Traumatic Brain Injury Leads to Increased Expression of Peripheral-Type Benzodiazepine Receptors, Neuronal Death, and Activation of Astrocytes and Microglia in Rat Thalamus

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 inc...

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Veröffentlicht in:Experimental neurology 2000-01, Vol.161 (1), p.102-114
Hauptverfasser: Raghavendra Rao, Vemuganti L., Dogan, Aclan, Bowen, Kellie K., Dempsey, Robert J.
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Sprache:eng
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Zusammenfassung: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 [3H]PK11195 (by 106 to 185%, P
ISSN:0014-4886
1090-2430
DOI:10.1006/exnr.1999.7269