The effects of post-stress exposure to alcohol upon the development of alcohol consumption in rats

Boyd, Thomas L.; Callen, Edward J.; House, William J.

doi:10.1016/0005-7967(89)90117-4

Cited by 12 publications

(4 citation statements)

References 14 publications

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“…This finding indicates that phosphory-lation and activation of NR2A/B subunits through Fyn is not a critical mechanism in the expression of an ADE. In agreement with previous reports, a simple stressor was shown to lead to a marked increase in ethanol consumption (Bowers et al, 1997;Boyd et al, 1989). The transient nature of the response is in agreement with previous reports of the effect of a simple stressor on ethanol consumption (Bowers et al, 1997;Boyd et al, 1989).…”

Section: Discussionsupporting

confidence: 92%

Role of Fyn Tyrosine Kinase in Ethanol Consumption by Mice

Cowen

Schumann

Yagi

et al. 2003

Alcoholism Clin & Exp Res

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Deletion of the Fyn tyrosine kinase gene may be involved in ethanol sensitivity but this effect may depend on a gene-environment interaction. Fyn does not influence ethanol consumption, neither under basal conditions nor following a deprivation period or stress. This finding indicates that phosphorylation and activation of N-methyl-D-aspartate (NMDA) receptors through Fyn is not a critical mechanism in alcohol drinking or relapse behavior.

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Section: Discussionsupporting

confidence: 92%

Role of Fyn Tyrosine Kinase in Ethanol Consumption by Mice

Cowen

Schumann

Yagi

et al. 2003

Alcoholism Clin & Exp Res

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“…In the present study, we used SPS method to establish PTSD, and found that stress induced alcohol CPP. Our results were compatible with the clinical situation in which PTSD is often associated with alcohol dependence (Boyd et al, 1989). In addition, some animal studies on maternal separation showed that this stress could have profound long-term effects on the first alcohol consumption in adult rats (Holter et al , 2000) or mouse (Cruz et al , 2008), which is consistent with our findings.…”

Section: Discussionsupporting

confidence: 92%

“…Experimentally studies on the relationship between stress and alcohol seeking usually use a variety of types of stress, such as footshock stress, immobilization stress, and isolation stress (Matsuzawa et al , 2000). However, in experimental animals, studies on the effect of stress on alcohol consumption have produced conflicting results: Some studies have reported that footshock stress increases alcohol intake (van Erp et al , 2001) whereas other studies have shown that footshock decreases (Funk et al , 2004) or has no effects on alcohol intake (Boyd et al , 1989).…”

Section: Introductionmentioning

confidence: 99%

Role of single prolonged stress in acquisition of alcohol conditioned place preference in rats

Wang

Zhao

et al. 2016

Life Sciences

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“…Because anxiety has been linked to EtOH consumption (Boyd et al, 1989) we also measured behavioral correlates of anxiety using an elevated plus maze prior to electrophysiological experiments. More time spent in the open arms and more open arm rearings suggest an animal is less anxious.…”

Section: Dor Modulation Of Gaba In the Vta Correlates With Anxiety-limentioning

confidence: 99%

δ-Opioid Receptor Expression in the Ventral Tegmental Area Protects Against Elevated Alcohol Consumption

Margolis¹,

Fields²,

Hjelmstad³

et al. 2008

J. Neurosci.

106

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Alcoholism is a complex and debilitating syndrome affecting ϳ140 million people worldwide. However, not everyone who consumes ethanol develops abuse, raising the possibility that some individuals have a protective mechanism that inhibits elevated alcohol consumption. We tested the hypothesis that the ␦-opioid receptor (DOR) plays such a protective role. Here we show that DOR activity in the ventral tegmental area (VTA) robustly decreases ethanol consumption in rats and that these effects depend on baseline ethanol consumption. Intra-VTA microinjection of the DOR agonist DPDPE decreases drinking, particularly in low-drinking animals. Furthermore, VTA microinjection of the DOR selective antagonist TIPP-⌿ increases drinking in low, but not high, drinkers and this increase is blocked by comicroinjection of the GABA A antagonist bicuculline. Using electrophysiological techniques we found that in VTA brain slices from drinking rats DPDPE presynaptically inhibits GABA A receptor mediated IPSCs in low drinkers, but not in high drinkers or naive animals, most likely through activation of DORs on GABA terminals. This DOR-mediated inhibition of IPSCs also correlates inversely with behavioral correlates of anxiety measured in the elevated plus maze. In contrast, presynaptic inhibition of VTA GABA A IPSCs by theopioid receptor agonist DAMGO is significantly reduced in both high-and low-drinking rats (Ͻ30%) compared with age-matched nondrinking controls (Ͼ70%). Together, our findings demonstrate the protective nature of VTA DORs and identify an important new target for therapeutic intervention for alcoholism.

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The effects of post-stress exposure to alcohol upon the development of alcohol consumption in rats

Cited by 12 publications

References 14 publications

Role of Fyn Tyrosine Kinase in Ethanol Consumption by Mice

Role of Fyn Tyrosine Kinase in Ethanol Consumption by Mice

Role of single prolonged stress in acquisition of alcohol conditioned place preference in rats

δ-Opioid Receptor Expression in the Ventral Tegmental Area Protects Against Elevated Alcohol Consumption

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