The soft mechanical signature of glial scars in the central nervous system

Emad Moeendarbary (), Isabell P. Weber, Graham K. Sheridan, David E. Koser, Sara Soleman, Barbara Haenzi, Elizabeth J. Bradbury, James Fawcett and Kristian Franze ()
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Emad Moeendarbary: Development and Neuroscience, University of Cambridge
Isabell P. Weber: Development and Neuroscience, University of Cambridge
Graham K. Sheridan: Development and Neuroscience, University of Cambridge
David E. Koser: Development and Neuroscience, University of Cambridge
Sara Soleman: John van Geest Centre for Brain Repair, University of Cambridge, Robinson Way
Barbara Haenzi: John van Geest Centre for Brain Repair, University of Cambridge, Robinson Way
Elizabeth J. Bradbury: Wolfson Centre for Age-Related Diseases, King's College London
James Fawcett: John van Geest Centre for Brain Repair, University of Cambridge, Robinson Way
Kristian Franze: Development and Neuroscience, University of Cambridge

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: Abstract Injury to the central nervous system (CNS) alters the molecular and cellular composition of neural tissue and leads to glial scarring, which inhibits the regrowth of damaged axons. Mammalian glial scars supposedly form a chemical and mechanical barrier to neuronal regeneration. While tremendous effort has been devoted to identifying molecular characteristics of the scar, very little is known about its mechanical properties. Here we characterize spatiotemporal changes of the elastic stiffness of the injured rat neocortex and spinal cord at 1.5 and three weeks post-injury using atomic force microscopy. In contrast to scars in other mammalian tissues, CNS tissue significantly softens after injury. Expression levels of glial intermediate filaments (GFAP, vimentin) and extracellular matrix components (laminin, collagen IV) correlate with tissue softening. As tissue stiffness is a regulator of neuronal growth, our results may help to understand why mammalian neurons do not regenerate after injury.

Date: 2017
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DOI: 10.1038/ncomms14787

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