Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/498
Title: Cellular markers of neuroinflammation and neurogenesis after ischemic brain injury in the long-term survival rat model
Authors: Šekeljić, Vera 
Bataveljic, Danijela
Stamenković, Stefan 
Ułamek, Marzena
Jabłoński, Mirosław
Radenović, Lidija 
Pluta, Ryszard
Anđus, Pavle 
Keywords: Blood-brain barrier;Brain ischemia;Microglia/macrophages;MRI;Neurogenesis;T cells
Issue Date: 1-Apr-2012
Journal: Brain Structure and Function
Abstract: 
MRI was employed to follow the neurodegenerative foci and the localization of inflammatory cells by magnetically labeled CD4+ or CD8+ lymphocytes in the ischemia/reperfusion long-lived rats (9 and 13 months after 10 min of cardiac arrest). MRI of ischemic rats showed: (1) blood-brain barrier (BBB) leakage in the area of the dorsal hippocampus and brainstem-hindbrain level in basal cerebellum, (2) unlike anti-CD8 magnetic antibodies anti-CD4 ultra small paramagnetic iron oxide particles (USPIO) antibodies revealed hypointense areas in the brainstem-interbrain region and caudoputamen not found in animals that were not injected with USPIO antibodies, and (3) dilation in the retrosplenial area. Immunocytochemistry revealed microglial activation in the hippocampus and striatum, with indications of activation in thalamic lateral dorsal nuclei and the subventricular zone. In the CA1 and CA3 regions, it was noted that OX42- and ED1-positive granules appear in neuronal somata. Immunostaining of lymphocytes with TCR confirmed the T-cell presence in ischemic brain parenchyma of the hippocampus and striatum. The above observations thus point to a persistent dysfunction of BBB that in long-term may still lead to infiltration of T cells that are predominantly of helper (CD4+) type. Such inflammatory processes are backed by microglial activity even up to 1 year after ischemia/reperfusion. Moreover, in these animals an augmented expression of neurogenesis markers and neuroblast migration was also revealed in the subventricular zone. Thus, a balance of degenerative processes and inflammatory surveillance with neurogenesis could determine the long-term outcome of global ischemia survival or the previously proposed formation of amyloid plaques and Alzheimer's-type dementia. © Springer-Verlag 2011.
URI: https://biore.bio.bg.ac.rs/handle/123456789/498
ISSN: 1863-2653
DOI: 10.1007/s00429-011-0336-7
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