Exercise reverses ethanol inhibition of neural stem cell proliferation

Crews, Fulton T.; Nixon, Kimberly; Wilkie, Mary E.

doi:10.1016/s0741-8329(04)00081-3

Cited by 120 publications

(52 citation statements)

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“…Ethanol preference and consumption were maintained regardless of wheel access. These results support earlier findings by Crews et al (2004) that ethanol consumption does not differ for mice with or without access to running wheels. It has been previously reported that voluntary wheel running reduces the effects of acute ethanol (delivered via i.p.…”

Section: Wheel Access Modifies Ethanol Drinking Patternssupporting

confidence: 93%

“…It is of interest to point out that Crews et al (2004) reported no difference in wheel running distance between ethanol drinking and water drinking mice, indicating a similar stability in normal reward-related processes. Without the experience of chronic self-administration followed by forced deprivation, hedonic substitution processes are not recruited.…”

Section: Wheel Running Increases During Ethanol Deprivation and Decrementioning

confidence: 96%

“…Crews et al (2004) reported that ethanol consumption does not differ for mice with or without access to a running wheel, however these mice had not chronically consumed ethanol prior to wheel running. For rats that had ethanol consumption experience, it has been shown that wheel running during alcohol deprivation increases subsequent ethanol consumption in rats (Werme et al, 2002).…”

Section: Introductionmentioning

confidence: 97%

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Wheel running, voluntary ethanol consumption, and hedonic substitution

Ozburn

Harris

Blednov

2008

Alcohol

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Few studies have examined the relationship between naturally rewarding behaviors and ethanol drinking behaviors in mice. Although natural and drug reinforcers activate similar brain circuitry, there is behavioral evidence suggesting food and drug rewards differ in perceived value (Bickel et al., 1995;DeGrandpre et al., 1993;Petry and Heyman, 1995). The primary goal of the present study was to investigate the relationships between naturally reinforcing stimuli and consumption of ethanol in ethanol preferring C57BL/6J mice. Mouse behaviors were observed after the following environmental manipulations: standard or enhanced environment, accessible or inaccessible wheel, and presence or absence of ethanol. Using a high resolution volumetric drinking monitor and wheel running monitor, we evaluated whether alternating access to wheel running modified ethanol-related behaviors and whether alternating access to ethanol modified wheel running or subsequent ethanolrelated behaviors. We found that ethanol consumption remains stable with alternating periods of wheel running. Wheel running increases in the absence of ethanol and decreases upon reintroduction of ethanol. Upon reintroduction of ethanol, an alcohol deprivation effect was seen. Collectively, the results support theories of hedonic substitution and suggest that female C57BL/6J mice express ethanol seeking and craving under these specific conditions.

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Section: Wheel Access Modifies Ethanol Drinking Patternssupporting

confidence: 93%

Section: Wheel Running Increases During Ethanol Deprivation and Decrementioning

confidence: 96%

Section: Introductionmentioning

confidence: 97%

See 1 more Smart Citation

Wheel running, voluntary ethanol consumption, and hedonic substitution

Ozburn

Harris

Blednov

2008

Alcohol

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“…In this profile counting methodology, cell counts were divided by the area of the section, expressed as cells/mm 2 , and compared by ANOVA. We have shown previously that profile counting and stereological estimations show identical results in percentage change (Crews et al, 2004). In addition, BrdUϩ cells are not a homogenously distributed population of cells; therefore, stereology may not be an appropriate method of quantification (Popken and Farel, 1997).…”

Section: Methodsmentioning

confidence: 98%

Temporally Specific Burst in Cell Proliferation Increases Hippocampal Neurogenesis in Protracted Abstinence from Alcohol

Nixon¹,

Crews²

2004

J. Neurosci.

203

252

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Adult neurogenesis is a newly considered form of plasticity that could contribute to brain dysfunction in psychiatric disease. Chronic alcoholism, a disease affecting over 8% of the adult population, produces cognitive impairments and decreased brain volumes, both of which are partially reversed during abstinence. Clinical data and animal models implicate the hippocampus, a region important in learning and memory. In a model of alcohol dependence (chronic binge exposure for 4 d), we show that adult neurogenesis is inhibited during dependence with a pronounced increase in new hippocampal neuron formation after weeks of abstinence. This increase is attributable to a temporally and regionally specific fourfold increase in cell proliferation at day 7 of abstinence, with a majority of those cells surviving and differentiating at percentages similar to controls, effects that doubled the formation of new neurons. Although increases in cell proliferation correlated with alcohol withdrawal severity, proliferation remained increased when diazepam (10 mg/kg) was used to reduce withdrawal severity. Indeed, those animals with little withdrawal activity still show a twofold burst in cell proliferation at day 7 of abstinence. Thus, alcohol dependence and recovery from dependence continues to alter hippocampal plasticity during abstinence. Because neurogenesis may contribute to hippocampal function and/or learning, memory, and mood, compensatory neurogenesis and the return of normal neurogenesis may also have an impact on hippocampal structure and function. For the first time, these data provide a neurobiological mechanism that may underlie the return of human cognitive function and brain volume associated with recovery from addiction.

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“…Previous studies have demonstrated biphasic alterations in NPC proliferation associated with alcohol exposure and withdrawal (Aberg et al, 2005;Crews et al, 2004;He et al, 2005;Nixon and Crews, 2002). To determine if abstinence from chronic drinking (and depression-like behavior) is associated with changes in NPC proliferation, serial sections of hippocampus were immunolabeled with PCNA, which is a cell cycle-specific nuclear protein belonging to the replication complex that permits DNA synthesis needed for G1 to S transition (Krude, 1999;Yew et al, 2001) and correlates with the proliferative state of cells (Celis et al, 1987).…”

Section: Proliferation Of Neural Progenitor Cellsmentioning

confidence: 99%

Abstinence following Alcohol Drinking Produces Depression-Like Behavior and Reduced Hippocampal Neurogenesis in Mice

Stevenson

Schroeder

Nixon

et al. 2008

Neuropsychopharmacol

131

102

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Alcoholism and depression show high degrees of comorbidity. Clinical evidence also indicates that depression that emerges during abstinence from chronic alcohol use has a greater negative impact on relapse than pre-existing depression. Although no single neurobiological mechanism can account for the behavioral pathologies associated with these devastating disorders, converging evidence suggests that aspects of both alcoholism and depression are linked to reductions in hippocampal neurogenesis. Here, we report results from a novel preclinical behavioral model showing that abstinence from voluntary alcohol drinking leads to the emergence of depressionlike behavior and reductions in neurogenesis. C57BL/6J mice were allowed to self-administer ethanol (10% v/v) vs H 2 O in the home cage for 28 days. Alcohol was then removed for 1 or 14 days, and mice were tested in the forced swim test to measure depression-like behavior. After 14 days, but not 1 day of abstinence from alcohol drinking, mice showed a significant increase in depression-like behavior. The significant increase in depression-like behavior during abstinence was associated with a reduction in proliferating cell nuclear antigen (PCNA) and doublecortin (DCX) immunoreactivity in the dentate gyrus of the hippocampus indicating that both the number of proliferating neural progenitor cells (NPC) and immature neurons were reduced, respectively. The number of NPCs that were labeled with bromo-deoxyuridine (BrdU) at the beginning of alcohol exposure was not altered indicating that survival of NPCs is not linked to abstinence-induced depression. Chronic treatment (14 days) with the antidepressant desipramine during abstinence prevented both the emergence of depression-like behavior and the reduction in hippocampal neurogenesis indicating that abstinence-induced depression is associated with structural plasticity in the hippocampus. Overall, the results of this study support the conclusion that profound functional (ie behavioral) and structural changes occur during abstinence from alcohol use and suggest that antidepressant treatment may alleviate some of these pathological neurobehavioral adaptations.

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Exercise reverses ethanol inhibition of neural stem cell proliferation

Cited by 120 publications

References 0 publications

Wheel running, voluntary ethanol consumption, and hedonic substitution

Wheel running, voluntary ethanol consumption, and hedonic substitution

Temporally Specific Burst in Cell Proliferation Increases Hippocampal Neurogenesis in Protracted Abstinence from Alcohol

Abstinence following Alcohol Drinking Produces Depression-Like Behavior and Reduced Hippocampal Neurogenesis in Mice

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