کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9426415 | 1295920 | 2005 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The TRPV1/2/3 activator 2-aminoethoxydiphenyl borate sensitizes native nociceptive neurons to heat in wildtype but not TRPV1 deficient mice
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کلمات کلیدی
DRGTRPV2TRPV32-aminoethoxydiphenyl borate2-APBCMHTRPVCGRPSIFHEPESTrpCMC4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid - 4- (2-hydroxyethyl) -1-piperazineethanesulfonic acidsynthetic interstitial fluid - مایع بینابینی مصنوعیwildtype - نوع وحشیcalcitonin gene-related peptide - پپتید مرتبط با ژن کلسی تونینTransient receptor potential channel - کانال بالقوه گیرنده گذراdorsal root ganglia - گانگلیس ریشه پشتیCapsaicin receptor - گیرنده کپسی سایین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
TRPV1 gene disruption results in a loss of capsaicin and proton responsiveness, but has minimal effects on heat-induced nocifensive behavior, suggesting that sensory transduction of heat is independent of TRPV1. TRPV3, another heat-activated ion channel but insensitive to capsaicin, was shown to be expressed in keratinocytes as well as in sensory neurons projecting to the skin. Recently, 2-aminoethoxydiphenyl borate was introduced as a TRPV3 agonist, but its selectivity was questioned by showing that it activated recombinant TRPV1 and TRPV2 as well. We used the isolated mouse skin-saphenous nerve preparation and whole-cell patch-clamping of cultured dorsal root ganglia neurons from TRPV1â/â and wildtype mice. We found no phenotypic differences between the heat responses of polymodal C-fibers, whereas cultured dorsal root ganglia neurons of TRPV1â/â hardly showed any heat-activated currents. Only C-fibers of wildtype but not TRPV1â/â mice were clearly sensitized to heat by 2-aminoethoxydiphenyl borate 10 and 100 μM; heat-activated current in wildtype neurons was only facilitated at 100 μM. Noxious heat-induced calcitonin gene-related peptide release showed clear deficits (<50%) in TRPV1 deficient skin, but the stimulated calcitonin gene-related peptide release from the isolated skull dura was unaffected. In both models, 2-aminoethoxydiphenyl borate was able to potentiate the heat response (46°C, 5 min) in a concentration-dependent manner, again, only in wildtype but not TRPV1â/â mice, suggesting that TRPV2/3 are not involved in this sensitization to heat. The results further suggest that TRPV1 is not responsible for the normal heat response of native nociceptors but plays the essential role in thermal sensitization and a prominent one in controlling dermal calcitonin gene-related peptide release, i.e. neurogenic inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 135, Issue 4, 2005, Pages 1277-1284
Journal: Neuroscience - Volume 135, Issue 4, 2005, Pages 1277-1284
نویسندگان
K. Zimmermann, A. Leffler, M.M.J. Fischer, K. Messlinger, C. Nau, P.W. Reeh,