title: Chronic hyperperfusion and angiogenesis follow subacute hypoperfusion in the thalamus of rats with focal cerebral ischemia.
abstract: Cerebral blood flow (CBF) is disrupted after focal ischemia in rats. We examined long-term hemodynamic and cerebrovascular changes in the rat thalamus after focal cerebral ischemia. Cerebral blood flow quantified by arterial spin labeling magnetic resonance imaging was decreased in the ipsilateral and contralateral thalamus 2 days after cerebral ischemia. Partial thalamic CBF recovery occurred by day 7, then the ipsilateral thalamus was chronically hyperperfused at 30 days and 3 months compared with its contralateral side. This contrasted with permanent hypoperfusion in the ipsilateral cortex. Angiogenesis was indicated by endothelial cell (RECA-1) immunohistochemistry that showed increased blood vessel branching in the ipsilateral thalamus at the end of the 3-month follow-up. Only transient thalamic IgG extravasation was observed, indicating that the blood-brain barrier was intact after day 2. Angiogenesis was preceded by transiently altered expression levels of cadherin family adhesion molecules, cadherin-7, protocadherin-1, and protocadherin-17. In conclusion, thalamic pathology after focal cerebral ischemia involved long-term hemodynamic changes and angiogenesis preceded by altered expression of vascular adhesion factors. Postischemic angiogenesis in the thalamus represents a novel type of remote plasticity, which may support removal of necrotic brain tissue and aid functional recovery.
authors.affiliation: Department of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
authors.forename: Nick M E A
authors.initials: NM
authors.lastname: Hayward
authors.forename: Pavel
authors.initials: P
authors.lastname: Yanev
authors.forename: Annakaisa
authors.initials: A
authors.lastname: Haapasalo
authors.forename: Riitta
authors.initials: R
authors.lastname: Miettinen
authors.forename: Mikko
authors.initials: M
authors.lastname: Hiltunen
authors.forename: Olli
authors.initials: O
authors.lastname: Gröhn
authors.forename: Jukka
authors.initials: J
authors.lastname: Jolkkonen
mesh_terms: D000818:Animals; D034961:Antigens, Nuclear / Q000378:metabolism; D001522:Behavior, Animal / Q000502:physiology; D001812:Blood-Brain Barrier / Q000473:pathology / Q000502:physiology; D002545:Brain Ischemia / Q000473:pathology* / Q000503:physiopathology* / Q000523:psychology; D015820:Cadherins / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism; D002540:Cerebral Cortex / Q000098:blood supply; D002560:Cerebrovascular Circulation / Q000502:physiology*; D002561:Cerebrovascular Disorders / Q000473:pathology* / Q000503:physiopathology* / Q000523:psychology; D006614:Hindlimb / Q000502:physiology; D007074:Immunoglobulin G / Q000378:metabolism; D007150:Immunohistochemistry; D008279:Magnetic Resonance Imaging; D008297:Male; D018919:Neovascularization, Physiologic / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000378:metabolism; D004856:Postural Balance / Q000502:physiology; D011597:Psychomotor Performance / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D013788:Thalamus / Q000098:blood supply* / Q000473:pathology; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D034961:Antigens, Nuclear; D015820:Cadherins; D015815:Cell Adhesion Molecules; D007074:Immunoglobulin G; D009419:Nerve Tissue Proteins; C546339:Rbfox3 protein, rat; D042461:Vascular Endothelial Growth Factor A