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Journal of Neuroscience, Vol 15, 5263-5274, Copyright © 1995 by Society for Neuroscience
Peripheral benzodiazepine receptors are colocalized with activated microglia following transient global forebrain ischemia in the rat
DT Stephenson, DA Schober, EB Smalstig, RE Mincy, DR Gehlert and JA Clemens
Eli Lilly and Company, CNS Division, Lilly Research Laboratories, Indianapolis, Indiana 46285, USA.
In mammalian brain the expression of peripheral benzodiazepine receptors
(PBRs) can be markedly induced following different types of neuronal
injury. PBRs are believed to be expressed on non-neuronal cells in the
brain, yet the specific cell type that expresses these receptors following
CNS insult has not been defined. In the present study, we investigated the
effects of transient global forebrain ischemia on PBRs by autoradiographic
localization of 3H-PK11195 binding. The distribution of PBRs was compared
to glial fibrillary acidic protein (GFAP) as a marker for astrocytes and
OX42 as a marker for microglia. Five to 6 d following four-vessel occlusion
(4-VO), an increase in PBRs was seen in the CA1 region of all 15 brains
examined. In brains from rats subjected to 4-VO, microglia were selectively
activated in stratum pyramidale of the CA1 layer. In contrast, astrocytes
appeared to be activated in multiple hippocampal cell layers including
stratum radiatum and stratum oriens. Activated astrocytes were also found
in regions that did not exhibit increased 3H-PK11195 binding. In some
brains, selected regions of secondary lesion, specifically necrotic
thalamic nuclei and the isocortex were found to be strongly immunoreactive
for OX42 but lacked GFAP immunoreactive cells. In adjacent sections, these
same regions displayed high densities of 3H-PK1195 binding. These
observations lend further support to the application of 3H-PK11195 binding
as a marker of neuronal injury in the brain. Furthermore, the data strongly
suggest that activated microglia rather than astrocytes express PBRs
following ischemic insults.
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