دورية أكاديمية

Muscarinic Acetylcholine Receptors Activate TRPC6 Channels in PC12D Cells via Ca2+ Store-Independent Mechanisms

التفاصيل البيبلوغرافية
العنوان: Muscarinic Acetylcholine Receptors Activate TRPC6 Channels in PC12D Cells via Ca2+ Store-Independent Mechanisms
المؤلفون: Zhang, Lei, Guo, Feifan, Kim, Ju Young, Saffen, David
بيانات النشر: Oxford University Press
سنة النشر: 2006
المجموعة: HighWire Press (Stanford University)
مصطلحات موضوعية: Regular Papers
الوصف: In this paper we report that stimulation of mAChRs in PC12D cells activates Ca2+ channels that are regulated independently of intracellular Ca2+ stores. In nominally Ca2+-free medium, exposure of PC12D cells to carbachol stimulates a robust influx of Ba2+, a Ca2+ substitute. This influx is blocked by atropine, but not by inhibitors of the nicotinic acetylcholine receptor or L-, N-, or T-type voltage-regulated Ca2+ channels. By contrast, depletion of intracellular Ca2+ stores with thapsigargin only weakly stimulates Ba2+ influx. Unlike store-operated Ca2+ channels (SOCCs), which close only after intracellular Ca2+ stores refill, channels mediating carbachol-stimulated Ba2+ influx rapidly close following the inactivation of mAChRs with atropine. Ba2+ influx is inhibited by extracellular Ca2+, by the Ca2+ channel blocker SKF-96365, and by activation of protein kinase C (PKC). Exogenous expression of antisense RNA encoding the rat c anonical- t ransient r eceptor p otential Ca2+ channel subtype 6 (TRPC6) or the N-terminal domain of TRPC6 blocks carbachol-stimulated Ba2+ influx in PC12D cells. Expression of TRPC6 antisense RNA or the TRPC6 N-terminal domain also blocks Ba2+ influx stimulated by 1-oleoyl-2-acetyl- sn -glycerol (OAG), a diacylglycerol analog previously shown to activate exogenously expressed TRPC6 channels. These data show that mAChRs in PC12D cells activate endogenous Ca2+ channels that are regulated independently of Ca2+ stores and require the expression of TRPC6.
نوع الوثيقة: text
وصف الملف: text/html
اللغة: English
العلاقة: http://jb.oxfordjournals.org/cgi/content/short/139/3/459Test; http://dx.doi.org/10.1093/jb/mvj065Test
DOI: 10.1093/jb/mvj065
الإتاحة: https://doi.org/10.1093/jb/mvj065Test
http://jb.oxfordjournals.org/cgi/content/short/139/3/459Test
حقوق: Copyright (C) 2006, Japanese Biochemical Society
رقم الانضمام: edsbas.E852AAE3
قاعدة البيانات: BASE