کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8516790 | 1556581 | 2018 | 34 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inhalational anesthetics accelerate desensitization of acid-sensing ion channels
ترجمه فارسی عنوان
بیهوشی استنشاقی باعث کاهش حساسیت کانال های یون های حساس به اسید می شود
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
ASICminimal alveolar concentrationPcTx1Inhalational anestheticPsalmotoxin 1CNS - دستگاه عصبی مرکزیcentral nervous system - سیستم عصبی مرکزیperipheral nervous system - سیستم عصبی پیرامونیNeuroprotection - محافظت نورونی یا محافظت از عصبMAC - مکPNS - کارمندان دولتAcid-sensing ion channel - کانال یون حساس به اسیدIon channel - کانال یونیDesensitization - کاهش حساسیت
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب رفتاری
چکیده انگلیسی
Acid-sensing ion channels (ASICs) are neuronal Na+ channels that are activated by extracellular acidification. Inhibiting ASICs is neuroprotective in mouse models of ischemic stroke. As inhalational anesthetics interact with many ion channels and as some of them have neuroprotective effects, we hypothesized that inhalational anesthetics modulate ASICs. We expressed different homo- and heteromeric ASICs heterologously in Xenopus oocytes. We co-applied with acidic pH the halogenated inhalational anesthetics sevoflurane, desflurane, and isoflurane and the noble gases xenon and argon at concentrations that are roughly equivalent to their minimal alveolar concentrations and analyzed their effect on current kinetics and amplitude. Sevoflurane, desflurane, and isoflurane as well as xenon and argon accelerated by a factor of â¼1.5 channel desensitization of the main ASICs of the central nervous system: homomeric ASIC1a and heteromeric ASIC1a/2a and ASIC1a/2b. Moreover, they decreased current amplitudes by â¼25%. For example, isoflurane accelerated desensitization of homomeric ASIC1a from 1.0â¯Â±â¯0.4â¯s (meanâ¯Â±â¯SD) to 0.6â¯Â±â¯0.2â¯s (nâ¯=â¯12; pâ¯=â¯0.0003) and decreased current amplitudes from 12.1â¯Â±â¯7.5â¯Î¼A to 9.3â¯Â±â¯5.6â¯Î¼A (nâ¯=â¯12; pâ¯=â¯0.0009). While inhalational anesthetics had similar effects on homomeric ASIC3, desensitization of ASIC1b was only accelerated by halogenated anesthetics but not noble gases; desensitization of homomeric ASIC2a was not modulated. In summary, we found a significant modulation of ASICs by different inhalational anesthetics. We conclude that ASICs should be considered as relevant targets of inhalation anesthetics.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuropharmacology - Volume 135, June 2018, Pages 496-505
Journal: Neuropharmacology - Volume 135, June 2018, Pages 496-505
نویسندگان
Linda Lehmke, Mark Coburn, Manfred Möller, Rosmarie Blaumeiser-Debarry, Pia Lenzig, Dominik Wiemuth, Stefan Gründer,