RGD Reference Report - Effects of chronic ethanol intake and its withdrawal on the expression and phosphorylation of the creb gene transcription factor in rat cortex. - Rat Genome Database

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Effects of chronic ethanol intake and its withdrawal on the expression and phosphorylation of the creb gene transcription factor in rat cortex.

Authors: Pandey, S C  Roy, A  Mittal, N 
Citation: Pandey SC, etal., J Pharmacol Exp Ther. 2001 Mar;296(3):857-68.
RGD ID: 401959326
Pubmed: PMID:11181917   (View Abstract at PubMed)

This investigation examined the effects of chronic ethanol treatment (15 days) and its withdrawal (24 h) on the expression and phosphorylation of cyclic AMP-response element-binding (CREB) protein in the rat cortex. The effects of chronic ethanol treatment and withdrawal on protein kinase A (PKA) activity and on the expression of the regulatory RII-beta- and the alpha-subtype catalytic subunits of PKA, and on the protein expression of Ca(2+)/calmodulin-dependent protein kinase IV (CaM kinase IV) and calcineurin in the rat cortex were also investigated. It was found that ethanol withdrawal but not ethanol treatment produced a significant decrease in the phosphorylated CREB (p-CREB) and CaM kinase IV protein levels in the frontal, parietal, and piriform cortex. Ethanol treatment and its withdrawal had no effect on the protein levels of total CREB in the frontal, parietal, and piriform cortex. On the other hand, ethanol treatment produced a significant reduction in the protein levels of CREB, p-CREB, and CaM kinase IV in the cingulate gyrus, and these changes reverted to normal levels during ethanol withdrawal. Total CREB protein levels were significantly higher in the cingulate gyrus during ethanol withdrawal. It was also observed that mRNA levels of CREB were significantly higher in the rat cortex during ethanol withdrawal but not during ethanol treatment. The protein levels of RII-beta- and alpha-subtype catalytic subunits of PKA and PKA activity were not modified in the rat cortex by chronic ethanol treatment and its withdrawal. Furthermore, the expression of calcineurin in the rat cortex was not altered during ethanol treatment and withdrawal. Taken together, these results suggest the possibility that decreased CREB-dependent events in the neurocircuitry of the frontal, parietal, and piriform cortex may play an important role in the phenomenon of alcohol dependence and also that decreased CREB-dependent events in the neurocircuitry of the cingulate gyrus may play a role in alcohol tolerance.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
alcohol use disorder  ISOCamk4 (Rattus norvegicus)401959326; 401959326protein:decreased expression:brain and cingulate gyrusRGD 
alcohol use disorder  IEP 401959326protein:decreased expression:brain and cingulate gyrusRGD 
withdrawal disorder  ISOCamk4 (Rattus norvegicus)401959326; 401959326associated with alcohol use disorder and protein:decreased expression:brainRGD 
withdrawal disorder  ISOCreb1 (Rattus norvegicus)401959326; 401959326associated with alcohol use disorder more ...RGD 
withdrawal disorder  IEP 401959326associated with alcohol use disorder and protein:decreased expression:brainRGD 
withdrawal disorder  IDA 401959326associated with alcohol use disorder more ...RGD 

Objects Annotated

Genes (Rattus norvegicus)
Camk4  (calcium/calmodulin-dependent protein kinase IV)
Creb1  (cAMP responsive element binding protein 1)

Genes (Mus musculus)
Camk4  (calcium/calmodulin-dependent protein kinase IV)
Creb1  (cAMP responsive element binding protein 1)

Genes (Homo sapiens)
CAMK4  (calcium/calmodulin dependent protein kinase IV)
CREB1  (cAMP responsive element binding protein 1)


Additional Information