Linked Life Data

10683277

Source:http://linkedlifedata.com/resource/pubmed/id/10683277

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-3-23
pubmed:abstractText
In mammalian CNS, the peripheral-type benzodiazepine receptor (PTBR) is localized on the outer mitochondrial membrane within the astrocytes and microglia. PTBR transports cholesterol to the site of neurosteroid biosynthesis. Several neurodegenerative disorders were reported to be associated with increased densities of PTBR. In the present study, we evaluated the changes in the PTBR density and gene expression in the brains of rats as a function of time (6 h to 14 days) after traumatic brain injury (TBI). Sham-operated rats served as control. Between 3 and 14 days after TBI, there was a significant increased in the binding of PTBR antagonist [(3)H]PK11195 (by 106 to 185%, P < 0.01, as assessed by quantitative autoradiography and in vitro filtration binding) and PTBR mRNA expression (by 2- to 3. 4-fold, P < 0.01, as assessed by RT-PCR) in the ipsilateral thalamus. At 14 days after the injury, the neuronal number decreased significantly (by 85 to 90%, P < 0.01) in the ipsilateral thalamus. At the same time point, the ipsilateral thalamus also showed increased numbers of the glial fibrillary acidic protein positive cells (astrocytes, by approximately 3.5-fold) and the ED-1 positive cells (microglia/macrophages, by approximately 36-fold), the two cell types known to be associated with PTBR. Increased PTBR expression following TBI seems to be associated with microglia/macrophages than astrocytes as PTBR density at different periods after TBI correlated better with the number of ED-1 positive cells (r(2) = 0.95) than the GFAP positive cells (r(2) = 0.56). TBI-induced increased PTBR expression is possibly an adaptive response to cellular injury and may play a role in the pathophysiology of TBI.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0014-4886
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Academic Press.
pubmed:issnType
Print
pubmed:volume
161
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
102-14
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10683277-Animals, pubmed-meshheading:10683277-Antineoplastic Agents, pubmed-meshheading:10683277-Astrocytes, pubmed-meshheading:10683277-Autoradiography, pubmed-meshheading:10683277-Biological Markers, pubmed-meshheading:10683277-Brain Injuries, pubmed-meshheading:10683277-Cell Death, pubmed-meshheading:10683277-Functional Laterality, pubmed-meshheading:10683277-Gene Expression, pubmed-meshheading:10683277-Glial Fibrillary Acidic Protein, pubmed-meshheading:10683277-Isoquinolines, pubmed-meshheading:10683277-Male, pubmed-meshheading:10683277-Microglia, pubmed-meshheading:10683277-Neurons, pubmed-meshheading:10683277-RNA, Messenger, pubmed-meshheading:10683277-Radioligand Assay, pubmed-meshheading:10683277-Rats, pubmed-meshheading:10683277-Rats, Sprague-Dawley, pubmed-meshheading:10683277-Receptors, GABA-A, pubmed-meshheading:10683277-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:10683277-Thalamus, pubmed-meshheading:10683277-Tritium, pubmed-meshheading:10683277-Up-Regulation
pubmed:year
2000
pubmed:articleTitle
Traumatic brain injury leads to increased expression of peripheral-type benzodiazepine receptors, neuronal death, and activation of astrocytes and microglia in rat thalamus.
pubmed:affiliation
Department of Neurological Surgery, University of Wisconsin-Madison, Madison, Wisconsin, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't