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Robust Axonal Regeneration Occurs in the Injured CAST/Ei Mouse CNS

  • Author(s): Omura, T
  • Omura, K
  • Tedeschi, A
  • Riva, P
  • Painter, MW
  • Rojas, L
  • Martin, J
  • Lisi, V
  • Huebner, EA
  • Latremoliere, A
  • Yin, Y
  • Barrett, LB
  • Singh, B
  • Lee, S
  • Crisman, T
  • Gao, F
  • Li, S
  • Kapur, K
  • Geschwind, DH
  • Kosik, KS
  • Coppola, G
  • He, Z
  • Carmichael, ST
  • Benowitz, LI
  • Costigan, M
  • Woolf, CJ
  • et al.

Axon regeneration in the CNS requires reactivating injured neurons' intrinsic growth state and enabling growth in an inhibitory environment. Using an inbred mouse neuronal phenotypic screen, we find that CAST/Ei mouse adult dorsal root ganglion neurons extend axons more on CNS myelin than the other eight strains tested, especially when pre-injured. Injury-primed CAST/Ei neurons also regenerate markedly in the spinal cord and optic nerve more than those from C57BL/6 mice and show greater sprouting following ischemic stroke. Heritability estimates indicate that extended growth in CAST/Ei neurons on myelin is genetically determined, and two whole-genome expression screens yield the Activin transcript Inhba as most correlated with this ability. Inhibition of Activin signaling in CAST/Ei mice diminishes their CNS regenerative capacity, whereas its activation in C57BL/6 animals boosts regeneration. This screen demonstrates that mammalian CNS regeneration can occur and reveals a molecular pathway that contributes to this ability. Omura et al. screened for neuronal growth on myelin and find CAST/Ei inbred mice are uniquely able to regenerate axons in the injured CNS through Activin signaling. Enhancing Activin signaling confers a CNS-regenerative capacity in normally non-regenerative mouse strains.

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