轴突
轴突切开术
神经科学
再生(生物学)
神经元
细胞生物学
生物
神经胶质
化学
中枢神经系统
作者
Shannon Trombley,Jackson Powell,Pavithran Guttipatti,Andrew J. Matamoros,Xiaohui Lin,Tristan C D G O'Harrow,Tobias Steinschaden,Leann Miles,Qin Wang,Shuchao Wang,Jingyun Qiu,Qingyang Li,Feng Li,Yuanquan Song
标识
DOI:10.1038/s41467-023-42306-2
摘要
A neuron's regenerative capacity is governed by its intrinsic and extrinsic environment. Both peripheral and central neurons exhibit cell-type-dependent axon regeneration, but the underlying mechanism is unclear. Glia provide a milieu essential for regeneration. However, the routes of glia-neuron signaling remain underexplored. Here, we show that regeneration specificity is determined by the axotomy-induced Ca2+ transients only in the fly regenerative neurons, which is mediated by L-type calcium channels, constituting the core intrinsic machinery. Peripheral glia regulate axon regeneration via a three-layered and balanced modulation. Glia-derived tumor necrosis factor acts through its neuronal receptor to maintain calcium channel expression after injury. Glia sustain calcium channel opening by enhancing membrane hyperpolarization via the inwardly-rectifying potassium channel (Irk1). Glia also release adenosine which signals through neuronal adenosine receptor (AdoR) to activate HCN channels (Ih) and dampen Ca2+ transients. Together, we identify a multifaceted glia-neuron coupling which can be hijacked to promote neural repair.
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