期刊
JOURNAL OF NEUROSCIENCE RESEARCH
卷 99, 期 12, 页码 3222-3237出版社
WILEY
DOI: 10.1002/jnr.24939
关键词
brain infarction; endothelin-1; microglia; neurodegeneration; RRID; AB_10711153; RRID; AB_2811075; RRID; AB_566455; RRID; SCR_002798; RRID; SCR_017654; stroke; touchscreen
资金
- NHMRC [1094974, 1113352]
- Australian Research Council Future Fellowship [140101327]
- National Health and Medical Research Council of Australia [1113352, 1094974] Funding Source: NHMRC
Animal modeling has been crucial in understanding the pathobiology of stroke. This research highlights the importance of addressing progressive atrophy and chronic inflammation as additional targets for intervention in the chronic phase after injury, even in cases of mild ischemic insult.
Animal modeling has played an important role in our understanding of the pathobiology of stroke. The vast majority of this research has focused on the acute phase following severe forms of stroke that result in clear behavioral deficits. Human stroke, however, can vary widely in severity and clinical outcome. There is a rapidly building body of work suggesting that milder ischemic insults can precipitate functional impairment, including cognitive decline, that continues through the chronic phase after injury. Here we show that a small infarction localized to the frontal motor cortex of rats following injection of endothelin-1 results in an essentially asymptomatic state based on motor and cognitive testing, and yet produces significant histopathological change including remote atrophy and inflammation that persists up to 1 year. While there is understandably a major focus in stroke research on mitigating the acute consequences of primary infarction, these results point to progressive atrophy and chronic inflammation as additional targets for intervention in the chronic phase after injury. The present rodent model provides an important platform for further work in this area.
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