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Flinders sensitive line rats are resistant to infarction following transient occlusion of the middle cerebral artery

Journal article
Authors V. Bay
D. F. Happ
Maryam Ardalan
Alexandra Quist
Florian Oggiano
Tetyana Chumak
K. Hansen
M. Ding
C. Mallard
R. A. Tasker
G. Wegener
Published in Brain Research
Volume 1737
Pages 6
ISSN 0006-8993
Publication year 2020
Published at Institute of Neuroscience and Physiology, Department of Physiology
Pages 6
Language en
Links dx.doi.org/10.1016/j.brainres.2020....
Keywords Flinders sensitive line, Depression, Stroke, MCAo, TTC, depressive symptoms, major depression, stroke patients, model, risk, progression, calcification, inflammation, metaanalysis, predictors, Neurosciences & Neurology
Subject categories Clinical Medicine

Abstract

Background: Depression is a common complication of stroke and increases the risk of mortality and disability. Pre-stroke depression is a possible risk factor for stroke and has also been linked to adverse outcomes. The underlying mechanisms linking depression and stroke remain unclear. Preclinical models may provide novel insights, but models reflecting both conditions are lacking. Methods: In this study, we investigated the effects of a 45-min transient middle cerebral artery occlusion (MCAo) on infarct size in male adult Flinders Sensitive Line rats, a genetic animal model of depression, and their control strains Flinders Resistant Line and Sprague-Dawley rats. Infarct size was assessed by tetrazolium chloride (TTC) and microtubule-associated protein 2 (MAP2) staining after 48 h of reperfusion. Angiograms of the vascular structure of naive animals were produced with a mu-CT scanner. Results: Both Flinders strains had significantly smaller infarcts following MCAo compared to Sprague-Dawley rats. This effect does not appear to be due to changes in cerebrovascular architecture, as indicated by an initial exploration of vascular organization using angiograms, or body temperature regulation. Conclusions: Our study suggests that the rat strain does not influence infarct volumes following MCAo.

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