Margolis6, S. Rock Levinson7, Peter Shrager3, Dirk Montag1, Melitta Schachner4
1Department of Neurobiology, Swiss Federal Institute of Technology, Hönggerberg, CH 8093 Zürich, Switzerland
2Zentrum für Molekulare Neurobiologie, Universität Hamburg, D 20246 Hamburg, Germany,
3Department of Neurobiology and Anatomy, University of Rochester Medical Center, Rochester, New York 14642
4Zentrum für Molekulare Neurobiologie, Universität Hamburg, D-20246 Hamburg, Germany
5Department Roche Genetics, F. Hoffmann-LaRoche, CH 4070 Basel, Switzerland,
6Department of Pharmacology, New York University Medical Center, New York, New York 10016, and
7Department of Physiology, University of Colorado Medical School, Denver, Colorado 80262

Tóm tắt

Tenascin-R (TN-R), an extracellular matrix glycoprotein of the CNS, localizes to nodes of Ranvier and perineuronal nets and interactsin vitrowith other extracellular matrix components and recognition molecules of the immunoglobulin superfamily. To characterize the functional roles of TN-Rin 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 β2 subunit. The distribution of carbohydrate epitopes of perineuronal nets recognized by the lectinWisteria floribundaor 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.

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Journal of Neuroscience

Tập 19 Số 11

4245-4262

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