GeneSet Information

Tier III GS75753 • Gene expression in rat frontal cortex and amygdala following prolonged intermittent ethanol exposure

DESCRIPTION:

Expression analysis of cingulate cortex and amygdala reveals a set of long-term up-regulated transcripts in this model. Here lists the gene expression changes 3 wk after termination of 7 wk of intermittent ethanol exposure. Fold change values are ethanol exposed vs. control rats. From Rimondini et al., 2002.

LABEL:

intermittent ethanol rat

SCORE TYPE:

Effect

DATE ADDED:

2010-07-01

DATE UPDATED:

2020-05-06

SPECIES:

AUTHORS:

Rimondini R, Arlinde C, Sommer W, Heilig M

TITLE:

Long-lasting increase in voluntary ethanol consumption and transcriptional regulation in the rat brain after intermittent exposure to alcohol.

JOURNAL:

The FASEB journal : official publication of the Federation of American Societies for Experimental Biology Jan 2002, Vol 16, pp. 27-35

ABSTRACT:

Prolonged exposure of the brain to ethanol is a prerequisite for developing ethanol dependence, but the underlying neural adaptations are unknown. Here we demonstrate that rats subjected to repeated cycles of intoxication and withdrawal develop a marked and long-lasting increase in voluntary ethanol intake. Exposure-induced but not spontaneous alcohol intake is antagonized by acamprosate, a compound clinically effective in human alcoholism. Expression analysis of cingulate cortex and amygdala reveals a set of long-term up-regulated transcripts in this model. These include members of pathways previously implicated in alcohol dependence (glutamatergic, endocannabinoid, and monoaminergic neurotransmission), as well as pathways not previously thought to be involved in this disorder (e.g., members of the mitogen-activated protein kinase pathway). Thus, alternating periods of ethanol intoxication and withdrawal are sufficient to induce an altered functional brain state, which is likely to be encoded by long-term changes in gene expression. These observations may have important implications for how alcoholism is managed clinically. Novel clinically effective treatments may be possible to develop by targeting the products of genes found to be regulated in our model. PUBMED: 11772933
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Social Control, Formal (D012926)
Brain (D001921)
Frontal Lobe (D005625)
Animals (D000818)
Taurine (D013654)
Humans (D006801)
Corticosterone (D003345)
Gene Expression Profiling (D020869)
Behavior, Animal (D001522)
Alcohol Deterrents (D000427)
Conditioning, Operant (D003216)
Therapeutics (D013812)
Transcriptional Activation (D015533)
Adaptation, Physiological (D000222)
Amygdala (D000679)
Rats (D051381)
Up-Regulation (D015854)
Oligonucleotide Array Sequence Analysis (D020411)
Protein Kinases (D011494)
Phosphotransferases (D010770)
Gyrus Cinguli (D006179)
Set (Psychology) (D012718)
Kinetics (D007700)
Endocannabinoids (D043883)
Alcoholism (D000437)
Ethanol (D000431)
Rats, Wistar (D017208)
amygdala (MA:0000887)
frontal cortex (MA:0000905)
cingulate cortex (MA:0000904)
brain (MA:0000168)
gene expression (GO:0010467)

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Supported by NIH R01 AA18776 jointly funded by NIAAA and NIDA, and JAX Center for Precision Genetics NIH U54 OD 020351