Linked Life Data

12831873

Source:http://linkedlifedata.com/resource/pubmed/id/12831873

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-6-30
pubmed:abstractText
Traumatic brain injury (TBI) initiates immediate and secondary neuropathological cascades that can result in persistent neurological dysfunction. Previous studies from our laboratory have shown that experimental rat brain injury causes a rapid and persistent decrease in CNS alpha7* nicotinic cholinergic receptor (nAChr) expression. The purpose of this study was to investigate whether intermittent nicotine injections could improve cognitive performance in the Morris water maze (MWM) following experimental brain injury. Adult male rats were anesthetized and subjected to a 1.5 mm controlled cortical impact (CCI) injury of the somatosensory cortex. Animals received twice daily i.p. nicotine injections for 11 days prior to CCI, 11 days following CCI or during both pre- and post-surgical intervals. MWM training was initiated 12 days post-injury. In the training phase of cognitive testing, twice-daily nicotine treatment following injury attenuated trauma-induced deficits in the distance traveled to reach the escape platform. This group of animals also had improvements in several measures of the probe test, including time spent, distance traveled and total entries into the target quadrant. TBI caused significant deficits in alpha7* nAChr expression in several regions of the hippocampus and cerebral cortex, which were largely unaffected by intermittent nicotine treatment. However, nicotine treatment up-regulated [(3)H]-epibatidine binding to non-alpha7* nAChrs, attenuating TBI-induced deficits in receptor expression in several brain regions evaluated. These results suggest that nicotine is efficacious at attenuating CCI-induced cognitive deficits in a manner independent of changes in alpha7* nAChr expression, perhaps via up-regulation of non-alpha7* nAChrs.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
119
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1199-208
pubmed:dateRevised
2010-6-4
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Chronic intermittent nicotine administration attenuates traumatic brain injury-induced cognitive dysfunction.
pubmed:affiliation
Division of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY 40536-0082, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.