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

نویسندگان

  • Takao Omura
  • Kumiko Omura
  • Andrea Tedeschi
  • Priscilla Riva
  • Michio W. Painter
  • Leticia Rojas
  • Joshua Martin
  • Véronique Lisi
  • Eric A. Huebner
  • Alban Latremoliere
  • Yuqin Yin
  • Lee B. Barrett
  • Bhagat Singh
  • Stella Lee
  • Tom Crisman
  • Fuying Gao
  • Songlin Li
  • Kush Kapur
  • Daniel H. Geschwind
  • Kenneth S. Kosik
  • Giovanni Coppola
  • Zhigang He
  • S. Thomas Carmichael
  • Larry I. Benowitz
  • Michael Costigan
  • Clifford J. Woolf
چکیده

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.

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عنوان ژورنال:
  • Neuron

دوره 86  شماره 

صفحات  -

تاریخ انتشار 2015