Abstract
IntroductionExercise therapies during rehabilitation significantly promote recovery from various deficits after cerebral infarction, which is mediated by neuronal plasticity with distinct inputs. Although adult neurogenesis can also be modulated by neuronal activity before synaptogenesis, how distinct exercises contribute to the neurological reorganization of the injured cerebral cortex remains unclear. In the present study, we aimed to elucidate the effects of different exercise therapies on motor recovery and neuronal reorganization after photochemically induced focal cerebral infarction.MethodsHere, we examined the effects of three different exercises—(a) forced lower‐intensity and (b) higher‐intensity treadmill exercises, and (c) voluntary exercise with wheel running—on motor recovery and adult neurogenesis in a rat model of focal cerebral infarction. Photochemically induced thrombosis (PIT) was used to generate focal infarction in rats that was mostly confined to their motor cortices.ResultsBeam walking tests showed that recovery after PIT‐induced cortical infarction differed in acute and chronic stages and was influenced by the type of exercise. Furthermore, forced low‐intensity training had more positive effects on functional recovery than other exercises or control. To evaluate the production of newly generated cells including de novo neurogenesis, we performed lineage analysis with BrdU labeling and immunofluorescence experiments. Lower‐intensity treadmill exercise increased the number of BrdU/NeuN colabeled cells, but not total BrdU‐retaining or BrdU/Sox2‐colabeled cells, in the peri‐infarct region of the ipsilateral cortex. In contrast, high‐intensity treadmill or voluntary exercises had the opposite effects.ConclusionsThese results suggest that neuronal maturation can be differently modulated by distinct exercises and that low‐intensity treadmill exercise could result in more potent generation of mature neurons. This also suggests the possibility that the generation of neural stem/progenitor cells and differentiation might be modulated by rehabilitation‐mediated neural plasticity.
Highlights
Exercise therapies during rehabilitation significantly promote recovery from various deficits after cerebral infarction, which is mediated by neuronal plasticity with distinct inputs
In the current study, we examined the effects of different exercise programs on motor recovery after focal cerebral infarction caused by photochemically induced thrombosis (PIT)
To understand the mechanisms underlying the exercise-mediated recovery of motor functions and neuronal plasticity in local neuronal circuits, we developed a rat model of focal cerebral infarction in the motor area using Photochemically induced thrombosis (PIT)
Summary
During the rehabilitation period after a stroke, physical exercise plays a significant role in recovery from various deficits including motor dysfunction, which is mediated by neuronal plasticity (Nudo, 2013). Different exercises are believed to be accompanied by distinct activities of sensory motor circuits to affect neuronal plasticity. There is accumulating evidence that different types of physical exercises such as forced and voluntary running can affect recovery from motor or memory dysfunction (Choi et al, 2018; Cotman, Berchtold, & Christie, 2007; So et al, 2017). Central nervous system (CNS) injury often induces the generation of different types of cells derived from resident neural stem cells, which can reduce tissue damage and facilitate functional recovery (Sabelstrom et al, 2013). In the current study, we examined the effects of different exercise programs (forced exercise by treadmill running with lower- and higher-intensity and voluntary exercise with wheel running) on motor recovery after focal cerebral infarction caused by photochemically induced thrombosis (PIT). We assessed whether these exercises could affect the distribution of newly generated cells 4 weeks after injury
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