生物谷报道：炎症和创伤能增加一个人对疼痛的敏感性，部分地因为发炎能改变脊髓如何处理疼痛感。Hiroshi Ikeda和奥地利的同事 现在发现了脊髓中的一个疼痛“放大器”，它能被模仿炎症的低水平和无规律的疼痛输入启动。这种无规律的疼痛输入能提高脊髓中感觉疼痛的神经元的钙离子水平，导致长时程增强(LTP)或突触强度的增强，这也许会改变这些神经元与疼痛通路下一步的其它脊髓神经元的最初关键突触。研究人员说，突触的变化放大了疼痛信号，潜在地增加了一个人对疼痛的敏感性。最新的Science上报道这一研究成果。
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 (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.
原始出处：
Synaptic Amplifier of Inflammatory Pain in the Spinal Dorsal Horn.
H. Ikeda, J. Stark, H. Fischer, M. Wagner, R. Drdla, T. Jager, and J. Sandkuhler (2006).
Science 312: 1659-1662 | Abstract » | Full Text » | PDF »
