The Impact of Short and Long-Term Exercise on the Expression of Arc and AMPARs During Evolution of the 6-Hydroxy-Dopamine Animal Model of Parkinson’s Disease

Garcia, Priscila Crespo; Real, Caroline Cristiano; Britto, Luiz Roberto Giorgetti de

doi:10.1007/s12031-017-0896-y

Cited by 33 publications

(14 citation statements)

References 56 publications

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“…Additionally, our studies indicate that DA denervation decreased the expression of GluR2 in the striatum in 6-OHDA rat PD model, and our treadmill exercise intervention regimen described above normalized this decrease in GluR2 expression (Chen et al, 2015a ), largely consistent with the results of Garcia et al ( 2017 ). GluR2 subunit-lacking AMPA-type glutamate receptors can form Ca-permeable glutamatergic receptor ion channels, conduct inwardly rectifying EPSCs, and Ca may trigger multiple molecular and cellular mechanisms in the MSNs (Cull-Candy et al, 2006 ; Liu and Savtchouk, 2012 ; Lalanne et al, 2016 ; Whitehead et al, 2017 ).…”

Section: Exercise Effects On Msn Anatomy Intrinsic Physiology and Cosupporting

confidence: 89%

“…Schallert and his collaborators also expanded their forced limb use paradigm in unilateral 6-OHDA lesioned rats to the more quantifiable exercise on treadmill and running wheels in unilateral 6-OHDA rats and bilateral MPTP-lesioned mice, and replicated their earlier results of limb use's (i.e., exercise's) protection of the DA neurons or exercise's promotion of DA neuron recovery from MPTP lesion in mice and 6-OHDA lesion in rats (Tillerson et al, 2003 ). Since then, other laboratories have performed follow-up studies and confirmed and expanded the original findings on exercise's neuroprotective effects on DA neurons in mouse MPTP and rat 6-OHDA PD models (Tillerson et al, 2003 ; Garcia et al, 2017 ; Real et al, 2017 ; Shi et al, 2017 ). For example, using intrastriatal 6-OHDA DA lesion in rats, Yoon et al ( 2007 ) and Tajiri et al ( 2010 ) reported similarly strong DA neuron protection in unilateral 6-OHDA rat PD model produced by treadmill exercise that was initiated 1 day before lesion and resumed 24 h after lesion and continued for 2–4 weeks.…”

Section: Exercise Effects On the Nigrostriatal Da System In Animal Pdmentioning

confidence: 85%

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Exercise-Induced Neuroprotection of the Nigrostriatal Dopamine System in Parkinson's Disease

Hou

Chen

Liu

et al. 2017

Front. Aging Neurosci.

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Epidemiological studies indicate that physical activity and exercise may reduce the risk of developing Parkinson's disease (PD), and clinical observations suggest that physical exercise can reduce the motor symptoms in PD patients. In experimental animals, a profound observation is that exercise of appropriate timing, duration, and intensity can reduce toxin-induced lesion of the nigrostriatal dopamine (DA) system in animal PD models, although negative results have also been reported, potentially due to inappropriate timing and intensity of the exercise regimen. Exercise may also minimize DA denervation-induced medium spiny neuron (MSN) dendritic atrophy and other abnormalities such as enlarged corticostriatal synapse and abnormal MSN excitability and spiking activity. Taken together, epidemiological studies, clinical observations, and animal research indicate that appropriately dosed physical activity and exercise may not only reduce the risk of developing PD in vulnerable populations but also benefit PD patients by potentially protecting the residual DA neurons or directly restoring the dysfunctional cortico-basal ganglia motor control circuit, and these benefits may be mediated by exercise-triggered production of endogenous neuroprotective molecules such as neurotrophic factors. Thus, exercise is a universally available, side effect-free medicine that should be prescribed to vulnerable populations as a preventive measure and to PD patients as a component of treatment. Future research needs to establish standardized exercise protocols that can reliably induce DA neuron protection, enabling the delineation of the underlying cellular and molecular mechanisms that in turn can maximize exercise-induced neuroprotection and neurorestoration in animal PD models and eventually in PD patients.

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Section: Exercise Effects On Msn Anatomy Intrinsic Physiology and Cosupporting

confidence: 89%

Section: Exercise Effects On the Nigrostriatal Da System In Animal Pdmentioning

confidence: 85%

Exercise-Induced Neuroprotection of the Nigrostriatal Dopamine System in Parkinson's Disease

Hou

Chen

Liu

et al. 2017

Front. Aging Neurosci.

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“…For example, chronic forced running prior to testing blocks the reinforcing effects of MDMA and MDMA-induced NAc dopamine release (63), indicating that exercise-induced adaptations may blunt the dopaminergic response to drugs of abuse. Exercise can also normalize glutamatergic signaling (64), and these effects may protect against drug use escalation and the development of substance use disorder (for review see 65). For example, chronic treadmill running reduced markers of hyper-excitability (e.g., upregulation of GluA2/3, and downregulation of GluA1 receptors) in a Parkinson’s Disease model, which is also characterized by depletion of dopamine and hyper-excitability/abnormal glutamatergic transmission (64).…”

Section: Overview Of Recent Findings In Male and Female Animalsmentioning

confidence: 99%

“…Exercise can also normalize glutamatergic signaling (64), and these effects may protect against drug use escalation and the development of substance use disorder (for review see 65). For example, chronic treadmill running reduced markers of hyper-excitability (e.g., upregulation of GluA2/3, and downregulation of GluA1 receptors) in a Parkinson’s Disease model, which is also characterized by depletion of dopamine and hyper-excitability/abnormal glutamatergic transmission (64). Exercise can also produce modifications at the level of chromatin, which induce long-term changes in gene expression (66).…”

Section: Overview Of Recent Findings In Male and Female Animalsmentioning

confidence: 99%

Exercise as a Prevention for Substance Use Disorder: a Review of Sex Differences and Neurobiological Mechanisms

et al. 2017

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Purpose of Review This report provides an update on clinical and preclinical findings for the efficacy of exercise to prevent substance use disorder with a focus on recent evidence for sex differences and neurobiological mechanisms. Recent Findings Exercise/physical activity is associated with decreased drug use in humans. Preclinical results further indicate that exercise decreases vulnerability to drug use and the development of features of substance use disorder, and suggest that females have an enhanced sensitivity to its reward-substitution effects. However, certain exercise conditions may sensitize the reward pathway and enhance vulnerability suggesting that parallel observations in humans (e.g., increased prescription opioid misuse and heroin use in high-school athletes) may be biologically-based. Summary Exercise is a promising prevention strategy for substance use disorder. Further work is needed to establish its efficacy as a sex-specific strategy using larger samples, and to understand the exercise conditions that induce beneficial versus risk-enhancing effects.

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“…Glutamatergic signaling in the reward pathway is another likely candidate given strong evidence implicating AMPA receptors in the incubation effect (81). While few studies have examined this possibility in addiction models, results from findings in males using models of Parkinson’s Disease, which is also characterized by hyper-excitability/abnormal glutamatergic drive, show that moderate levels of forced running reduce hyper-excitability (upregulation of GluA2/3, and downregulation of GluA1 receptors) in cortical and striatal regions (e.g., 82). …”

Section: Neurobiological Mechanismsmentioning

confidence: 99%

Exercise as a Sex-Specific Treatment for Substance Use Disorder

et al. 2017

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Purpose of Review Exercise is a promising treatment for substance use disorder that may reduce withdrawal symptoms and prevent relapse. In this review, we discuss recent evidence from clinical and preclinical studies for its efficacy, from a behavioral to a molecular level, in order to understand the exercise conditions that lead to beneficial effects. We also highlight the few recent findings of sex-specific differences. Recent Findings Clinical and preclinical findings show that exercise decreases withdrawal symptoms, including craving, in both males and females. Evidence from clinical studies support the efficacy of exercise to prevent relapse to smoking, although further research is needed to examine sex differences, establish long-term efficacy, and to determine if effects extend to other substance use disorders. Preclinical findings also support the potential utility of exercise to prevent relapse with evidence suggesting that its efficacy is enhanced in males, and mediated by blocking drug-induced adaptations that occur during early abstinence. Summary Sex differences and timing of exercise availability during abstinence should be considered in future studies examining exercise as an intervention for relapse. A better understanding of the neurobiological mechanisms underlying the efficacy of exercise to reduce withdrawal symptoms and prevent relapse is needed to guide its development as a sex-specific treatment.

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The Impact of Short and Long-Term Exercise on the Expression of Arc and AMPARs During Evolution of the 6-Hydroxy-Dopamine Animal Model of Parkinson’s Disease

Cited by 33 publications

References 56 publications

Exercise-Induced Neuroprotection of the Nigrostriatal Dopamine System in Parkinson's Disease

Exercise-Induced Neuroprotection of the Nigrostriatal Dopamine System in Parkinson's Disease

Exercise as a Prevention for Substance Use Disorder: a Review of Sex Differences and Neurobiological Mechanisms

Exercise as a Sex-Specific Treatment for Substance Use Disorder

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