Endothelial Transient Receptor Potential Conical Channel (TRPC)-3 Activation Induces Vasogenic Edema Formation in the Rat Piriform Cortex Following Status Epilepticus

التفاصيل البيبلوغرافية
العنوان: Endothelial Transient Receptor Potential Conical Channel (TRPC)-3 Activation Induces Vasogenic Edema Formation in the Rat Piriform Cortex Following Status Epilepticus
المؤلفون: So Yeon Choi, Yeon-Joo Kim, Ji-Eun Kim, Tae-Cheon Kang, Won Il Kim, Ji-Yang Kim, Min-Ju Kim, Hea Jin Ryu
المصدر: Cellular and Molecular Neurobiology. 33:575-585
بيانات النشر: Springer Science and Business Media LLC, 2013.
سنة النشر: 2013
مصطلحات موضوعية: Male, Cell type, Brain Edema, Status epilepticus, Rats, Sprague-Dawley, Cellular and Molecular Neuroscience, Transient receptor potential channel, Status Epilepticus, TRPC3, Piriform cortex, medicine, Animals, RNA, Messenger, Receptor, TRPC, TRPC Cation Channels, Cerebral Cortex, Chemistry, Imidazoles, Antagonist, Endothelial Cells, Cell Biology, General Medicine, Rats, Cell biology, medicine.symptom, Neuroscience
الوصف: Transient receptor potential canonical channel (TRPC) is a nonselective cation channel permeable to Ca(2+), which express in many cell types, including neurons. However the alterations in TRPC receptor expressions in response to status epilepticus (SE) have not been explored. Therefore, the present study was designated to elucidate the roles of TRPC3 in neuronal death and vasogenic edema within the rat piriform cortex (PC) following SE. In non-SE animals, TRPC3 immunoreactivity was abundantly detected in the PC. Following SE, TRPC3 immunoreactivity was increased in neurons. Furthermore, TRPC3 expression was detected in endothelial cells that did not contain it in non-SE animals. Loss of SMI-71 (a blood-brain barrier antigen) immunoreactivity was also observed in TRPC3 positive endothelial cells. In addition, FJB positive neurons and vasogenic edema were noticeably detected in the PC. To directly determine whether TRPC3 activation is correlated to SE-induced vasogenic edema formation and neuronal damages in the PC, the effect of Pyr-3 (a TRPC3 antagonist) on SE-induced insults were investigated. Pyr-3 infusion effectively attenuated vasogenic edema in the PC as compared to the vehicle. Therefore, our findings indicate that TRPC3 activation/overexpression induced by SE may involve BBB disruption and neuronal damages in the rat PC following SE. Therefore, the present study was TRPC3 may play an important role in SE-induced vasogenic edema formation through BBB disruptions in the rat PC.
تدمد: 1573-6830
0272-4340
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::194e25c6a2ab4e8548e9bb4f6ce64c24Test
https://doi.org/10.1007/s10571-013-9931-xTest
حقوق: CLOSED
رقم الانضمام: edsair.doi.dedup.....194e25c6a2ab4e8548e9bb4f6ce64c24
قاعدة البيانات: OpenAIRE