Up-regulation of the peripheral-type benzodiazepine receptor expression and [H-3]PK11195 binding in gerbil hippocampus after transient forebrain ischemia

In mammalian CNS, the peripheral-type benzodiazepine receptor (PTBR) is loc alized on the outer mitochondrial membrane within the astrocytes and microg lia. The main function of PTBR is to transport cholesterol across the mitoc hondrial membrane to the site of neurosteroid biosynthesis. The present stu dy evaluated the changes in the PTBR density, gene expression and immunorea ctivity in gerbil hippocampus as a function of reperfusion time after trans ient forebrain ischemia, Between 3 to 7 days of reperfusion, there was a si gnificant increase in the maximal binding site density (B-max) of the PTBR antagonist [H-3]PK11195 (by 94-156%; P < 0.01) and PTBR mRNA levels (by 1.8 - to 2.9-fold; P < 0.01). At 7 days of reperfusion, in the hippocampal CA1 (the brain region manifesting selective neuronal death), PTBR immunoreactiv ity increased significantly. Increased PTBR expression after transient fore brain ischemia may lead to increased neurosteroid biosynthesis, and thus ma y play a role in the ischemic pathophysiology, (C) 2001 Wiley-Liss, Inc.