Ischemia-induced slowly progressive neuronal damage in the rat brain
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Cited by (100)
Transgenic mice over-expressing endothelial endothelin-1 show cognitive deficit with blood-brain barrier breakdown after transient ischemia with long-term reperfusion
2013, Neurobiology of Learning and MemoryCitation Excerpt :These morphological changes might due to the neuronal cell death after the ischemia/reperfusion injury and ET-1over-expression further exacerbated the damage. In addition, Nakano has described a phenomenon of “slowly progressive neuronal damage” after short-term ischemia (Nakano, Kogure, & Fujikura, 1990). The delayed neuronal damage in the brain was observed weeks or months after 15 to 45 min MCAO (Nakano et al., 1990), in contrast to the previous opinion that this process only continues for several days after transient ischemia injury (Kirino, 1982; Pulsinelli, Brierley, & Plum, 1982).
Characterizing infarction and selective neuronal loss following temporary focal cerebral ischemia in the rat: A multi-modality imaging study
2013, Neurobiology of DiseaseCitation Excerpt :This diversity of local tissue outcome likely reflects inter- and intra-subject differences in severity of hypoperfusion during MCAo, previously documented in this model (Buchan et al., 1992; Kaplan et al., 1991) including by us (Hughes et al., 2010). Following proximal tMCAo, SNL is commonly observed in the striatum (Fujioka et al., 1999; Garcia et al., 1997; Katchanov et al., 2003; Li et al., 1999, 2000; Sicard et al., 2006a; Wegener et al., 2006; Winter et al., 2005), but is milder and much less consistent in the neocortex (Garcia et al., 1997; Lehrmann et al., 1997; Li et al., 1999; Nakano et al., 1990; Sicard et al., 2006a), where it tends to affect the borders of the infarct (Garcia et al., 1997; Mies et al., 1983; Nedergaard, 1987). In non-human primates (DeGirolami et al., 1984) and man (Nedergaard et al., 1986; Torvik and Svindland, 1986), definite SNL has so far been observed only as an inconsistent rim bordering the infarct, though this may reflect among other factors biases in duration of ischemia and occurrence of reperfusion, as well as lack of IHC analysis.
Therapeutic neuroprotective effects of ginkgolide B on cortex and basal ganglia in a rat model of transient focal ischemia
2011, European Journal of Pharmaceutical SciencesCitation Excerpt :Later than 2 h after MCAO, has only the chance to protect cortical tissue, which is viable for up to 12–24 h after focal ischemia (Garcia, 1992). Nakano et al. (1990) studied neuronal damage in the dorsolateral striatum and neocortex following various ischemia time subjected in rats, and some articles reported slowly progressive neuronal damage after MCAO. It remains unclear how the ischemic injury progress in different brain regions after MCAO and whether ischemic injury could be reversible after ischemia injury.
Mapping selective neuronal loss and microglial activation in the salvaged neocortical penumbra in the rat
2010, NeuroImageCitation Excerpt :With brief proximal tMCAo, SNL has been frequently reported in the striatum (Fujioka et al., 1999; Garcia et al., 1997; Katchanov et al., 2003; Li et al., 1999, 2000; Sicard et al., 2006; Wegener et al., 2006). Mild degrees of neocortical SNL have also been occasionally reported after brief proximal tMCAo (Garcia et al., 1997; Lehrmann et al., 1997; Li et al., 1999; Nakano et al., 1990; Sicard et al., 2006). For instance, cortical “selective neuronal necrosis” was found by Garcia et al. (1997) to affect 40% of rats subjected to 10–25 min thread tMCAo; in this study, dead neurons were only seen using H&E within 7 days of the insult, while after this date only vanishing neuron “ghosts” were barely identifiable.
A new model of transient focal cerebral ischemia for inducing selective neuronal necrosis
2009, Brain Research Bulletin