Linked Life Data

16191445

Source:http://linkedlifedata.com/resource/pubmed/id/16191445

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-11-28
pubmed:abstractText
Chronic alcohol consumption (CAC) provokes intense neurobiological alterations, which lead, notably, to an important abstinence syndrome upon withdrawal with deleterious cognitive consequences. We here examined the effect of activation or inactivation of the sigma(1) receptor during CAC withdrawal on the cognitive abilities of Swiss mice. Animals consumed an alcohol 10%/sucrose 30 g/l solution during 4 months. Control groups consumed only the sucrose vehicle solution. Then, animals experienced a progressive, 16 days long, CAC withdrawal, during which they were administered once daily with saline, igmesine (10 mg/kg i.p.), a sigma(1) receptor agonist, or BD1047 (10 mg/kg i.p.), a sigma(1) antagonist. Mice were then tested using an object exploration task, to evaluate their locomotor and exploratory activities and reactions to object habituation, spatial change or novel object presentation. CAC-treated animals showed augmentation of locomotion, anxiety and object exploration, which impeded correct reaction to object habituation, spatial change or novelty. Treatment with the sigma(1) ligands, ineffective in control groups, resulted in decrease of the hyper-responsiveness and restored habituation. However, correct reactions to spatial change and novelty were only produced by the sigma(1) agonist treatment. Moreover, the sigma(1) receptor hippocampal expression was increased in CAC-treated mice. Treatments with both sigma(1) ligands regulated its expression, but subcellular fractionation experiments revealed that the agonist treatment increased [(3)H](+)-pentazocine binding to sigma(1) sites in the plasma membrane fraction, while the antagonist maintained it only in the microsomal, putatively endoplasmic reticulum, fraction. In conclusion, CAC increased the sigma(1) receptor expression in the hippocampus of mice. Regulation of its expression during withdrawal, notably using a selective agonist, allowed not only to attenuate the CAC-induced hyper-responsiveness, but also to restore correct cognitive abilities.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0166-4328
pubmed:author
pubmed:issnType
Print
pubmed:day
6
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
166-76
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16191445-Alcohol Drinking, pubmed-meshheading:16191445-Alcohols, pubmed-meshheading:16191445-Analysis of Variance, pubmed-meshheading:16191445-Animals, pubmed-meshheading:16191445-Behavior, Animal, pubmed-meshheading:16191445-Blotting, Western, pubmed-meshheading:16191445-Cell Fractionation, pubmed-meshheading:16191445-Cinnamates, pubmed-meshheading:16191445-Cyclopropanes, pubmed-meshheading:16191445-Drug Interactions, pubmed-meshheading:16191445-Ethylenediamines, pubmed-meshheading:16191445-Exploratory Behavior, pubmed-meshheading:16191445-Gene Expression Regulation, pubmed-meshheading:16191445-Habituation, Psychophysiologic, pubmed-meshheading:16191445-Male, pubmed-meshheading:16191445-Mice, pubmed-meshheading:16191445-Neuropsychological Tests, pubmed-meshheading:16191445-Pentazocine, pubmed-meshheading:16191445-Radioligand Assay, pubmed-meshheading:16191445-Receptors, sigma, pubmed-meshheading:16191445-Recognition (Psychology), pubmed-meshheading:16191445-Substance Withdrawal Syndrome, pubmed-meshheading:16191445-Time Factors, pubmed-meshheading:16191445-Tritium
pubmed:year
2006
pubmed:articleTitle
Compensatory effect by sigma1 (sigma1) receptor stimulation during alcohol withdrawal in mice performing an object recognition task.
pubmed:affiliation
CNRS FRE 2693, Université de Montpellier II, cc 090, Place Eugène Bataillon, 34095 Montpellier cedex 5, France.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't