Abstract:While it is well established that exercise can improve cognitive performance, it is unclear how long these benefits endure after exercise has ended. Accordingly, the effects of voluntary exercise on cognitive function and brain-derived neurotrophic factor (BDNF) protein levels, a major player in the mechanisms governing the dynamics of memory formation and storage, were assessed immediately after a 3-week running period, or after a 1-week or 2-week delay following the exercise period. All exercised mice showed… Show more
“…Unlimited access to voluntary wheel running generally improves memory in C57BL/6J mice [36,37]. The lack of behavioural and cognitive effects of intermittent wheel running in our study raises the question of whether there are optimal levels of exercise for behavioural changes to occur.…”
Section: Intermittent Voluntary Wheel Running Does Not Alter Behavioumentioning
Number of tables: 1Number of words in the abstract: 248Number of words in the manuscript (including tables and figure legends): 6,639Number of words in the introduction: 1,290Number of words in the discussion: 1,243 ABSTRACT Physical exercise can improve cognition but whether this is related to motivation levels is unknown. Voluntary wheel running is a rewarding activity proposed as a model of motivation to exercise. To question the potential effects of exercise motivation on subsequent behaviour, we used a pharmacological approach targeting some reward mechanisms. The stress hormone corticosterone has rewarding effects mediated by activation of low affinity glucocorticoid receptors (GR). To investigate whether corticosterone synthesis motivates exercise via activation of GRs and subsequently, impacts on behaviour, we treated C57BL/6J mice acutely with the inhibitor of corticosterone synthesis metyrapone (35 mg/kg) or repeatedly with the GR antagonist mifepristone (30 mg/kg) prior to 1-hour running wheel sessions. To investigate whether reducing motivation to exercise impacts on behaviour, we antagonised running-induced dopamine D2/D3 receptors activation with sulpiride (25 or 50 mg/kg) and assessed locomotor, anxiety-related and memory performance after 20 running sessions over 4 weeks. We found that corticosterone synthesis contributes to running levels, but the maintenance of running behaviour was not mediated by activation of GRs. Intermittent exercise was not associated with changes in behavioural or cognitive performance. The persistent reduction in exercise levels triggered by sulpiride also had limited impact on behavioural performance, although the level of performance for some behaviours was related to the level of exercise. Altogether, these findings indicate that corticosterone and dopamine D2/D3 receptor activation contribute to the motivation for wheel running, but suggest that motivation for exercise is not a sufficient factor to alter behaviour in healthy mice.
“…Unlimited access to voluntary wheel running generally improves memory in C57BL/6J mice [36,37]. The lack of behavioural and cognitive effects of intermittent wheel running in our study raises the question of whether there are optimal levels of exercise for behavioural changes to occur.…”
Section: Intermittent Voluntary Wheel Running Does Not Alter Behavioumentioning
Number of tables: 1Number of words in the abstract: 248Number of words in the manuscript (including tables and figure legends): 6,639Number of words in the introduction: 1,290Number of words in the discussion: 1,243 ABSTRACT Physical exercise can improve cognition but whether this is related to motivation levels is unknown. Voluntary wheel running is a rewarding activity proposed as a model of motivation to exercise. To question the potential effects of exercise motivation on subsequent behaviour, we used a pharmacological approach targeting some reward mechanisms. The stress hormone corticosterone has rewarding effects mediated by activation of low affinity glucocorticoid receptors (GR). To investigate whether corticosterone synthesis motivates exercise via activation of GRs and subsequently, impacts on behaviour, we treated C57BL/6J mice acutely with the inhibitor of corticosterone synthesis metyrapone (35 mg/kg) or repeatedly with the GR antagonist mifepristone (30 mg/kg) prior to 1-hour running wheel sessions. To investigate whether reducing motivation to exercise impacts on behaviour, we antagonised running-induced dopamine D2/D3 receptors activation with sulpiride (25 or 50 mg/kg) and assessed locomotor, anxiety-related and memory performance after 20 running sessions over 4 weeks. We found that corticosterone synthesis contributes to running levels, but the maintenance of running behaviour was not mediated by activation of GRs. Intermittent exercise was not associated with changes in behavioural or cognitive performance. The persistent reduction in exercise levels triggered by sulpiride also had limited impact on behavioural performance, although the level of performance for some behaviours was related to the level of exercise. Altogether, these findings indicate that corticosterone and dopamine D2/D3 receptor activation contribute to the motivation for wheel running, but suggest that motivation for exercise is not a sufficient factor to alter behaviour in healthy mice.
“…Various protocols of differing intensities of exercise can also lead to different effects on the neurological function (40). Furthermore, based on learning definition, relatively stable are as the learning aspects.…”
Background: Stress induced by sleep deprivation can cause degradation of learning in the acquisition phase, and low-intensity exercise can prevent the negative effects of stress.
“…In the same study it was found that inhibition of BDNF during running prevents the enhanced memory function associated with running. Other studies in mice have shown that BDNF levels are increased in the hippocampus within 3 weeks of voluntary exercise and levels remain high up to 2 weeks after the end of the exercise period (15). BDNF levels did not return to baseline until after 3-4 weeks after the running period, and the performance in the radial arm maze was best when performed 1 week after the end of running.…”
Section: Molecular Mechanisms Of Adaptive Responses To Oxidative Stressmentioning
As is generally true with other age-related diseases, Alzheimer's disease (AD) involves oxidative damage to cellular components in the affected tissue, in this case the brain. The causes and consequences of oxidative stress in neurons in AD are not fully understood, but considerable evidence points to important roles for accumulation of amyloid b-peptide upstream of oxidative stress and perturbed cellular Ca 2+ homeostasis and energy metabolism downstream of oxidative stress. The identification of mutations in the b-amyloid precursor protein and presenilin-1 as causes of some cases of early onset inherited AD, and the development of cell culture and animal models based on these mutations has greatly enhanced our understanding of the AD process, and has greatly expanded opportunities for preclinical testing of potential therapeutic interventions. In this regard, and of particular interest to us, is the elucidation of adaptive cellular stress response pathways (ACSRP) that can counteract multiple steps in the AD neurodegenerative cascades, thereby limiting oxidative damage and preserving cognitive function. ACSRP can be activated by factors ranging from exercise and dietary energy restriction, to drugs and phytochemicals. In this article we provide an overview of oxidative stress and AD, with a focus on ACSRP and their potential for preventing and treating AD. Antioxid. Redox Signal. 14, 1519-1534.
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