RT Journal Article
SR Electronic
T1 Axonal Localization of Integrins in the CNS Is Neuronal Type and Age Dependent
JF eneuro
JO eneuro
FD Society for Neuroscience
SP ENEURO.0029-16.2016
DO 10.1523/ENEURO.0029-16.2016
VO 3
IS 4
A1 Melissa R. Andrews
A1 Sara Soleman
A1 Menghon Cheah
A1 David A. Tumbarello
A1 Matthew R. J. Mason
A1 Elizabeth Moloney
A1 Joost Verhaagen
A1 Jean-Charles Bensadoun
A1 Bernard Schneider
A1 Patrick Aebischer
A1 James W. Fawcett
YR 2016
UL http://www.eneuro.org/content/3/4/ENEURO.0029-16.2016.abstract
AB The regenerative ability of CNS axons decreases with age, however, this ability remains largely intact in PNS axons throughout adulthood. These differences are likely to correspond with age-related silencing of proteins necessary for axon growth and elongation. In previous studies, it has been shown that reintroduction of the α9 integrin subunit (tenascin-C receptor, α9) that is downregulated in adult CNS can improve neurite outgrowth and sensory axon regeneration after a dorsal rhizotomy or a dorsal column crush spinal cord lesion. In the current study, we demonstrate that virally expressed integrins (α9, α6, or β1 integrin) in the adult rat sensorimotor cortex and adult red nucleus are excluded from axons following neuronal transduction. Attempts to stimulate transport by inclusion of a cervical spinal injury and thus an upregulation of extracellular matrix molecules at the lesion site, or cotransduction with its binding partner, β1 integrin, did not induce integrin localization within axons. In contrast, virally expressed α9 integrin in developing rat cortex (postnatal day 5 or 10) demonstrated clear localization of integrins in cortical axons revealed by the presence of integrin in the axons of the corpus callosum and internal capsule, as well as in the neuronal cell body. Furthermore, examination of dorsal root ganglia neurons and retinal ganglion cells demonstrated integrin localization both within peripheral nerve as well as dorsal root axons and within optic nerve axons, respectively. Together, our results suggest a differential ability for in vivo axonal transport of transmembrane proteins dependent on neuronal age and subtype.