کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9425813 | 1295893 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Acute effects of glucocorticoids on ATP-induced Ca2+ mobilization and nitric oxide production in cochlear spiral ganglion neurons
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کلمات کلیدی
nNOSethylene glycol-bis (β-aminoethyl ether) N,N,N′,N′-tetraacetic acidintracellular Ca2+ concentrationsS-nitroso-N-acetylpenicillamineSGNsDAF-2 DADAF-2eNOSiNOSNOSEGTAPSSDIC4,5-diaminofluorescein diacetate - 4،5-دی آمین فلوئورسین دی سکته4,5-diaminofluorescein - 4،5-دیامین فلوئورسینDMSO - DMSOl-NAME - L-NAMEl-NG-Nitroarginine methyl ester - L-NG-Nitroarginine متیل استر[Ca2+]i - [Ca2 +] iadenosine 5′-triphosphate - آدنوزین 5'-تری فسفاتATP - آدنوزین تری فسفات یا ATPNon-genomic effect - اثر غیر ژنومیIntracellular Ca2+ - داخل سلولی Ca2 +Dexamethasone - دگزامتازونDimethyl sulfoxide - دیمتیل سولفواکسیدinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییendothelial nitric oxide synthase - سنتاز اکسید نیتریک اندوتلیالneuronal nitric oxide synthase - سنتاز اکسید نیتریک عصبیSNAP - ضربه محکم و ناگهانیSpiral ganglion neurons - نورونهای گانگلیونی اسپیرالNitric oxide - نیتریک اکسیدnitric oxide synthase - نیتریک اکسید سنتازdifferential interference contrast - کنتراست تداخل دیفرانسیلP2 receptor - گیرنده P2
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Rapid, non-genomic effects of glucocorticoids on extracellular adenosine 5â²-triphosphate (ATP)-induced intracellular Ca2+ concentration ([Ca2+]i) changes and nitric oxide (NO) production were investigated in type I spiral ganglion neurons (SGNs) of the guinea-pig cochlea using the Ca2+-sensitive dye fura-2 and the NO-sensitive dye 4,5-diaminofluorescein (DAF-2). Pretreatment of SGNs with 1 μM dexamethasone for 10 min, a synthetic glucocorticoid hormone, enhanced the ATP-induced [Ca2+]i increase in SGNs. RU 38486, a competitive glucocorticoid receptor antagonist eliminated the effects of dexamethasone on the ATP-induced [Ca2+]i increase in SGNs. These acute effects of dexamethasone were dependent on the presence of extracellular Ca2+, thereby suggesting that dexamethasone may rapidly enhance the Ca2+ influx through the activation of ionotropic P2X receptors which may interact with glucocorticoid-mediated membrane receptors. Extracellular ATP increased the intensity of DAF-2 fluorescence, indicating NO production in SGNs. The ATP-induced NO production was mainly due to the Ca2+ influx through the activation of P2 receptors. S-nitroso-N-acetylpenicillamine, a NO donor, enhanced the ATP-induced [Ca2+]i increase in SGNs while l-NG-nitroarginine methyl ester (l-NAME), a NO synthesis inhibitor, inhibited it. Dexamethasone enhanced the ATP-induced NO production in SGNs. The augmentation of dexamethasone on ATP-induced NO production was abolished in the presence of l-NAME. It is concluded that the ATP-induced [Ca2+]i increase induces NO production which enhances a [Ca2+]i increase in SGNs by a positive-feedback mechanism. Dexamethasone enhances the ATP-induced [Ca2+]i increase in SGNs which results in the augmentation of NO production. The present study suggests that NO may play an important role in auditory signal transduction. Our results also indicate that glucocorticoids may rapidly affect auditory neurotransmission due to a novel non-genomic mechanism.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 130, Issue 2, 2005, Pages 485-496
Journal: Neuroscience - Volume 130, Issue 2, 2005, Pages 485-496
نویسندگان
H. Yukawa, J. Shen, N. Harada, H. Cho-Tamaoka, T. Yamashita,