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I.序論
Gruneberg2)により分離系統化されたHy−3 mouseは常染色体劣性遺伝により10〜20%に生後水頭症を発症してくる動物で先天性水頭症実験モデルとしては最適であり,多くの研究結果が報告されている1,3,4,8,9)。Hy−3mouseの水頭症の成因についてはBerry1)らのクモ膜下腔欠損による髄液吸収障害説があり,Raimondi9)らも腔室内に投与されたtracerが脳表のクモ膜下腔に侵入しないことを認めている。著者らはhydrocephalicHy−3 mouseのleptomeningesおよびクモ膜下腔の微細構造を観察するとともにhorseradish peroxidase(HRP)をtracerとして用いて水頭症mouseにおける髄液循環動態を観察しHy−3 mouseの水頭症の成因につき考察を加えた。
Congenital murine hydrocephalus occuring in the Hy-3 strain has certain similarities to human con-genital hydrocephalus. In order to elucidate the pathophysiology and etiology of congenital hydro-cephalus, ultrastructual study of the brain and the leptomeninges in the Hy-3 hydrocephalic mice was undertaken.
The cerebral cortex was invested with the thick cellular layer which had similar features of primi-tive arachnoid barrier cells. No appearent sub-arachnoid space was found.
Horseradish peroxidase, introduced into the lateral ventricle, crossed the ependymal cells and penetrated into parenchymal extracellular spaces. However no horseradish peroxidase activity was found over the cerebral hemispheres.
Those results suggested that the hydrocephalus in the Hy-3 strain is due to developmental anomaly of the leptomeninges and to defect of cerebral subarachnoid space.
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