Mouse brain PSA-NCAM levels are altered by graded-controlled cortical impact injury.

Abstract:

:Traumatic brain injury (TBI) is a worldwide endemic that results in unacceptably high morbidity and mortality. Secondary injury processes following primary injury are composed of intricate interactions between assorted molecules that ultimately dictate the degree of longer-term neurological deficits. One comparatively unexplored molecule that may contribute to exacerbation of injury or enhancement of recovery is the posttranslationally modified polysialic acid form of neural cell adhesion molecule, PSA-NCAM. This molecule is a critical modulator of central nervous system plasticity and reorganization after injury. In this study, we used controlled cortical impact (CCI) to produce moderate or severe TBI in the mouse. Immunoblotting and immunohistochemical analysis were used to track the early (2, 24, and 48 hour) and late (1 and 3 week) time course and location of changes in the levels of PSA-NCAM after TBI. Variable and heterogeneous short- and long-term increases or decreases in expression were found. In general, alterations in PSA-NCAM levels were seen in the cerebral cortex immediately after injury, and these reductions persisted in brain regions distal to the primary injury site, especially after severe injury. This information provides a starting point to dissect the role of PSA-NCAM in TBI-related pathology and recovery.

journal_name

Neural Plast

journal_title

Neural plasticity

authors

Budinich CS,Chen H,Lowe D,Rosenberger JG,Bernstock JD,McCabe JT

doi

10.1155/2012/378307

subject

Has Abstract

pub_date

2012-01-01 00:00:00

pages

378307

eissn

2090-5904

issn

1687-5443

journal_volume

2012

pub_type

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