Synaptic amplifier of inflammatory pain in the spinal dorsal horn
Synaptic amplifier of inflammatory pain in the spinal dorsal horn
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DOI：
10.1126/science.1127233
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发表时间：
2006-06-16
期刊：
影响因子：
56.9
通讯作者：
Sandkuhler, Jurgen
中科院分区：
文献类型：
--
作者：
Ikeda, Hiroshi;Stark, Johanna;Sandkuhler, Jurgen
炎症和创伤导致疼痛敏感性增强（痛觉过敏），这部分是由于脊髓中感觉处理的改变。痛觉过敏的突触假说认为痛觉过敏是由脊髓中的活动依赖性长时程增强（activity-dependent long-term potentiation，LTP）引起的，但这一假说受到了挑战，因为在以往的疼痛通路研究中，LTP是由高频（类似于100赫兹）神经刺激引起的。然而，这并不像炎症时发生的真实的低频传入阻滞。我们发现了一个突触放大器的起源，一个上行疼痛通路，是开关上的低水平活动的伤害性神经纤维。该模型整合了已知的痛觉过敏信号转导通路，没有矛盾。
Inflammation and trauma lead to enhanced pain sensitivity ( hyperalgesia), which is in part due to altered sensory processing in the spinal cord. The synaptic hypothesis of hyperalgesia, which postulates that hyperalgesia is induced by the activity-dependent long-term potentiation (LTP) in the spinal cord, has been challenged, because in previous studies of pain pathways, LTP was experimentally induced by nerve stimulation at high frequencies (similar to 100 hertz). This does not, however, resemble the real low-frequency afferent barrage that occurs during inflammation. We identified a synaptic amplifier at the origin of an ascending pain pathway that is switched-on by low-level activity in nociceptive nerve fibers. This model integrates known signal transduction pathways of hyperalgesia without contradiction.