کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4346970 1296814 2009 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Comparative roles of ATP-sensitive K+ channels and Ca2+-activated BK+ channels in posthypoxic hyperexcitability and rapid hypoxic preconditioning in hippocampal CA1 pyramidal neurons in vitro
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
Comparative roles of ATP-sensitive K+ channels and Ca2+-activated BK+ channels in posthypoxic hyperexcitability and rapid hypoxic preconditioning in hippocampal CA1 pyramidal neurons in vitro
چکیده انگلیسی
The aim of this study was to investigate the comparative effects of glibenclamide (GC), a selective blocker of K+ATP channels, and iberiotoxin (IbTX), a selective blocker of BK+Ca channels, on the repeated brief hypoxia-induced posthypoxic hyperexcitability and rapid hypoxic preconditioning in hippocampal CA1 pyramidal neurons in vitro. The method of field potentials measurement in CA1 region of the rat hippocampal slices was used. In contrast to GC (10 μM), IbTX (10 nM) significantly abolished both posthypoxic hyperexcitability and rapid hypoxic preconditioning induced by brief hypoxic episodes. These effects of IbTX did not depend on its ability to reduce the hypoxia-induced decrease of population spike (PS) amplitude during hypoxic episodes since GC (10 μM), comparatively with IbTX (10 nM), significantly reduced the depressive effect of hypoxia on the PS amplitude during hypoxic episodes but did not abolish both posthypoxic hyperexcitability and rapid hypoxic preconditioning in CA1 pyramidal neurons. Our results indicated that BK+Ca channels, in comparison with K+ATP channels, play a more important role in such repeated brief hypoxia-induced forms of neuroplasticity in hippocampal CA1 pyramidal neurons as posthypoxic hyperexcitability and rapid hypoxic preconditioning.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 461, Issue 2, 11 September 2009, Pages 90-94
نویسندگان
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