生物谷報(bào)道：炎癥和創(chuàng)傷能增加一個(gè)人對(duì)疼痛的敏感性,，部分地因?yàn)榘l(fā)炎能改變脊髓如何處理疼痛感,。Hiroshi Ikeda和奧地利的同事 現(xiàn)在發(fā)現(xiàn)了脊髓中的一個(gè)疼痛“放大器”，它能被模仿炎癥的低水平和無規(guī)律的疼痛輸入啟動(dòng),。這種無規(guī)律的疼痛輸入能提高脊髓中感覺疼痛的神經(jīng)元的鈣離子水平,，導(dǎo)致長時(shí)程增強(qiáng)(LTP)或突觸強(qiáng)度的增強(qiáng),，這也許會(huì)改變這些神經(jīng)元與疼痛通路下一步的其它脊髓神經(jīng)元的最初關(guān)鍵突觸,。研究人員說,，突觸的變化放大了疼痛信號(hào)，潛在地增加了一個(gè)人對(duì)疼痛的敏感性,。最新的Science上報(bào)道這一研究成果,。
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.
原始出處：
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 »
