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Published Abstract
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Title: Determining the requirement of progenitor cells in stroke recovery
Author: Lee K, Carter A, Jeffers M, Cameron H, Corbett D, Lagace D
DOI: https://doi.org/10.1111/ijs.12633
Appeared in: International Journal of Stroke
Published: October 16, 2015
Please cite this abstract as: Lee K, Carter A, Jeffers M, Cameron H, Corbett D, Lagace D.
(2015). Determining the requirement of progenitor cells in stroke recovery. Int J Stroke,
10, 21.
This is a PDF file of an unedited abstract was published based on a poster presented at
the 6th Canadian Stroke Congress, September 17-19, 2015. All abstracts were collated
and published online in the International Journal of Stroke. The final publisher version of
this abstract can be viewed at the DOI provided above.
HP1.3: Determining the requirement of progenitor cells in stroke recovery
Lee K1, Carter A1, Jeffers M1, Cameron H2, Corbett D1,3, Lagace D1
1University of Ottawa, Ottawa, Canada
2National Institute of Health, Bethesda, USA
3Canadian Partnership for Stroke Recovery, Ottawa, Canada
Background: Preclinical rodent studies have shown post-stroke there is a significant
increase in the number of progenitor cells (PCs), ectopic migration of PCs, and a
correlation between increases in neurogenesis and improved recovery. Loss-of-
function studies have shown that PC ablation prior to stroke impedes recovery.
However, is it the PCs per se that are mediating recovery and do these PCs affect
motor and/or cognitive function? This study aims to determine if neurogenesis per
se is required during stroke recovery.
Methods: PCs were ablated using an unpublished GFAP-TK rat model that allows for
the inducible deletion of GFAP-expressing stem cells in the adult brain by treatment
with valganciclovir (vgcv). A stroke was produced through injection of ET-1, a
vasoconstrictive peptide, into the forelimb motor cortex and recovery was measured
using the staircase, cylinder and beam walk tests. Spatial learning and memory was
measured using the Barnes Maze.
Results: Treatment with vgcv in the GFAP-TK rats produced an ablation of PCs.
Control and GFAP-TK (vgcv treated) rats showed a similar amount of motor recovery
up to 7 weeks post-stroke. Control and GFAP-TK rats also showed no differences in
spatial learning and memory on the Barnes Maze at 1 week post-stroke. Histological
assessment of stroke volume is on-going, but preliminary findings show similar lesion
volumes between control and GFAP-TK rats.
Conclusions: The GFAP-TK rat model appears to be useful in order to ablate
neurogenesis and assess recovery from stroke. Rats without PCs prior to and following
the induction of stroke showed a similar pattern of motor recovery and spatial learning
and memory, suggesting that PCs are not required for either one of these tasks. These
results conflict with the few other published studies reporting that PCs are required for
motor and/or cognitive functioning, and suggest that neurogenesis may not mediate
innate recovery.
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