We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
from
Section B2
-
Determinants of regeneration in the injured nervous system
By
Jared H. Miller, Department of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, OH, USA,
Jerry Silver, Department of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, OH, USA
Edited by
Michael Selzer, University of Pennsylvania,Stephanie Clarke, Université de Lausanne, Switzerland,Leonardo Cohen, National Institute of Mental Health, Bethesda, Maryland,Pamela Duncan, University of Florida,Fred Gage, Salk Institute for Biological Studies, San Diego
This chapter discusses the environment of the glial scar, with particular focus on the role of chondroitin sulfate proteoglycans (CSPGs) in regeneration failure. Many injuries of the central nervous system (CNS) occur with an accompanying opening of the blood-brain barrier. Non-CNS molecules entering the brain parenchyma through the disrupted blood-brain barrier have significant effects on the immune system and subsequent development of the glial scar. It should be reiterated that following injury in the vicinity of blood-brain barrier extravasation, much of the glial scar forms without astrocyte proliferation, but rather with a switch to the reactive state followed by inhibitory extracellular matrix (ECM) production and then hypertrophy. The growth inhibitory and growth promoting molecules exist in a balance that favors stalled regeneration of axons, but it is important to reiterate that non-regenerating axons still need to be supported if they are to remain indefinitely in the vicinity of the lesion.
Recommend this
Email your librarian or administrator to recommend adding this to your organisation's collection.