Effects of voluntary exercise on hippocampal long-term potentiation in morphine-dependent rats

Miladi‐Gorji, Hossein; Rashidy-Pour, Ali; Fathollahi, Yaghoub; Semnanian, Saeed; Jadidi, Majid

doi:10.1016/j.neuroscience.2013.09.056

Cited by 19 publications

(19 citation statements)

References 46 publications

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“…In line with our study, it was shown that the hippocampal DG (as a source of neural stem cells) continues to generate new neurons throughout the lifespan, and physical activity also causes an increase in neurogenesis in the DG of the hippocampus, a brain area important for learning, memory (10), and synaptic plasticity (17). Our finding is consistent with previous results showing that exerciseassociated changes in synaptic plasticity occurred in the same region where neurogenesis occurred by running, suggesting that newborn cells have a functional role in this process (9).…”

Section: Discussionsupporting

confidence: 90%

“…In human subjects and in rodents, voluntary or forced exercises promote neurogenesis in the adult dentate gyrus (DG) (7) and brain-derived neurotrophic factor (BDNF) might have a potential role in exercise-induced neurogenesis, synaptic plasticity, and memory through its actions on the tyrosine kinase B (TrkB) receptor (8)(9)(10)(11)(12)(13)(14). We have recently demonstrated that voluntary exercise diminishes the severity of morphine dependency (15) and the anxiogenic-like behaviors in both morphine-dependent and withdrawn rats (16), enhances LTP in hippocampal DG area (17), and ameliorates the spatial memory deficits in morphine-dependent rats through TrkB receptor of BDNF (15).…”

Section: Introductionmentioning

confidence: 99%

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Enhancing Hippocampal Neuronal Numbers in Morphine-Dependent Rats by Voluntary Exercise Through a Brain-Derived Neurotrophic Factor-Mediated Mechanism

Rashidy-Pour

Fathollahi

Miladi‐Gorji

et al. 2015

Middle East J Rehabil Health

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Background: Exposure to morphine decreases neurogenesis in the hippocampus. Recent studies have shown that voluntary running decreases the severity of anxiety behaviors and cognitive deficits, and increased synaptic plasticity in morphine-dependent rats. Objectives: This study aimed to investigate whether the morphine dependence-induced attenuation of hippocampal neuron number in rats would be reversed by voluntary running through a brain-derived neurotrophic factor (BDNF)-mediated mechanism. Materials and Methods: The rats were received injections of 10 mg/kg of morphine twice a day over ten days of voluntary running. A specific antagonist of BDNF action (TrkB-IgG) was used to block the hippocampal BDNF action during the study period; cytochrome C (Cyt C) was used as the control drug. Results: We found that chronic exposure to morphine had decreased the number of dentate gyrus neurons in sedentary rats receiving Cyt C or IgG in comparison to the control rats (P < 0.05). Moreover, exercise groups receiving saline or morphine showed an increase in the number of neurons following ten days running; blocking the BDNF action with TrkB-IgG fully inhibited this effect (both, P = 0.0001). Conclusions: This study demonstrates that that voluntary exercise can ameliorate the attenuation of hippocampal neuron number induced by morphine dependence through a BDNF-mediated mechanism. Thus, physical activity might have a potential role in ameliorating chronic morphine-induced neuronal changes in the hippocampus.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Enhancing Hippocampal Neuronal Numbers in Morphine-Dependent Rats by Voluntary Exercise Through a Brain-Derived Neurotrophic Factor-Mediated Mechanism

Rashidy-Pour

Fathollahi

Miladi‐Gorji

et al. 2015

Middle East J Rehabil Health

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“…On the other hand, there is considerable evidence that exercise can induce changes in neuroplasticity and regulate drug reward processing via the mesolimbic reward pathway (Zlebnik et al , 2014a; Greenwood et al , 2011; Werme et al , 2000; Werme et al , 2002b). Above all, the effects of drug addiction and exercise on these reward network signaling molecules are sex-dependent and regulated by steroid hormones (Miladi-Gorji et al , 2014; Berchtold et al , 2001; Peterson et al , 2014; Lynch et al , 2002; Becker and Hu, 2008). In this section, we present a brief overview of the sex differences in neural changes underlying the efficacy of exercise in drug addiction as indicated in Figure 1.…”

Section: Underlying Neurobiological Mechanisms For the Sex-specifimentioning

confidence: 99%

“…In addition, voluntary exercise also stimulates histone deacetylase and DNA demethylation of BDNF promoter IV to regulate brain plasticity by engaging mechanisms of epigenetic regulation (Gomez-Pinilla et al , 2011). Recent studies found that short-term exercise enhanced hippocampal LTP and cognitive functions as well as increased numbers of spike LTP in morphine-dependent rats (Miladi-Gorji et al , 2014). Moreover, the 30-day intensive treadmill exercise increased dendritic spine density and arborization in mouse striatal, reducing drug-induced cognitive deficit (Toy et al , 2014).…”

Section: Underlying Neurobiological Mechanisms For the Sex-specifimentioning

confidence: 99%

Sex differences in drug addiction and response to exercise intervention: From human to animal studies

Zhou

Zhao

Zhou

et al. 2016

Frontiers in Neuroendocrinology

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Accumulated research supports the idea that exercise could be an option of potential prevention and treatment for drug addiction. During the past few years, there has been increased interest in investigating of sex differences in exercise and drug addiction. This demonstrates that sex-specific exercise intervention strategies may be important for preventing and treating drug addiction in men and women. However, little is known about how and why sex differences are found when doing exercise-induced interventions for drug addiction. In this review, we included both animal and human that pulled subjects from a varied age demographic, as well as neurobiological mechanisms that may highlight the sex-related differences in these potential to assess the impact of sex-specific roles in drug addiction and exercise therapies.

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“…Increasing evidence suggests that exercise can prevent and treat a variety of neurocognitive disorders (Smith et al, ). For example, exercise not only improves spatial learning and memory in rodents with or without brain diseases but also ameliorates learning and memory deficits induced by alcohol (Christie et al, ), methylphenidate (Motaghinejad, Motevalian, Larijani, & Khajehamedi, ), and morphine (Miladi‐Gorji et al, ). Unfortunately, few studies have focused on the relationship between exercise and learning–memory dysfunction related to nicotine withdrawal.…”

Section: Discussionmentioning

confidence: 99%

Exercise improves nicotine reward‐associated cognitive behaviors and related α7 nAChR‐mediated signal transduction in adolescent rats

Zhou

et al. 2018

Journal Cellular Physiology

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The adolescent brain is vulnerable to long-lasting cognitive disturbances resulting from nicotine exposure. Although exercise has been used as an intervention for ameliorating cognitive deficits in various disorders, the effect on cognitive changes induced by nicotine exposure and its underlying mechanisms remain unclear. The purpose of this study was to investigate the effects of exercise on nicotine reward-associated cognitive behaviors in adolescent rats subjected to nicotine conditioned place preference paradigm (CPP). Male adolescent rats were trained on the Go/NoGo task, then subjected to nicotine CPP, and then randomly separated into four groups: sedentary (SED), high- (HE), moderate- (ME), and low-intensity (LE) exercise. Rats in exercise groups performed treadmill running 30 min daily for 10 days. Results showed that MEs had shorter escape latencies in the Morris water maze (MWM) test compared to SEDs. Although time spent and distance swam in the target quadrant significantly increased in both the MEs and HEs, the number of target quadrant crosses increased significantly only in MEs. MEs and HEs showed higher performance accuracy on NoGo and lower scores on CPP tasks. Expression of α7 nicotinic acetylcholine receptors (nAChRs) and downstream signaling molecules increased in MEs in prefrontal cortex but not hippocampus, with α7 nAChRs expression positively associated with NoGo accuracy and MWM probe test performance, but negatively correlated with CPP scores. The findings of this study suggest that moderate-intensity exercise can improve nicotine induced cognitive behaviors, and implicates prefrontal cortical α7 nAChR-mediated signal transduction as a possible mechanism.

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Effects of voluntary exercise on hippocampal long-term potentiation in morphine-dependent rats

Cited by 19 publications

References 46 publications

Enhancing Hippocampal Neuronal Numbers in Morphine-Dependent Rats by Voluntary Exercise Through a Brain-Derived Neurotrophic Factor-Mediated Mechanism

Enhancing Hippocampal Neuronal Numbers in Morphine-Dependent Rats by Voluntary Exercise Through a Brain-Derived Neurotrophic Factor-Mediated Mechanism

Sex differences in drug addiction and response to exercise intervention: From human to animal studies

Exercise improves nicotine reward‐associated cognitive behaviors and related α7 nAChR‐mediated signal transduction in adolescent rats

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