کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9425740 | 1295889 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Action of neuropeptide Y on nociceptive transmission in substantia gelatinosa of the adult rat spinal dorsal horn
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
DRGguanosine-5′-O-(2-thiodiphosphate)HEPESGDP-β-SEGTABIBP 3226mIPSCSTTsEPSCNPYmEPSCTTXdorsal root ganglion - گانگلیون ریشه پشتی6-Cyano-7-nitroquinoxaline-2,3-dione - 6-Cyano-7-nitroquinoxaline-2،3-dioneEPSC - EPSCoRImmunoreactivity - ایمنی فعالTetraethylammonium - تترا اتیل آمونیومtetrodotoxin - تترو دوتوکسین spontaneous excitatory postsynaptic current - جریان Post-synaptic جبری خودبخودیminiature inhibitory postsynaptic current - جریان ممانعت کننده پستانیپتیک مینیاتوریexcitatory postsynaptic current - جریان پستیینپتیک تحریک کنندهminiature excitatory postsynaptic current - جریان پستیینپتیک مضر تحریک آمیزCNS - دستگاه عصبی مرکزیConduction velocity - سرعت هدایتSomatostatin - سوماتواستاتینCNQX - سیانکیوایکسcentral nervous system - سیستم عصبی مرکزیAntinociception - ضد انعقادsubstantia gelatinosa - محرک ژلاتینوزاnoradrenaline - نورآدرنالین TEA - چایNeuropeptide Y - یوروپروتئین Y
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Effects of neuropeptide Y (NPY) on substantia gelatinosa neurons were investigated in adult rat spinal cord slices using blind whole-cell patch-clamp technique. Bath application of NPY (1μM) induced a membrane hyperpolarization, resulting in a suppression of the dorsal root stimulation-induced action potentials in 24% of the substantia gelatinosa neurons tested. In voltage clamp mode, NPY produced an outward current dose-dependently in about one third of substantia gelatinosa neurons at the holding potential of â60 mV, which was not affected by tetrodotoxin (1μM). The NPY-induced current was suppressed by perfusion with a Ba2+-containing external solution and a Cs2SO4 or tetraethylammonium-containing pipette solution. In addition, The NPY-induced outward currents reversed its polarity near the equilibrium potential of K+ ions (â93 mV). The response to NPY recorded with guanosine-5â²-O-(2-thiodiphosphate)-β-S (GDP-β-S) containing pipette solution was abolished 30 min after patch formation, suggesting that the response was mediated by the G-protein-coupled receptors. Application of an NPY-Y1 selective agonist, [Leu31, Pro-34]-NPY (1μM), for 30 s also induced an outward current with a similar time course and amplitude to that induced by NPY. On the other hand, the NPY response was blocked by a simultaneous application of NPY-Y1 selective antagonist, BIBP 3226 (1μM). No significant changes were found in amplitude and frequency of miniature excitatory postsynaptic currents and dorsal root evoked excitatory postsynaptic currents by NPY. In addition, NPY did not affect both of the miniature inhibitory postsynaptic currents and evoked inhibitory postsynaptic currents, mediated by either the GABA or glycine receptor. These findings, taken together, suggest that NPY produces an outward current in substantia gelatinosa neurons through G-protein coupled, and NPY-Y1 receptor-mediated activation of K+ channels without affecting presynaptic components. The inhibition of the synaptic transmission from the primary fibers to the substantia gelatinosa neurons is considered to contribute to the antinociceptive effects of NPY.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 134, Issue 2, 2005, Pages 595-604
Journal: Neuroscience - Volume 134, Issue 2, 2005, Pages 595-604
نویسندگان
A. Miyakawa, H. Furue, T. Katafuchi, N. Jiang, T. Yasaka, G. Kato, M. Yoshimura,