Citation

Paniagua-Torija B, Arevalo-Martin A, Molina-Holgado E, Molina-Holgado F, Garcia-Ovejero D. Neuroscience 2014; 284C: 283-289.

Affiliation

Laboratory of Neuroinflammation, Unidad de Neurologia Experimental, Hospital Nacional de Paraplejicos (SESCAM), 45071 Toledo, Spain. Electronic address: dgarciao@sescam.jccm.es.

Copyright

(Copyright © 2014, International Brain Research Organization, Publisher Elsevier Publishing)

DOI

10.1016/j.neuroscience.2014.10.013

PMID

25453765

Abstract

Under inflammatory conditions, interleukin-1β (IL-1β) modulates neural stem cells at neurogenic niches. Here we show that spinal cord injury in rats increases IL-1β expression in astrocytes located around the spinal cord ependyma, a region that also holds a neurogenic potential. IL-1β increases from day 1 after lesion, reaches maximal levels between days 3 and 7, and declines from 14days to low levels after 28days. At the time of maximal expression, periependymal upregulation of IL-1β extends beyond 5mm from the epicenter of the lesion both rostral and caudally. Since IL-1β controls proliferation and cell fate of neural stem/precursor cells, its modulation in periependymal astrocytes might create an appropriate environment for cell replacement after injury.

Language: en