Exercise intensity influences cell injury in rat hippocampal slices exposed to oxygen and glucose deprivation

Scopel, Denise; Fochesatto, Cíntia; Cimarosti, Helena; Rabbo, Maristela Padilha de Souza; Belló‐Klein, Adriane; Salbego, Christianne Gazzana; Netto, Carlos Alexandre; Siqueira, Ionara Rodrigues

doi:10.1016/j.brainresbull.2006.08.011

Cited by 59 publications

(35 citation statements)

References 30 publications

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“…Each training session lasted 20 min because great improvements in physical fitness were found at this time (ASCM, 1998). The treadmill controls (0) were always habituated to the experimental room and handled as treadmill runners, but they were not submitted to the running protocol (adapted from Scopel et al, 2006). The treadmill controls were placed in the treadmill off 3 days/week during 20 min.…”

Section: Treadmill Exercise Protocolmentioning

confidence: 99%

The impact of the frequency of moderate exercise on memory and brain-derived neurotrophic factor signaling in young adult and middle-aged rats

et al. 2012

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Section: Treadmill Exercise Protocolmentioning

confidence: 99%

The impact of the frequency of moderate exercise on memory and brain-derived neurotrophic factor signaling in young adult and middle-aged rats

et al. 2012

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“…Training consisted of 20 min of running sessions on an adapted motorized rodent treadmill (INBRAMEDTK01, Porto Alegre, Brazil), three times per week [33]. Animals from the control group (sedentary) were transported to the experimental room, handled exactly as the exercised ones and maintained in the turned off treadmill for 20 min [34].…”

Section: Exercise Trainingmentioning

confidence: 99%

“…A moderate intensity exercise protocol was used [33][34][35], i.e., exercise intensity was set at 60% of animal's maximal oxygen uptake [36]. The oxygen uptake (VO 2 ) peak was estimated for all animals before training, considering the exhaustion, as follows: each rat ran on a treadmill at a low initial speed followed by increases in speed of 5 m/min every 3 min until the point of exhaustion (i.e., failure of the rats to continue running); the time to fatigue (in min) and workload (in m/min) were taken as indexes of exercise capacity, that was assigned as VO 2 max [36,37].…”

Section: Exercise Trainingmentioning

confidence: 99%

Physical Exercise Reverses Cognitive Impairment in Rats Subjected to Experimental Hyperprolinemia

et al. 2011

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This study investigated whether physical exercise would reverse proline-induced performance deficits in water maze tasks, as well as its effects on brain-derived neurotrophic factor (BDNF) immunocontent and brain acetylcholinesterase (AChE) activity in Wistar rats. Proline administration followed partial time (6th-29th day of life) or full time (6th-60th day of life) protocols. Treadmill exercise was performed from 30th to 60th day of life, when behavioral testing was started. After that, animals were sacrificed for BDNF and AChE determination. Results show that proline impairs cognitive performance, decreases BDNF in cerebral cortex and hippocampus and increases AChE activity in hippocampus. All reported effects were prevented by exercise. These results suggest that cognitive, spatial learning/memory, deficits caused by hyperprolinemia may be associated, at least in part, to the decrease in BDNF levels and to the increase in AChE activity, as well as support the role of physical exercise as a potential neuroprotective strategy.

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“…Studies have shown decreased expression of DNA methyltransferases [118] and increased expression of HAT [119] in the hippocampus of rats which exert their epigenetic influence by increasing the expression of neurotrophic factors in brain. Further evidence was provided by Scopel et al [120] by showing that exercise regime of 20 minutes for 2 weeks for wistar rat attenuates the damage in hippocampal slices submitted to ischemia in-vitro opening the field for further investigation.…”

Section: Introductionmentioning

confidence: 97%

Role of early life exposure and environment on neurodegeneration: implications on brain disorders

Modgil

Lahiri

Sharma

et al. 2014

Transl Neurodegener

108

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Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS) and retinal degeneration have been studied extensively and varying molecular mechanisms have been proposed for onset of such diseases. Although genetic analysis of these diseases has also been described, yet the mechanisms governing the extent of vulnerability to such diseases remains unresolved. Recent studies have, therefore, focused on the role of environmental exposure in progression of such diseases especially in the context of prenatal and postnatal life, explaining how molecular mechanisms mediate epigenetic changes leading to degenerative diseases. This review summarizes both the animal and human studies describing various environmental stimuli to which an individual or an animal is exposed during in-utero and postnatal period and mechanisms that promote neurodegeneration. The SNPs mediating gene environment interaction are also described. Further, preventive and therapeutic strategies are suggested for effective intervention.

show abstract

Exercise intensity influences cell injury in rat hippocampal slices exposed to oxygen and glucose deprivation

Cited by 59 publications

References 30 publications

The impact of the frequency of moderate exercise on memory and brain-derived neurotrophic factor signaling in young adult and middle-aged rats

The impact of the frequency of moderate exercise on memory and brain-derived neurotrophic factor signaling in young adult and middle-aged rats

Physical Exercise Reverses Cognitive Impairment in Rats Subjected to Experimental Hyperprolinemia

Role of early life exposure and environment on neurodegeneration: implications on brain disorders

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