INFLAMMATORY LEUKOCYTIC RECRUITMENT AND DIFFUSE NEURONAL DEGENERATIONARE SEPARATE PATHOLOGICAL PROCESSES RESULTING FROM TRAUMATIC BRAIN INJURY

Citation
Hd. Soares et al., INFLAMMATORY LEUKOCYTIC RECRUITMENT AND DIFFUSE NEURONAL DEGENERATIONARE SEPARATE PATHOLOGICAL PROCESSES RESULTING FROM TRAUMATIC BRAIN INJURY, The Journal of neuroscience, 15(12), 1995, pp. 8223-8233
Citations number
79
Categorie Soggetti
Neurosciences,Neurosciences
Journal title
ISSN journal
02706474
Volume
15
Issue
12
Year of publication
1995
Pages
8223 - 8233
Database
ISI
SICI code
0270-6474(1995)15:12<8223:ILRADN>2.0.ZU;2-E
Abstract
The present study characterized whether inflammatory leukocytic infilt ration is temporally and regionally correlated with neuronal degenerat ion and/or blood brain barrier (BBB) breakdown resulting from traumati c brain injury. Adult rats were sacrificed at 5 min, 2, 4, 12, 24, and 72 hr after lateral fluid percussion brain injury. BBB breakdown, neu ronal degeneration and leukocyte infiltration were assessed using immu nocytochemistry silver impregnation and toluidine blue and eosin stain ing. BBB breakdown and neuronal degeneration occurred concomitantly in injured cortex, hippocampus, and along the dorsolateral quadrant of t he diencephalon. However, neuronal degeneration within deep diencephal ic structures transpired in the absence of IgG extravasation. Neutroph ils were observed only in regions exhibiting BBB damage and were first apparent in injured cortex and hippocampus between 2-12 hr posttrauma lining the vasculature and filling subarachnoid/subdural spaces. Neut rophils then migrated from damaged vasculature into traumatized cortic al and hippocampal parenchyma by 24 hr after lateral fluid percussion injury. Macrophages were also observed within cortical parenchyma at 2 4 hr and completely filled the cortical lesion site by 72 hr after inj ury. Macrophages were not as abundant throughout hippocampal parenchym a and were found only in hippocampal regions exhibiting focal hemorrha ge at 72 hr. Finally, neutrophils did not migrate to deep diencephalic structures that showed no BBB damage despite extensive neuronal degen eration. Indeed, lateral fluid percussion elicits inflammatory leukocy tic recruitment only in regions experiencing concomitant BBB damage an d neuronal degeneration. In summary, inflammatory leukocytic recruitme nt and diffuse neuronal degeneration are separate pathological process es resulting from traumatic brain injury.