Abstract：
:Increased permeability of the brain-blood barrier (BBB) in the piriform cortex (PC) has been reported in various animal models of temporal lobe epilepsy. Since BBB disruption induced by epileptogenic insult has not fully clarified, we attempted to determine whether changes in BBB-related molecules are associated with vasogenic edema in the PC. One day after status epilepticus (SE), PC neurons and astrocytes showed a pyknotic nucleus and shrunken cytoplasm accompanied by vasogenic edema. At this time point, SMI-71 (an endothelial barrier antigen) immunoreactivity had decreased in the PC. Prior to vasogenic edema formation (12 h after SE), dystrophin immunoreactivity disappeared within astrocytes, while the change in glial fibrillary acidic protein immunoreactivity was negligible. However, glucose transporter-1 (an endothelial cell marker) had increased at 12 h after SE. These findings indicate that dysfunction of dystrophin induced by SE may result in endothelial and astroglial damage with BBB breakdown and increase vascular permeability, leading to vasogenic edema that is involved in pathogenesis of epileptogenesis.
journal_name
Brain Resjournal_title
Brain researchauthors
Sheen SH,Kim JE,Ryu HJ,Yang Y,Choi KC,Kang TCdoi
10.1016/j.brainres.2010.10.080subject
Has Abstractpub_date
2011-01-19 00:00:00pages
173-83eissn
0006-8993issn
1872-6240pii
S0006-8993(10)02385-1journal_volume
1369pub_type
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