期刊
BMB REPORTS
卷 48, 期 9, 页码 507-512出版社
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
DOI: 10.5483/BMBRep.2015.48.9.013
关键词
Astroglial death; Blood-brain barrier; Epilepsy; Mannitol; Status epilepticus
资金
- Healthcare Technology R&D Project, Ministry for Health, Welfare and Family Affairs [A111313]
- National Research Foundation of Korea (MEST) - Korean government [2012R1A2A1A01001775, 2009-0093812]
- Hallym University [HRF-201410-016]
- National Research Foundation of Korea [2012R1A2A1A01001775, 2009-0093812] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
In the present study, we addressed the question of whether treatment with mannitol, an osmotic diuretic, affects astroglio-vascular responses to status epilepticus (SE). In saline-treated animals, astrocytes exhibited reactive astrogliosis in the CA1-3 regions 2-4 days after SE. In the mannitol-treated animals, a large astroglial empty zone was observed in the CA1 region 2 days after SE. This astroglial loss was unrelated to vasogenic edema formation. There was no difference in SE-induced neuronal loss between saline-and mannitol-treated animals. Furthermore, mannitol treatment did not affect astroglial loss and vasogenic edema formation in the dentate gyrus and the piriform cortex. These findings suggest that mannitol treatment induces selective astroglial loss in the CA1 region independent of vasogenic edema formation following SE. These findings support the hypothesis that the susceptibility of astrocytes to SE is most likely due to the distinctive heterogeneity of astrocytes independent of hemodynamics.
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