NDLI: Cellular markers of neuroinflammation and neurogenesis after ischemic brain injury in the long-term survival rat model

Content Provider	Springer Nature Link
Author	Sekeljic, Vera Bataveljic, Danijela Stamenkovic, Stefan Ułamek, Marzena Jabłoński, Mirosław Radevic, Lidija Pluta, Ryszard Andjus, Pavle R.
Copyright Year	2011
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.
Starting Page	411
Ending Page	420
Page Count	10
File Format	PDF
ISSN	18632653
Journal	Anatomy and Embryology
Volume Number	217
Issue Number	2
e-ISSN	18632661
Language	English
Publisher	Springer-Verlag
Publisher Date	2011-06-26
Publisher Place	Berlin/Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Brain ischemia Blood–brain barrier Microglia/macrophages T cells Neurogenesis MRI Cell Biology Neurology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Neuroscience Anatomy Histology

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