Microglial and astrocytic reactions prior to onset of thalamic cell death after traumatic lesion of the rat sensorimotor cortex

Citation
Dm. Hermann et al., Microglial and astrocytic reactions prior to onset of thalamic cell death after traumatic lesion of the rat sensorimotor cortex, ACT NEUROP, 99(2), 2000, pp. 147-153
Citations number
27
Categorie Soggetti
Neurosciences & Behavoir
Journal title
ACTA NEUROPATHOLOGICA
ISSN journal
00016322 → ACNP
Volume
99
Issue
2
Year of publication
2000
Pages
147 - 153
Database
ISI
SICI code
0001-6322(200002)99:2<147:MAARPT>2.0.ZU;2-8
Abstract
The temporospatial relationship between microglial and astrocytic reactions and delayed thalamic cell death was examined 1-7 days following a traumati c cold lesion of the rat sensorimotor cortex using immunocytochemistry in c ombination with terminal deoxynucleo-tidyltransferase-mediated biotinylated dUTP nick end labeling (TUNEL) of nuclear DNA fragmentation. No or only oc casional TUNEL-positive cells were found in the thalamic relay nuclei up to 3 days after trauma. After 7 days, on the other hand, a considerable numbe r of TUNEL-positive cells were seen in the ventrobasal, the ventrolateral a nd posterior thalamic nuclei. Already 3 days after trauma, i.e., before cel l injury was detectable, many protoplasmic astrocytes, which were reactive for glial fibrillary acidic protein, and ramified microglia, which were pos itive for complement receptor type 3b (CR3b) but negative for major histoco mpatibility complex (MHC) class II antigen, were noticed in the thalamus. T he number of labeled astro- and microglia further increased after 7 days, w hen DNA fragmentation became evident. At this time, the morphology of micro glia shifted towards bushy and rod-like cells, and microglia became also re active for MHC class LI antigen. Clusters of CR3b- and MHC class II-positiv e microglia were found in the ventrobasal thalamus. The present findings de monstrate that trauma-induced microglial and astrocytic reactions appear in the thalamus prior the onset of cell damage.