中枢神経系の脱髄機序に関する研究 Study on the Mechanism of Demyelination in Central Nervous System
Study on the Mechanism of Demyelination in Central Nervous System
柳沢, 勝彦, 1954-
学位の種類: 博士（医学）. 報告番号: 乙第1141号. 学位記番号: 新大院博（医）乙第1060号. 学位授与年月日: 平成3年4月16日
新潟医学会雑誌. 1991, 105(5), 326-333.
Calcium-dependent protease was extracted from human brain myelin membrane and partially purified on a phenyl Sepharose CL, 4B column. It was activated by calcium ion in the millimolar range, and therefore was determined to be calpain II. This enzyme fraction was electrophoresed and immunostained with anti-chicken muscle calpain antibody, resulting in staining as a single band with apparent molecular weight of 80K. This protease degraded exogenous myelin-associated glycoprotein. From the present result, it is suggested that calpain is bound to myelin membranes and involved in the turnover of myelin proteins. The vacuolar degeneration was produced by oral administration of triethyl tin （TET）. The wet weight of brain stems which seems to reflect the degree of accumulation of water increased during the administration of the toxin, whereas the activity of 2', 3'-cyclic nucleotide 3'-phosphodiesterase altered less remarkably. When TET was withdrawed from the drinking water, the rats showed a dramatic clinical improvement along with reduction in wet weight of brain stems. Treatment with acetazolamide following TET inhibited the clinical improvement and reduction in wet weight of brain stems. The present results indicates that central myelin has plasticity in recovering from the vacuolar degeneration by removing the accumulated fluid and carbonic anhydrase is possibly involved in the dehydration of myelin in such a recovery phase.