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논문 기본 정보

자료유형
학술저널
저자정보
Ehn-Kyoung Choi (충북대학교) Dongsun Park (충북대학교) Tae Kyun Kim (충북대학교) Sun Hee Lee (충북대학교) Dae-Kwon Bae (충북대학교) Goeun Yang (충북대학교) Yun-Hui Yang (충북대학교) Jangbeen Kyung (충북대학교) Dajeong Kim (충북대학교) Woo Ryoung Lee (순천향대학교) Jun-Gyo Suh (한림대학교) Eun-Suk Jeong (서울벤처정보대학원대학교) Seung U. Kim (University of British Columbia Hospital) Yun-Bae Kim (충북대학교)
저널정보
한국실험동물학회 Laboratory Animal Research Laboratory Animal Research Vol.27 No.2
발행연도
2011.6
수록면
77 - 84 (8page)

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초록· 키워드

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Periventricular leukomalacia, specifically characterized as white matter injury, in neonates is strongly associated with the damage of pre-myelinating oligodendrocytes. Clinical data suggest that hypoxiaischemia during delivery and intrauterine or neonatal infection-inflammation are important factors in the etiology of periventricular leukomalacia including cerebral palsy, a serious case exhibiting neurobehavioral deficits of periventricular leukomalacia. In order to explore the pathophysiological mechanisms of white matter injury and to better understand how infectious agents may affect the vulnerability of the immature brain to injury, novel animal models have been developed using hypoperfusion, microbes or bacterial products (lipopolysaccharide) and excitotoxins. Such efforts have developed rat models that produce predominantly white matter lesions by adopting combined hypoxia-ischemia technique on postnatal days 1-7, in which unilateral or bilateral carotid arteries of animals are occluded (ischemia) followed by 1-2 hour exposure to 6-8% oxygen environment (hypoxia). Furthermore, low doses of lipopolysaccharide that by themselves have no adverse-effects in 7-day-old rats, dramatically increase brain injury to hypoxicischemic challenge, implying that inflammation sensitizes the immature central nervous system. Therefore, among numerous models of periventricular leukomalacia, combination of hypoxia-ischemialipopolysaccharide might be one of the most-acceptable rodent models to induce extensive white matter injury and ensuing neurobehavioral deficits for the evaluation of candidate therapeutics.

목차

Neuropathology of Infantile PVL
Etiology of Infantile PVL
Animal Models of PVL
Conclusion
Acknowledgments
References

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