Treadmill running improves motor function and alters dendritic morphology in the striatum after collagenase-induced intracerebral hemorrhage in rats

Takamatsu, Yasuyuki; Ishida, Atsushi; Hamakawa, Michiru; Tamakoshi, Keigo; Jung, Cha-Gyun; Ishida, Kenji

doi:10.1016/j.brainres.2010.07.070

Cited by 32 publications

(22 citation statements)

References 45 publications

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“…Analysis was performed by a customized Sholl analysis plug-in (Available at: http://www.biology.ucsd.edu/labs/ghosh/software/index.html) for ImageJ software (National Institutes of Health, Bethesda, MD, USA). As shown in Figure 1, concentric rings of increasing radius equivalent to 10 µm apart were used, and the numbers of intersections of the dendritic branches with each concentric ring were recorded [19].…”

Section: Methodsmentioning

confidence: 99%

Effects of Exercise Intensity on Spatial Memory Performance and Hippocampal Synaptic Plasticity in Transient Brain Ischemic Rats

Shih

Yang²,

Wang³

2013

PLoS ONE

100

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Memory impairment is commonly noted in stroke survivors, and can lead to delay of functional recovery. Exercise has been proved to improve memory in adult healthy subjects. Such beneficial effects are often suggested to relate to hippocampal synaptic plasticity, which is important for memory processing. Previous evidence showed that in normal rats, low intensity exercise can improve synaptic plasticity better than high intensity exercise. However, the effects of exercise intensities on hippocampal synaptic plasticity and spatial memory after brain ischemia remain unclear. In this study, we investigated such effects in brain ischemic rats. The middle cerebral artery occlusion (MCAO) procedure was used to induce brain ischemia. After the MCAO procedure, rats were randomly assigned to sedentary (Sed), low-intensity exercise (Low-Ex), or high-intensity exercise (High-Ex) group. Treadmill training began from the second day post MCAO procedure, 30 min/day for 14 consecutive days for the exercise groups. The Low-Ex group was trained at the speed of 8 m/min, while the High-Ex group at the speed of 20 m/min. The spatial memory, hippocampal brain-derived neurotrophic factor (BDNF), synapsin-I, postsynaptic density protein 95 (PSD-95), and dendritic structures were examined to document the effects. Serum corticosterone level was also quantified as stress marker. Our results showed the Low-Ex group, but not the High-Ex group, demonstrated better spatial memory performance than the Sed group. Dendritic complexity and the levels of BDNF and PSD-95 increased significantly only in the Low-Ex group as compared with the Sed group in bilateral hippocampus. Notably, increased level of corticosterone was found in the High-Ex group, implicating higher stress response. In conclusion, after brain ischemia, low intensity exercise may result in better synaptic plasticity and spatial memory performance than high intensity exercise; therefore, the intensity is suggested to be considered during exercise training.

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Section: Methodsmentioning

confidence: 99%

Effects of Exercise Intensity on Spatial Memory Performance and Hippocampal Synaptic Plasticity in Transient Brain Ischemic Rats

Shih

Yang²,

Wang³

2013

PLoS ONE

100

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“…Furthermore, MAP-2 plays in the growth, differentiation, and plasticity of neurons, with key roles in neuronal responses to growth factors, neurotransmitters, synaptic activity, and neurotoxins [30, 45]. The increase of MAP-2-positive dendrites is connected with neural activity regeneration after injury cerebrovascular [17, 46], and dendritic morphological changes may be involved in motor learning [21]. Since modification and rearrangement of MAP-2 are obligatory steps in many processes that modify neuronal function, we decided to investigate the effects of skilled and unskilled training after ICH on functional recovery and MAP-2 expression.…”

Section: Discussionmentioning

confidence: 99%

“…It was demonstrated that treadmill running training improves motor function after ICH, and this improvement may be related to changes in dendritic morphology in the striatum [21]. Still, previous studies found that synapse formation in the motor cortex begins immediately when learning a new task [22].…”

Section: Introductionmentioning

confidence: 99%

Motor Skill Training Promotes Sensorimotor Recovery and Increases Microtubule-Associated Protein-2 (MAP-2) Immunoreactivity in the Motor Cortex after Intracerebral Hemorrhage in the Rat

et al. 2013

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Motor skill learning may induce behavioral and neurophysiological adaptations after intracerebral hemorrhage (ICH). Learning a new motor skill is associated with dendritic reorganization and requires protein synthesis and expression of MAP-2. The purpose of this study was to evaluate motor performance and expression of MAP-2 in the motor cortex of rats submitted to intracerebral hemorrhage model (ICH) and skill task training (SK) or unskilled training (US) during 4 weeks. The Staircase test was used for behavioral evaluation, and relative optical densities and morphometrical analysis were used to estimate MAP-2 immunoreactivity and parameters of brain tissue in both motor cortices. Results show that skill task training performed with the impaired forelimb was able to increase MAP-2 immunoreactivity in the motor cortex either in sham or in ICH groups in both cortices: ipsilesional [F (5,35) = 14.25 (P < 0.01)] and contralesional hemispheres [F (5,35) = 9.70 (P < 0.01)]. ICH alone also increased MAP-2 immunoreactivity despite the absence of functional gains. Behavioral evaluation revealed that ICH-SK group performed better than ICH and ICH-US animals in the Staircase test. Data suggest that motor skill training induces plastic modifications in both motor cortices, either in physiological or pathological conditions and that skill motor training produces higher brain plasticity and positive functional outcomes than unskilled training after experimental intracerebral hemorrhage.

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“…Work in rat ICH has shown promising beneficial effect of exercise on functional recovery (MacLellan et al 2011; Tamakoshi et al 2014; Takamatsu et al 2010), but less is known in mouse models. Jin and colleagues tested exercise in a mouse model of collagenase-induced ICH and found that mice that received voluntary exercise showed increased proliferation and survival of neural progenitor cells (NPCs), with migration of cells to the injured site in comparison with no exercise mice.…”

Section: Transgenic Mouse Studiesmentioning

confidence: 99%

Intracerebral hemorrhage in mouse models: therapeutic interventions and functional recovery

Kathirvelu

Carmichael

2014

Metab Brain Dis

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There has been strong pre-clinical research on mechanisms of initial cell death and tissue injury in intracerebral hemorrhage (ICH). This data has led to the evaluation of several therapeutics for neuroprotection or the mitigation of early tissue damage. Most of these studies have been done in the rat. Also, there has been little study of the mechanisms of tissue repair and recovery. This review examines the testing of candidate therapeutics in mouse models of ICH for their effect on tissue protection and repair. This review will help the readers compare it to the extensively researched rat model of ICH and thus enhance work that are pending in mouse model.

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Treadmill running improves motor function and alters dendritic morphology in the striatum after collagenase-induced intracerebral hemorrhage in rats

Cited by 32 publications

References 45 publications

Effects of Exercise Intensity on Spatial Memory Performance and Hippocampal Synaptic Plasticity in Transient Brain Ischemic Rats

Effects of Exercise Intensity on Spatial Memory Performance and Hippocampal Synaptic Plasticity in Transient Brain Ischemic Rats

Motor Skill Training Promotes Sensorimotor Recovery and Increases Microtubule-Associated Protein-2 (MAP-2) Immunoreactivity in the Motor Cortex after Intracerebral Hemorrhage in the Rat

Intracerebral hemorrhage in mouse models: therapeutic interventions and functional recovery

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