Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 109, Issue 35, Pages 14206-14211Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1119853109
Keywords
axon regeneration; cerebellum; neural development; lentiviral vectors
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Funding
- Centre National de la Recherche Scientifique
- Universite Pierre et Marie Curie [ANR-07-NEURO-043-01]
- International Foundation for Research in Paraplegia
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Neurons in the CNS of higher vertebrates lose their ability to regenerate their axons at a stage of development that coincides with peak circulating thyroid hormone (T-3) levels. Here, we examined whether this peak in T-3 is involved in the loss of axonal regenerative capacity in Purkinje cells (PCs). This event occurs at the end of the first postnatal week in mice. Using organotypic culture, we found that the loss of axon regenerative capacity was triggered prematurely by early exposure of mouse PCs to T-3, whereas it was delayed in the absence of T-3. Analysis of mutant mice showed that this effect was mainly mediated by the T-3 receptor alpha 1. Using gain- and loss-of-function approaches, we also showed that Kruppel-like factor 9 was a key mediator of this effect of T-3. These results indicate that the sudden physiological increase in T-3 during development is involved in the onset of the loss of axon regenerative capacity in PCs. This loss of regenerative capacity might be part of the general program triggered by T-3 throughout the body, which adapts the animal to its postnatal environment.
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