Glia instruct axon regeneration via a ternary modulation of neuronal calcium channels in Drosophila

Shannon Trombley, Jackson Powell, Pavithran Guttipatti, Andrew Matamoros, Xiaohui Lin, Tristan O’Harrow, Tobias Steinschaden, Leann Miles, Qin Wang, Shuchao Wang, Jingyun Qiu, Qingyang Li, Feng Li () and Yuanquan Song ()
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Shannon Trombley: The Children’s Hospital of Philadelphia
Jackson Powell: The Children’s Hospital of Philadelphia
Pavithran Guttipatti: The Children’s Hospital of Philadelphia
Andrew Matamoros: The Children’s Hospital of Philadelphia
Xiaohui Lin: Fudan University
Tristan O’Harrow: The Children’s Hospital of Philadelphia
Tobias Steinschaden: The Children’s Hospital of Philadelphia
Leann Miles: The Children’s Hospital of Philadelphia
Qin Wang: The Children’s Hospital of Philadelphia
Shuchao Wang: The Children’s Hospital of Philadelphia
Jingyun Qiu: The Children’s Hospital of Philadelphia
Qingyang Li: Fudan University
Feng Li: Fudan University
Yuanquan Song: The Children’s Hospital of Philadelphia

Nature Communications, 2023, vol. 14, issue 1, 1-18

Abstract: Abstract 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.

Date: 2023
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DOI: 10.1038/s41467-023-42306-2

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