A role for corticotropin releasing factor (CRF) in ethanol consumption, sensitivity, and reward as revealed by CRF-deficient mice

Mehmert, Kristin K.; Koenig, Heather N.; Camarini, Rosana; Kim, Joseph A.; Nannini, Michelle; Ou, Christine J.; Hodge, Clyde W.

doi:10.1007/s00213-002-1248-2

Cited by 79 publications

(53 citation statements)

References 45 publications

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“…Corticotropin releasing factor (CRF) is another CREB target gene, and it has previously been shown that CRF expression is lower in the CeA of P rats compared with NP rats (16). Since CRF is implicated in anxiety and alcohol-drinking behaviors (8,58), it possible that CREB may regulate anxiety and alcohol-drinking behaviors of P rats via the CRF system. Future studies are needed to investigate the role of CRF or other CREB-related genes (27) in the neural circuitry of the CeA and MeA with the phenomenon of anxiety and alcohol preference in P rats or in other animal models.…”

Section: Figurementioning

confidence: 99%

Deficits in amygdaloid cAMP-responsive element–binding protein signaling play a role in genetic predisposition to anxiety and alcoholism

Pandey¹,

Zhang²,

Roy³

et al. 2005

J. Clin. Invest.

185

178

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We investigated the role of cAMP-responsive element-binding protein (CREB) in genetic predisposition to anxiety and alcohol-drinking behaviors using alcohol-preferring (P) and -nonpreferring (NP) rats. The levels of CREB, phosphorylated CREB, and neuropeptide Y (NPY) were innately lower in the central amygdala (CeA) and medial amygdala (MeA), but not in the basolateral amygdala (BLA), of P rats compared with NP rats. P rats displayed higher baseline anxiety-like behaviors and consumed higher amounts of alcohol compared with NP rats. Ethanol injection or voluntary intake reduced the higher anxiety levels in P rats. Ethanol also increased CREB function in the CeA and MeA, but not in the BLA, of P rats. Infusion of the PKA activator Sp-cAMP or NPY into the CeA decreased the alcohol intake and anxiety-like behaviors of P rats. PKA activator infusion also increased CREB function in the CeA of P rats. On the other hand, ethanol injection or voluntary intake did not produce any changes either in anxiety levels or on CREB function in the amygdaloid structures of NP rats. Interestingly, infusion of the PKA inhibitor Rp-cAMP into the CeA provoked anxiety-like behaviors and increased alcohol intake in NP rats. PKA inhibitor decreased CREB function in the CeA of NP rats. These novel results provide the first evidence to our knowledge that decreased CREB function in the CeA may be operative in maintaining the high anxiety and excessive alcohol-drinking behaviors of P rats.

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Section: Figurementioning

confidence: 99%

Deficits in amygdaloid cAMP-responsive element–binding protein signaling play a role in genetic predisposition to anxiety and alcoholism

Pandey¹,

Zhang²,

Roy³

et al. 2005

J. Clin. Invest.

185

178

View full text Add to dashboard Cite

show abstract

“…CRF over-expressing mice exhibit abnormalities that involve the HPA axis, including elevated levels of ACTH and glucocorticoids as well as other symptoms of Cushing's syndrome (Stenzel-Poore et al 1992;Coste et al 2001). We postulated that overexpression of CRF would have an effect opposite to that seen in CRF KO mice, which showed increased EtOH drinking (Olive et al 2003). Once we identified differences in EtOH drinking, we postulated that these differences might be due to differences in taste, in EtOH sensitivity, or in sensitivity to the aversive properties of EtOH.…”

Section: Introductionmentioning

confidence: 96%

“…We are unaware of similar studies in the replicated high and low alcohol drinking (HAD and LAD) rat lines or high and low alcohol preferring (HAP and LAP) mouse lines that would substantiate these findings. However, CRF knockout (KO) mice that carry a targeted deletion of the CRF gene, and thus express no CRF, voluntarily consumed significantly more EtOH when compared with wild type mice of a similar genetic background (Olive et al 2003). These CRF deficient mice also failed to show EtOH conditioned place preference (CPP) at lower doses, but did exhibit CPP at higher EtOH doses.…”

Section: Introductionmentioning

confidence: 98%

Corticotropin-releasing factor overexpression decreases ethanol drinking and increases sensitivity to the sedative effects of ethanol

et al. 2004

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“…Voluntary ethanol consumption Increased ethanol consumption in KO mice(Olive et al 2003) Voluntary ethanol consumption No effect of KO…”

mentioning

confidence: 99%

Pharmacogenetic studies of alcohol self-administration and withdrawal

Crabbe

Phillips

2003

Psychopharmacology

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A role for corticotropin releasing factor (CRF) in ethanol consumption, sensitivity, and reward as revealed by CRF-deficient mice

Abstract: CRF deficiency may lead to excessive ethanol consumption by reducing sensitivity to the locomotor stimulant and rewarding effects of ethanol.

Cited by 79 publications

References 45 publications

Deficits in amygdaloid cAMP-responsive element–binding protein signaling play a role in genetic predisposition to anxiety and alcoholism

Deficits in amygdaloid cAMP-responsive element–binding protein signaling play a role in genetic predisposition to anxiety and alcoholism

Corticotropin-releasing factor overexpression decreases ethanol drinking and increases sensitivity to the sedative effects of ethanol

Pharmacogenetic studies of alcohol self-administration and withdrawal

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