Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-11-24
pubmed:abstractText
Brain tissue inflammatory responses, including neuronal loss and gliosis at the neural electrode/tissue interface, limit the recording stability and longevity of neural probes. The neural adhesion molecule L1 specifically promotes neurite outgrowth and neuronal survival. In this study, we covalently immobilized L1 on the surface of silicon-based neural probes and compared the tissue response between L1 modified and non-modified probes implanted in the rat cortex after 1, 4, and 8 weeks. The effect of L1 on neuronal health and survival, and glial cell reactions were evaluated with immunohistochemistry and quantitative image analysis. Similar to previous findings, persistent glial activation and significant decreases of neuronal and axonal densities were found at the vicinity of the non-modified probes. In contrast, the immediate area (100 ?m) around the L1 modified probe showed no loss of neuronal bodies and a significantly increased axonal density relative to background. In this same region, immunohistochemistry analyses show a significantly lower activation of microglia and reaction of astrocytes around the L1 modified probes when compared to the control probes. These improvements in tissue reaction induced by the L1 coating are likely to lead to improved functionality of the implanted neural electrodes during chronic recordings.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1878-5905
pubmed:author
pubmed:copyrightInfo
Published by Elsevier Ltd.
pubmed:issnType
Electronic
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
681-92
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
The surface immobilization of the neural adhesion molecule L1 on neural probes and its effect on neuronal density and gliosis at the probe/tissue interface.
pubmed:affiliation
Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA 15261, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural