Article

The positive correlation between therapeutic exercise and memory
recovery in cases of ischemia has been extensively studied; however, long-term
exercise begun after ischemic neuronal death as a chronic neurorestorative
strategy has not yet been thoroughly examined. OBJECTIVE: The purpose of this
study is to investigate possible mechanisms by which exercise ameliorates
ischemia-induced memory impairment in the aged gerbil hippocampus after transient
cerebral ischemia. METHODS: Treadmill exercise was begun 5 days after
ischemia-reperfusion (I-R) and lasted for 1 or 4 weeks. The animals were
sacrificed 31 days after the induction of ischemia. Changes in short-term memory,
as well as the hippocampal expression of markers of cell proliferation,
neuroblast differentiation, neurogenesis, myelin and microvessel repair, and
growth factors were examined by immunohistochemistry and/or western blots.
RESULTS: Four weeks of exercise facilitated memory recovery despite neuronal
damage in the stratum pyramidale (SP) of the hippocampal CA1 region and in the
polymorphic layer (PoL) of the dentate gyrus (DG) after I-R. Long-term exercise
enhanced cell proliferation and neuroblast differentiation in a time-dependent
manner, and newly generated mature cells were found in the granule cell layer of
the DG, but not in the SP of the CA1 region or in the PoL of the DG. In addition,
long-term exercise ameliorated ischemia-induced damage of myelin and
microvessels, which was correlated with increased BDNF expression in the CA1
region and the DG. CONCLUSIONS: These results suggest that long-term treadmill
exercise after I-R can restore memory function through replacement of multiple
damaged structures in the ischemic aged hippocampus.
CI - (c) The Author(s) 2016.

Langue : ANGLAIS