Hung Johanna, Colicos Michael A
Department of Physiology and Biophysics and the Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.
PLoS One. 2008;3(11):e3692. doi: 10.1371/journal.pone.0003692. Epub 2008 Nov 12.
Activity plays a critical role in network formation during developmental, experience-dependent, and injury related remodeling. Here we report a mechanism by which axon trajectory can be altered in response to remote neuronal activity. Using photoconductive stimulation to trigger high frequency action potentials in rat hippocampal neurons in vitro, we find that activity functions as an attractive cue for growth cones in the local environment. The underlying guidance mechanism involves astrocyte Ca(2+) waves, as the connexin-43 antagonist carbenoxolone abolishes the attraction when activity is initiated at a distance greater than 120 microm. The asymmetric growth cone filopodia extension that precedes turning can be blocked with CNQX (10 microM), but not with the ATP and adenosine receptor antagonists suramin (100 microM) and alloxazine (4 microM), suggesting non-NMDA glutamate receptors on the growth cone mediate the interaction with astrocytes. These results define a potential long-range signalling pathway for activity-dependent axon guidance in which growth cones turn towards directional, temporally coordinated astrocyte Ca(2+) waves that are triggered by neuronal activity. To assess the viability of the guidance effect in an injury paradigm, we performed the assay in the presence of conditioned media from lipopolysaccharide (LPS) activated purified microglial cultures, as well as directly activating the glia present in our co-cultures. Growth cone attraction was not inhibited under these conditions, suggesting this mechanism could be used to guide regeneration following axonal injury.
在发育、经验依赖和损伤相关的重塑过程中,活动在网络形成中起着关键作用。在此,我们报告一种机制,通过该机制轴突轨迹可响应远程神经元活动而改变。利用光导刺激在体外触发大鼠海马神经元的高频动作电位,我们发现活动在局部环境中作为生长锥的一种吸引线索发挥作用。潜在的引导机制涉及星形胶质细胞的Ca(2+)波,因为当活动在大于120微米的距离处启动时,连接蛋白43拮抗剂卡贝缩酮消除了这种吸引力。在转向之前不对称的生长锥丝状伪足延伸可被CNQX(10微摩尔)阻断,但不能被ATP和腺苷受体拮抗剂苏拉明(100微摩尔)和咯嗪(4微摩尔)阻断,这表明生长锥上的非NMDA谷氨酸受体介导了与星形胶质细胞的相互作用。这些结果定义了一种潜在的依赖活动的轴突引导的长距离信号通路,其中生长锥转向由神经元活动触发的定向、时间协调的星形胶质细胞Ca(2+)波。为了评估在损伤模型中引导效应的可行性,我们在来自脂多糖(LPS)激活的纯化小胶质细胞培养物的条件培养基存在下进行了测定,以及直接激活我们共培养物中存在的胶质细胞。在这些条件下生长锥的吸引力没有受到抑制,这表明该机制可用于引导轴突损伤后的再生。