کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9426399 | 1295920 | 2005 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
O2 sensing by recombinant TWIK-related halothane-inhibitable K+ channel-1 background K+ channels heterologously expressed in human embryonic kidney cells
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کلمات کلیدی
HEPESN-(2-hydroxyethyl)piperazine-N′-(2-ethanesulphonic acid)THIKGPNHEK293PAODPII–V - I - VArachidonic acid - اسید آراشیدونیکPhenylarsine oxide - اکسید فنیلارسینcurrent–voltage - جریان ولتاژcarotid body - جسم کاروتید، جسم سباتیdiphenylene iodonium - دیوفنیلن یدونیومglossopharyngeal nerve - عصب glossopharyngealAcute hypoxia - هیپوکسی حادresting membrane potential - پتانسیل غشای استراحتhuman embryonic kidney - کلیه جنین انسان
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Hypoxic inhibition of K+ channels provides a link between low O2 and cell function, and in glossopharyngeal neurons hypoxic inhibition of a TWIK-related halothane-inhibitable K+ channel-1 (THIK-1)-like background K+ channel regulates neuronal function. In the present study, we examined directly the O2 sensitivity of recombinant THIK-1 channels, expressed in human embryonic kidney (HE293) cells. THIK-1 expression conferred a moderately outwardly rectifying halothane-inhibited and arachidonic acid-potentiated K+ current and invoked a strongly hyperpolarized resting membrane potential. Endogenous K+ currents in untransfected cells were unaffected by either agent. Hypoxia (PO2, 20 mm Hg) reversibly inhibited THIK-1 currents and caused membrane depolarization, effects that were occluded by halothane. Neither the mitochondrial complex I inhibitors rotenone, myxothiazol and sodium cyanide, nor the NADPH oxidase inhibitors diphenylene iodonium and phenylarsine oxide, were effective in inhibiting the O2-sensitivity of THIK-1. Thus, hypoxic inhibition of THIK-1 occurs by a mechanism dissimilar to that which regulates the activity of other members of the background K+ channel family. Given the O2 sensitivity of THIK-1 channels and their abundant expression in the CNS, we raise for the first time the possibility of a physiological and/or pathological role for these channels during brain ischemia.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 135, Issue 4, 2005, Pages 1087-1094
Journal: Neuroscience - Volume 135, Issue 4, 2005, Pages 1087-1094
نویسندگان
V.A. Campanucci, S.T. Brown, K. Hudasek, I.M. O'Kelly, C.A. Nurse, I.M. Fearon,