Duan Bo, Cheng Longzhen, Bourane Steeve, Britz Olivier, Padilla Christopher, Garcia-Campmany Lidia, Krashes Michael, Knowlton Wendy, Velasquez Tomoko, Ren Xiangyu, Ross Sarah, Lowell Bradford B, Wang Yun, Goulding Martyn, Ma Qiufu
Dana-Farber Cancer Institute and Department of Neurobiology, Harvard Medical School, 1 Jimmy Fund Way, Boston, Massachusetts 02115, USA.
Institute of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China.
Cell. 2014 Dec 4;159(6):1417-1432. doi: 10.1016/j.cell.2014.11.003. Epub 2014 Nov 20.
Pain information processing in the spinal cord has been postulated to rely on nociceptive transmission (T) neurons receiving inputs from nociceptors and Aβ mechanoreceptors, with Aβ inputs gated through feed-forward activation of spinal inhibitory neurons (INs). Here, we used intersectional genetic manipulations to identify these critical components of pain transduction. Marking and ablating six populations of spinal excitatory and inhibitory neurons, coupled with behavioral and electrophysiological analysis, showed that excitatory neurons expressing somatostatin (SOM) include T-type cells, whose ablation causes loss of mechanical pain. Inhibitory neurons marked by the expression of dynorphin (Dyn) represent INs, which are necessary to gate Aβ fibers from activating SOM(+) neurons to evoke pain. Therefore, peripheral mechanical nociceptors and Aβ mechanoreceptors, together with spinal SOM(+) excitatory and Dyn(+) inhibitory neurons, form a microcircuit that transmits and gates mechanical pain. PAPERCLIP:
脊髓中的疼痛信息处理被假定依赖于伤害性传递（T）神经元，这些神经元接收来自伤害感受器和Aβ机械感受器的输入，其中Aβ输入通过脊髓抑制性神经元（INs）的前馈激活进行门控。在这里，我们使用交叉遗传操作来识别疼痛转导的这些关键成分。标记并消融六组脊髓兴奋性和抑制性神经元，结合行为和电生理分析，表明表达生长抑素（SOM）的兴奋性神经元包括T型细胞，其消融会导致机械性疼痛丧失。以强啡肽（Dyn）表达标记的抑制性神经元代表INs，它们是使Aβ纤维无法激活SOM（+）神经元以诱发疼痛所必需的。因此，外周机械性伤害感受器和Aβ机械感受器，与脊髓SOM（+）兴奋性和Dyn（+）抑制性神经元一起，形成了一个传递和控制机械性疼痛的微回路。回形针：
