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000163651 0247_ $$2doi$$a10.1016/j.neuron.2021.10.007
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000163651 1001_ $$0P:(DE-2719)2812271$$aHilton, Brett J$$b0$$eFirst author$$udzne
000163651 245__ $$aAn active vesicle priming machinery suppresses axon regeneration upon adult CNS injury.
000163651 260__ $$aNew York, NY$$bElsevier$$c2022
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000163651 520__ $$aAxons in the adult mammalian central nervous system fail to regenerate after spinal cord injury. Neurons lose their capacity to regenerate during development, but the intracellular processes underlying this loss are unclear. We found that critical components of the presynaptic active zone prevent axon regeneration in adult mice. Transcriptomic analysis combined with live-cell imaging revealed that adult primary sensory neurons downregulate molecular constituents of the synapse as they acquire the ability to rapidly grow their axons. Pharmacogenetic reduction of neuronal excitability stimulated axon regeneration after adult spinal cord injury. Genetic gain- and loss-of-function experiments uncovered that essential synaptic vesicle priming proteins of the presynaptic active zone, but not clostridial-toxin-sensitive VAMP-family SNARE proteins, inhibit axon regeneration. Systemic administration of Baclofen reduced voltage-dependent Ca2+ influx in primary sensory neurons and promoted their regeneration after spinal cord injury. These findings indicate that functional presynaptic active zones constitute a major barrier to axon regeneration.
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000163651 650_7 $$2Other$$aBaclofen
000163651 650_7 $$2Other$$aMunc13
000163651 650_7 $$2Other$$aRIM1/2
000163651 650_7 $$2Other$$aactive zone
000163651 650_7 $$2Other$$aaxon injury
000163651 650_7 $$2Other$$aaxon regeneration
000163651 650_7 $$2Other$$aspinal cord injury
000163651 650_2 $$2MeSH$$aAnimals
000163651 650_2 $$2MeSH$$aAxons: metabolism
000163651 650_2 $$2MeSH$$aCentral Nervous System: metabolism
000163651 650_2 $$2MeSH$$aMammals
000163651 650_2 $$2MeSH$$aMice
000163651 650_2 $$2MeSH$$aNerve Regeneration: physiology
000163651 650_2 $$2MeSH$$aNeurons: metabolism
000163651 650_2 $$2MeSH$$aSpinal Cord Injuries: metabolism
000163651 7001_ $$0P:(DE-2719)2811971$$aHusch, Andreas$$b1$$udzne
000163651 7001_ $$0P:(DE-2719)2811123$$aSchaffran, Barbara$$b2$$udzne
000163651 7001_ $$0P:(DE-2719)2812342$$aLin, Tien-Chen$$b3$$udzne
000163651 7001_ $$0P:(DE-2719)9000509$$aBurnside, Emily R$$b4$$udzne
000163651 7001_ $$0P:(DE-2719)2810386$$aDupraz, Sebastian$$b5$$udzne
000163651 7001_ $$0P:(DE-2719)2811316$$aSchelski, Max$$b6$$udzne
000163651 7001_ $$0P:(DE-2719)2814235$$aKim, Jisoo$$b7$$udzne
000163651 7001_ $$0P:(DE-HGF)0$$aMüller, Johannes Alexander$$b8
000163651 7001_ $$0P:(DE-HGF)0$$aSchoch, Susanne$$b9
000163651 7001_ $$0P:(DE-HGF)0$$aImig, Cordelia$$b10
000163651 7001_ $$0P:(DE-HGF)0$$aBrose, Nils$$b11
000163651 7001_ $$0P:(DE-2719)2810270$$aBradke, Frank$$b12$$eLast author$$udzne
000163651 773__ $$0PERI:(DE-600)2001944-0$$a10.1016/j.neuron.2021.10.007$$gVol. 110, no. 1, p. 51 - 69.e7$$n1$$p51 - 69.e7$$tNeuron$$v110$$x0896-6273$$y2022
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