Maguire S, Strittmatter R, Chandra S, Barone FCStroke-prone rats exhibit prolonged behavioral deficits without increased brain injury: an indication of disrupted post-stroke brain recovery of function. Neurosci Lett 354:229-233

Department of Laboratory Animal Science, GlaxoSmithKline, King of Prussia, PA 19406, USA.
Neuroscience Letters (Impact Factor: 2.03). 01/2004; 354(3):229-33. DOI: 10.1016/j.neulet.2003.09.079
Source: PubMed


Stroke-prone rat strains exhibit an increased stroke risk and sensitivity, and reduced endogenous mechanisms of ischemic brain tolerance. This experiment provides a comparative, serial evaluation of neurological deficits and brain injury following middle cerebral artery occlusion/permanent focal stroke in this high-risk strain. Stroke-prone spontaneously hypertensive (SHR-SP), spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats were evaluated over 28 days using magnetic resonance imaging (MRI), histopathology, and neurobehavioral testing. T2- and diffusion weighted-MRI was performed after 1, 10 and 28 days to measure the degree of stroke-induced brain injury. Normotensive WKY rats receiving the same stroke and other SHR-SP rats receiving sham surgery were used for control comparisons. Functional deficits were scored after 1, 4, 11, 18 and 28 days. The degree of brain infarction/injury was practically identical in hypertensive and stroke-prone rats. WKY rats exhibited significantly smaller infarcts (P<0.05), with neurological function recovering quickly to normal by day 11 in this strain. Functional deficits persisted longer in hypertensive rats, with function recovering to normal by day 18 (P<0.05). Functional deficits in SHR-SP rats persisted the longest, and were observed even after 28 days (P<0.05). This increased and prolonged neurologic dysfunction exhibited by SHR-SP compared to SHR rats, while exhibiting practically identical degrees of brain injury/infarction, reflects the increased stroke risk and sensitivity of this strain and suggests a reduced SHR-SP brain plasticity following injury. Therefore, the stroke-prone rat provides an enhanced and prolonged functional deficit model that can be used to elucidate those mechanisms/novel targets critical to longitudinal neurobehavioral recovery post-stroke.

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    • "); Murphy et al (2004) IHR, inducible hypertensive rat; 3-NPA, 3-nitropropionic acid; SHR-SP, stroke-prone spontaneously hypertensive rat. a Reference list for SHR-SP (Okamoto et al, 1975; Yamori et al, 1976; Yamori and Horie, 1977; Hart et al, 1980; Ogata et al, 1981; Coyle and Jokelainen, 1983; Sadoshima et al, 1983; Fredriksson et al, 1984, 1985; Tamaki et al, 1984; Werber and Heistad, 1984; Paschen et al, 1985; Tobian et al, 1986; Mayhan et al, 1987; Tagami et al, 1987; Baumbach et al, 1988; Mayhan et al, 1988; Fredriksson et al, 1988a, b; Hajdu et al, 1991; Yang et al, 1991, 1993; Coyle and Feng, 1993a, b; Baumbach et al, 1994; Richer et al, 1994; Yamaguchi et al, 1994; Linz et al, 1997; Minami et al, 1997; Blezer et al, 1998; Brosnan et al, 1999; Carswell et al, 1999, 2000a, b, 2004; Chillon and Baumbach, 1999; Marks et al, 2001; Sironi et al, 2001, 2004a, b, 2005; Kawashima et al, 2003; Banfi et al, 2004; Maguire et al, 2004; Kim-Mitsuyama et al, 2005; Liebetrau et al, 2005; Nagotani et al, 2005; Jesmin et al, 2007; Lee et al, 2007; Ballerio et al, 2007). "
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