Action of neuropeptide Y on nociceptive transmission in substantia gelatinosa of the adult rat spinal dorsal horn
Action of neuropeptide Y on nociceptive transmission in substantia gelatinosa of the adult rat spinal dorsal horn
复制标题
DOI：
10.1016/j.neuroscience.2005.04.045
复制
发表时间：
2005-01-01
期刊：
影响因子：
3.3
通讯作者：
Yoshimura, M
中科院分区：
文献类型：
--
作者：
Miyakawa, A;Furue, H;Yoshimura, M
采用全细胞膜片钳技术，观察了神经肽Y（NPY）对大鼠脊髓胶状质神经元的作用。浴应用神经肽Y（1 μ M）诱导膜超极化，导致抑制背根刺激诱导的动作电位在24%的胶状质神经元测试。在电压钳模式下，NPY在-60 mV的保持电位下，在约三分之一的胶状质神经元中产生剂量依赖性的外向电流，这不受河豚毒素（1 μ M）的影响。NPY诱导的电流被抑制灌流与Ba 2 +-含有外部解决方案和Cs2 SO 4或四乙基铵含有移液管解决方案。在K+平衡电位附近（-93 mV），NPY诱导的外向电流极性发生逆转。用含有鸟苷-5 '-O-（2-硫代二磷酸）-β-S（GDP-β-S）的移液器溶液记录的对NPY的反应在贴片形成后30分钟被消除，表明该反应由G蛋白偶联受体介导。应用NPY-Y1选择性激动剂[Leu（31），Pro（-34）]-NPY（1 μ M）30 s也诱导了一个外向电流，其时程和幅度与NPY诱导的电流相似。另一方面，通过同时应用NPY-Y1选择性拮抗剂BIBP 3226（1 μ M）阻断NPY反应。NPY对微小兴奋性突触后电流和背根诱发兴奋性突触后电流的幅度和频率无明显影响。此外，NPY不影响由GABA或甘氨酸受体介导的微型抑制性突触后电流和诱发抑制性突触后电流。这些发现，综合起来，表明，NPY产生一个外向电流在胶状质神经元通过G-蛋白偶联，和NPY-Y1受体介导的K+通道的激活，而不影响突触前组件。抑制初级纤维向胶状质神经元的突触传递被认为有助于NPY的抗伤害性感受作用。(c)2005由Elsevier Ltd代表IBRO出版。
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 (1 mu M) 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 -60 mV, which was not affected by tetrodotoxin (1 mu M). 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 (-93 mV). The response to NPY recorded with guanosine-5'-O-(2-thiodiphosphate)-beta-S (GDP-beta-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, [Leu(31), Pro(-34)]-NPY (1 mu M), 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 (1 mu M). 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. (c) 2005 Published by Elsevier Ltd on behalf of IBRO.