Research article summary (published 30 May 2009):

Disruption of laminin in the peripheral nervous system impedes nonmyelinating Schwann cell development and impairs nociceptive sensory function.

Full Abstract

The mechanisms controlling the differentiation of immature Schwann cells (SCs) into nonmyelinating SCs is not known. Laminins are extracellular matrix proteins critical for myelinating SC differentiation, but their roles in nonmyelinating SC development have not been established. Here, we show that the peripheral nerves of mutant mice with laminin-deficient SCs do not form Remak bundles, which consist of a single nonmyelinating SC interacting with multiple unmyelinated axons. These mutant nerves show aberrant L1 and neural cell adhesion molecule (N-CAM) expression pattern during development. The homophilic and heterophilic interactions of N-CAM are also impaired in the mutant nerves. Other molecular markers for nonmyelinating SCs, including Egr-1, glial fibrillary acidic protein, and AN2/NG2, are all absent in adult mutant nerves. Analysis of expression of SC lineage markers demonstrates that nonmyelinating SCs do not develop in mutant nerves. Additionally, mutant mice are insensitive to heat stimuli and show a decreased number of C-fiber sensory neurons, indicating reduced nociceptive sensory function. These results show that laminin participates in nonmyelinating SC development and Remak bundle formation and suggest a possible role for laminin deficiency in peripheral sensory neuropathies. (c) 2008 Wiley-Liss, Inc.

Author information

Author/s: Yu, Wei-Ming (WM); Yu, Huaxu (H); Chen, Zu-Lin (ZL); Strickland, Sidney (S);

Affiliation: Laboratory of Neurobiology and Genetics, The Rockefeller University, New York, NY, USA.

Grants: NS 035704 (Agency:NINDS NIH HHS) ; NS 038472 (Agency:NINDS NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

Journal: Glia (Glia), published in United States. (Language: eng)

Reference: 2009-Jun; vol 57 (issue 8) : pp 850-9

Dates: Created 2009/04/16; Completed 2009/07/09;

PMID: 19053061, status: MEDLINE (last retrieval date: 7/24/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals Antigens - metabolism Calcitonin Gene-Related Peptide - metabolism Gene Expression Regulation - genetics Glial Fibrillary Acidic Protein - metabolism Laminin - genetics; metabolism Mice Mice, Transgenic Microscopy, Immunoelectron - methods N-Ethylmaleimide-Sensitive Proteins - genetics; metabolism

N-Ethylmaleimide-Sensitive Proteins - genetics; metabolism Nerve Fibers, Unmyelinated - physiology; ultrastructure Neural Cell Adhesion Molecules - genetics; metabolism Octamer Transcription Factor-6 - metabolism Peripheral Nervous System - cytology; metabolism Proteoglycans - metabolism Receptors, Purinergic P2 - metabolism Schwann Cells - physiology; ultrastructure Sensory Receptor Cells - metabolism; ultrastructure Somatosensory Disorders - genetics; physiopathology

Associated Chemicals: Antigens (0) ; Glial Fibrillary Acidic Protein (0) ; Laminin (0) ; Neural Cell Adhesion Molecules (0) ; Proteoglycans (0) ; Receptors, Purinergic P2 (0) ; chondroitin sulfate proteoglycan 4 (0) ; laminin gamma 1 (0) ; purinoceptor P2X3 (0) ; Octamer Transcription Factor-6 (132052-52-9) ; Calcitonin Gene-Related Peptide (83652-28-2) ; N-Ethylmaleimide-Sensitive Proteins (EC 3.6.4.6)

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