Inflammatory response and white matter damage after microinjections of endothelin-1 into the rat striatum.
Following acute and chronic neurodegenerative disorders, a cascade of pathological events including inflammatory response, excitotoxicity and oxidative stress induces secondary tissue loss in both gray and white matter. Axonal damage and demyelination are important components of the white matter demise during these diseases. In spite of this, a few studies have addressed the patterns of inflammatory response, axonal damage and demyelination following focal ischemic damage to the central nervous system (CNS). In the present study, we describe the patterns of inflammatory response, axonal damage and myelin impairment following microinjections of 10 pmol of endothelin-1 into the rat striatum. Animals were perfused at 1 day, 3 days and 7 days after injection. 20 mum sections were stained by hematoxylin and immunolabeled for neutrophils (anti-MBS-1), activated macrophages/microglia (anti-ED1), damaged axons (anti-betaAPP) and myelin (anti-MBP). The evolution of acute inflammation was quantitatively assessed by cell counts in different survival times. There was recruitment of both neutrophils and macrophages to the damaged striatal parenchyma with maximum recruitment at 1 day and 7 days, respectively. Progressive myelin impairment in the striatal white matter tracts has been observed mainly at later survival times. beta-APP+ endbulbs were not present in all evaluated time points. These results suggest that progress myelin impairment in the absence of damage to axonal cylinder is a feature of white matter pathology following endothelin-1-induced focal striatal ischemia.
Souza-Rodrigues
R D
RD
Laboratory of Experimental Neuroprotection and Neuroregeneration, Department of Morphology, Biological Sciences Center, Federal University of Pará, Belém-Pará, Brazil.
Costa
A M R
AM
Lima
R R
RR
Dos Santos
C D
CD
Picanço-Diniz
C W
CW
Gomes-Leal
W
W
D016229:Amyloid beta-Peptides / Q000032:analysis / Q000378:metabolism; D000818:Animals; D001369:Axons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D002545:Brain Ischemia / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D002536:Cerebral Arteries / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D002634:Chemotaxis, Leukocyte / Q000187:drug effects / Q000502:physiology; D003342:Corpus Striatum / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D003711:Demyelinating Diseases / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D018450:Disease Progression; D004660:Encephalitis / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D019332:Endothelin-1 / Q000633:toxicity*; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D017628:Microglia / Q000187:drug effects / Q000378:metabolism; D008845:Microinjections; D004676:Myelin Basic Protein / Q000032:analysis / Q000378:metabolism; D009413:Nerve Fibers, Myelinated / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
D016229:Amyloid beta-Peptides; D015415:Biomarkers; D019332:Endothelin-1; D004676:Myelin Basic Protein