Ikeda Hiroshi, Stark Johanna, Fischer Harald, Wagner Matthias, Drdla Ruth, Jäger Tino, Sandkühler Jürgen
Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.
Science. 2006 Jun 16;312(5780):1659-62. doi: 10.1126/science.1127233.
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 ( approximately 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.
炎症和创伤会导致痛觉敏感性增强（痛觉过敏），这部分是由于脊髓中感觉处理过程的改变。痛觉过敏的突触假说是，痛觉过敏是由脊髓中依赖活动的长时程增强（LTP）诱导产生的，但这一假说受到了挑战，因为在之前关于疼痛通路的研究中，LTP是通过高频（约100赫兹）神经刺激实验性诱导产生的。然而，这与炎症期间实际发生的低频传入神经冲动并不相似。我们在一条上行疼痛通路的起始处发现了一个突触放大器，它由伤害性神经纤维的低水平活动开启。该模型毫无矛盾地整合了已知的痛觉过敏信号转导通路。
