] Control or TLE mice were anesthetized with phenobarbital sodium (60 mg/kg, i.p.) and the brains were rapidly decapitated, removed and placed in an ice-cold sucrose-based dissecting solution (in mM): sucrose (300), KCl (2), NaH 2PO 4 (1.25), CaCl 2 (1), MgCl 2 (5), NaHCO 3 (26) and glucose (11). Implications of all the available evidence These characterizations of the relations between ClC and TLE advance the understanding of the mechanism of epileptogenesis in TLE. Furthermore, we identified ClC-3, a ClC gene family member, had higher expression in the hippocampus of TLE mice and TLE patients, and its expression was positively correlated with both the power and number of ictal HFOs per seizure in the sclerotic hippocampus. Additionally, NPPB and DIDS induced an outward current, which was likely a tonic inhibitory current in the hippocampal neurons of intractable TLE patients. In vivo study found that NPPB and DIDS reduced the seizure frequency and the power of ictal HFOs in the hippocampus of chronic TLE mice. Chloride channel blockers NPPB and DIDS efficiently reduced ClC-mediated current and increased the inhibitory transmission in hippocampal neurons of TLE mice. ClC-mediated outwardly rectified current was increased in the hippocampal neurons of chronic TLE mice and led to the elevation of intracellular chloride concentration in the neurons of epileptogenic lesions. In the present study, we presented evidence that ClC are significantly involved in the epileptogenesis of TLE. The Lancet Regional Health – Western Pacific.The Lancet Regional Health – Southeast Asia.The Lancet Gastroenterology & Hepatology.
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