The genomic determinants of alcohol preference in mice

Tabakoff, Boris; Saba, Laura; Kechris, Katerina; Hu, Wei; Bhave, Sanjiv V.; Finn, Deborah A.; Grahame, Nicholas J.; Hoffman, Paula L.

doi:10.1007/s00335-008-9115-z

Cited by 68 publications

(81 citation statements)

References 57 publications

(69 reference statements)

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“…FC, STR, VMB, and HIP contain structures and circuitry involved in both neuroadaptation to alcohol and the neurocognitive processes that underlie addiction behavior [24]. OB and CB are implicated in the initial preference drinking in rodents, and initial sensitivity and acute tolerance to the ataxic effects of alcohol respectively [25].…”

Section: Brain Harvest and Blood Alcohol Determinationmentioning

confidence: 99%

RETRACTED ARTICLE: Identification of gene expression profile in the rat brain resulting from acute alcohol intoxication

Kong

Yang

et al. 2014

Mol Biol Rep

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This study aimed to identify gene expression profile in the rat brain resulting from acute alcohol intoxication (AAI). Eighteen SD rats were divided into the alcohol-treated group (n = 9) and saline control group (n = 9). Periorbital blood samples were taken to determine their blood alcohol content by gas chromatography. Tissue sections were analyzed by H and E staining and biochemical assays. Real-time reverse transcription PCR was used to validate microarray data. Statistical analysis was carried out using SPSS18.0 software (Version 18.0, SPSS Inc., Chicago, IL, USA). H and E staining demonstrated that alcohol-treated rats showed no obvious pathological changes in nerve cells compared with those in the control group. Biochemical tests revealed that alcohol-treated rats had lower superoxide dismutase activity than those in the control group (167.3 ± 10.3 U/mg vs. 189.2 ± 5.9 U/mg, P < 0.05). Furthermore, the malondialdehyde levels in alcohol-treated rats were higher than those in the control group (3.48 ± 0.24 mmol/mg vs. 2.51 ± 0.23 mmol/mg, P < 0.05). Microarray data presented 366 up-regulated genes and 300 down-regulated genes in the AAI rat brain. Gene ontology analysis identified 31 genes up-regulated and 39 down-regulated among all differentially expressed genes. Twenty-four pathways showed significant differences, including 12 pathways involved with up-regulated genes and 12 pathways involved with down-regulated genes. Selected genes showed significantly different expression in both alcohol-treated and control groups (P < 0.05). Gene expression analysis enabled clustering of alcohol intoxication-related genes by function. These genes expression may be potential targets for treatment or drug screening for acute alcohol intoxication.

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Section: Brain Harvest and Blood Alcohol Determinationmentioning

confidence: 99%

RETRACTED ARTICLE: Identification of gene expression profile in the rat brain resulting from acute alcohol intoxication

Kong

Yang

et al. 2014

Mol Biol Rep

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“…The neuroimmune transcriptome & alcohol dependence: potential for targeted therapies Review identified immune and inflammatory transcripts and pathways in alcohol-exposed tissue from mice, rats and human tissue [3][4][5]34,[102][103][104]. Several immune genes found in these microarray studies were validated in rodent ethanol consumption paradigms, further corroborating a role for neuroimmune signaling in drinking behavior [14,105].…”

Section: Microglia Alcohol Activation Of Microglial Genesmentioning

confidence: 98%

The Neuroimmune Transcriptome and Alcohol Dependence: Potential for Targeted Therapies

et al. 2016

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Transcriptome profiling enables discovery of gene networks that are altered in alcoholic brains. This technique has revealed involvement of the brain's neuroimmune system in regulating alcohol abuse and dependence, and has provided potential therapeutic targets. In this review, we discuss Toll-like-receptor pathways, hypothesized to be key players in many stages of the alcohol addiction cycle. The growing appreciation of the neuroimmune system's involvement in alcoholism has also led to consideration of crucial roles for glial cells, including astrocytes and microglia, in the brain's response to alcohol abuse. We discuss current knowledge and hypotheses on the roles that specific neuroimmune cell types may play in addiction. Current strategies for repurposing US FDA-approved drugs for the treatment of alcohol use disorders are also discussed.

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“…Ethanol preference has been an important subject for studies in alcohol abuse and dependence (Green and Grahame 2008; Tabakoff et al 2008). Oral ethanol consumption is widely used to investigate the genetic and neurobiological basis for high ethanol preference (Murphy et al 2002; Tabakoff et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of phosphodiesterase-4 decreases ethanol intake in mice

Chen

et al. 2011

Psychopharmacology

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Rationale Cyclic AMP (cAMP)-protein kinase A (PKA) signaling has been implicated in the regulation of ethanol consumption. Phosphodiesterase-4 (PDE4) specifically hydrolyzes cAMP and plays a critical role in controlling intracellular cAMP levels in the brain. However, the role of PDE4 in ethanol consumption remains unknown. Objective To examine whether PDE4 was involved in regulating ethanol intake. Methods The two-bottle choice paradigm was used to assess intake of ethanol, sucrose, and quinine in C57BL/6J mice treated with the selective PDE4 inhibitor rolipram or Ro 20-1724; locomotor activity was also monitored using the open-field test in mice treated with rolipram. Results Administration (i.p.) of either rolipram (0.25 and 0.5 mg/kg) or Ro 20-1724 (10 mg/kg) reduced ethanol intake and preference by 60-80%, but did not alter total fluid intake. In contrast, rolipram even at the higher dose of 0.5 mg/kg was not able to affect intake of sucrose or quinine, alcohol-induced sedation, or blood ethanol elimination. At 0.5 mg/kg, rolipram did decrease locomotor activity, but the effect only lasted for approximately 40 min, which did not likely affect behavior of ethanol drinking. Conclusions These results suggest that PDE4 is a novel target for drugs that reduce ethanol intake; PDE4 inhibitors may be used for treatment of alcohol dependence.

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The genomic determinants of alcohol preference in mice

Cited by 68 publications

References 57 publications

RETRACTED ARTICLE: Identification of gene expression profile in the rat brain resulting from acute alcohol intoxication

RETRACTED ARTICLE: Identification of gene expression profile in the rat brain resulting from acute alcohol intoxication

The Neuroimmune Transcriptome and Alcohol Dependence: Potential for Targeted Therapies

Inhibition of phosphodiesterase-4 decreases ethanol intake in mice

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