Modulation of synaptic plasticity by exercise

Prenatal alcohol exposure is associated to different physical, behavioral, cognitive, and neurological impairments collectively known as fetal alcohol spectrum disorder. The underlying mechanisms of ethanol toxicity are not completely understood. Experimental studies during human pregnancy to identify new diagnostic biomarkers are difficult to carry out beyond genetic or epigenetic analyses in biological matrices. Therefore, animal models are a useful tool to study the teratogenic effects of alcohol on the central nervous system and analyze the benefits of promising therapies. Animal models of alcohol spectrum disorder allow the analysis of key variables such as amount, timing and frequency of ethanol consumption to describe the harmful effects of prenatal alcohol exposure. In this review, we aim to synthetize neurodevelopmental disabilities in rodent fetal alcohol spectrum disorder phenotypes, considering facial dysmorphology and fetal growth restriction. We examine the different neurodevelopmental stages based on the most consistently implicated epigenetic mechanisms, cell types and molecular pathways, and assess the advantages and disadvantages of murine models in the study of fetal alcohol spectrum disorder, the different routes of alcohol administration, and alcohol consumption patterns applied to rodents. Finally, we analyze a wide range of phenotypic features to identify fetal alcohol spectrum disorder phenotypes in murine models, exploring facial dysmorphology, neurodevelopmental deficits, and growth restriction, as well as the methodologies used to evaluate behavioral and anatomical alterations produced by prenatal alcohol exposure in rodents.

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“…Synaptic plasticity is the process through which long-term changes in synaptic communication occur (171).…”

Section: Synaptic Plasticitymentioning

confidence: 99%

Murine Models for the Study of Fetal Alcohol Spectrum Disorders: An Overview

et al. 2020

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“…However, its implication in synaptic dynamics during development has not been described yet. Synapse number can be altered due to the influence of physiological parameters (aging, hormonal state, exercise) [23][24][25][26], pathological (neurodegenerative process) [27,28] or induced conditions (mutants) [29] which alter cellular components and pathways [30]. The imbalance between the pro-and anti-synaptogenic pathways modulates the number of synapses [30].…”

Section: Introductionmentioning

confidence: 99%

Small heat shock proteins determine synapse number and neuronal activity during development

2020

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Environmental changes cause stress, Reactive Oxygen Species and unfolded protein accumulation which hamper synaptic activity and trigger cell death. Heat shock proteins (HSPs) assist protein refolding to maintain proteostasis and cellular integrity. Mechanisms regulating the activity of HSPs include transcription factors and posttranslational modifications that ensure a rapid response. HSPs preserve synaptic function in the nervous system upon environmental insults or pathological factors and contribute to the coupling between environmental cues and neuron control of development. We have performed a biased screening in Drosophila melanogaster searching for synaptogenic modulators among HSPs during development. We explore the role of two small-HSPs (sHSPs), sHSP23 and sHSP26 in synaptogenesis and neuronal activity. Both sHSPs immunoprecipitate together and the equilibrium between both chaperones is required for neuronal development and activity. The molecular mechanism controlling HSP23 and HSP26 accumulation in neurons relies on a novel gene (CG1561), which we name Pinkman (pkm). We propose that sHSPs and Pkm are targets to modulate the impact of stress in neurons and to prevent synapse loss.

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“…Aerobic training is also positively associated with synaptic plasticity, the essential biological change for memory, and learning. It is involved in both long-term potentiation enhancement and long-term depression induction (Bettio et al, 2019). Neuron density and gray matter volumes are increased in hippocampus, prefrontal and cingulate cortices after physical activity (Ruscheweyh et al, 2011;Kleemeyer et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Cognitive Gains of Aerobic Exercise in Patients With Ischemic Cerebrovascular Disorder: A Systematic Review and Meta-Analysis

Shu

Xie

et al. 2020

Front. Cell Dev. Biol.

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Background: Cognitive impairment has become an important problem in ischemic cerebrovascular disorder survivors as disease related deaths have been significantly reduced. Aerobic exercise, the most prevalent mode of physical activity, positively contributes to cognition in both healthy population and people with cognitive impairment. However, studies on its associations with cognitive gains in patients with ischemic cerebrovascular disease showed mixed findings.Objective: To explore the cognitive effects of aerobic exercise on ischemic cerebrovascular disorder survivors and investigate the possible moderators on exercise benefits.Method: Randomized controlled trials investigating the effects of sole aerobic exercise on cognitive function in population with ischemic intracranial vascular disorder compared to any control group who did not receive the intervention were enrolled in this systematic review and meta-analysis. Four online database (Pubmed, Cochrane Library, Embase, and Web of Science) were searched.Results: The initial search returned 1,522 citations and ultimately 11 studies were included in the systematic review. Analysis of seven studies showed the beneficial but not statistically significant impact of aerobic exercise on global cognitive function (0.13; 95% Cl −0.09 to 0.35; p = 0.25). Participants already with cognitive impairment benefited more from this intervention (0.31; 95% Cl 0.07–0.55; p = 0.01) and moderate intensity might be the optimal choice (0.34; 95% Cl −0.01 to 0.69; p = 0.06). The program duration and initiation time after stroke occurrence did not predict better cognitive outcome. Aerobic exercise was not associated with improvement of processing speed and executive function, the two subdomains of cognitive function.Conclusions: Aerobic exercise may contribute to cognitive gains in survivors of ischemic cerebrovascular disorder, especially for population already with cognitive decline. Our findings suggest that the adoption of moderate intensity aerobic exercise might improve cognition in such population.

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Modulation of synaptic plasticity by exercise

Cited by 52 publications

References 165 publications

Murine Models for the Study of Fetal Alcohol Spectrum Disorders: An Overview

Murine Models for the Study of Fetal Alcohol Spectrum Disorders: An Overview

Small heat shock proteins determine synapse number and neuronal activity during development

Cognitive Gains of Aerobic Exercise in Patients With Ischemic Cerebrovascular Disorder: A Systematic Review and Meta-Analysis

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