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Rescuing prefrontal cAMP-CREB pathway reverses working memory deficits during withdrawal from prolonged alcohol

G Dominguez1,2, M Dagnas1, L Decorte1

  • 1Institut de Neurosciences Cognitives et Intégratives d'Aquitaine, Nouvelle Université de Bordeaux, CNRS UMR 5287, Talence, France.

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Summary

Alcohol withdrawal impairs working memory by disrupting the protein kinase A (PKA)/cAMP-responsive element binding (CREB) pathway in the prefrontal cortex. This pathway is crucial for cognitive function during sustained withdrawal.

Keywords:
AlcoholismBehaviorHippocampusHistone acetylationPKAPrefrontal cortex

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Behavioral Science

Background:

  • Chronic alcohol consumption (CAC) and subsequent withdrawal negatively impact cognitive functions, particularly those mediated by the prefrontal cortex (PFC).
  • The protein kinase A (PKA)/cAMP-responsive element binding (CREB) signaling cascade is implicated in memory deficits during alcohol withdrawal, but its role in sustained withdrawal remains unclear.

Purpose of the Study:

  • To investigate the role of the PKA/CREB signaling cascade in the PFC and hippocampus during sustained alcohol withdrawal.
  • To determine the molecular mechanisms underlying working memory (WM) impairments following chronic alcohol consumption and withdrawal.

Main Methods:

  • Utilized a mouse model of chronic alcohol consumption and withdrawal.
  • Assessed working memory using the T-maze spontaneous alternation task.
  • Measured levels of phosphorylated CREB (pCREB) and histone H4 acetylation in the PFC and dorsal CA1 (dCA1) region of the hippocampus.
  • Administered rolipram (a CREB enhancer) and Sp-cAMPS (a PKA activator) via systemic injection or direct PFC/dCA1 infusion.

Main Results:

  • Withdrawal after 6-month CAC impaired WM and reduced pCREB in the PFC, but not dCA1.
  • Both unimpaired and withdrawn mice showed decreased pCREB in dCA1 and reduced histone H4 acetylation in PFC and dCA1 compared to controls.
  • Enhancing CREB activity improved WM in withdrawn mice but impaired it in control mice, correlating with increased PFC pCREB.
  • PKA activation in the PFC improved WM in withdrawn mice but impaired it in control mice, with no effect in the dCA1.

Conclusions:

  • Dysregulation of PKA/CREB signaling in prefrontal neurons is a key molecular mechanism underlying cognitive deficits during alcohol withdrawal.
  • The PFC, specifically its PKA/CREB-dependent processes, plays a critical role in mediating working memory impairments associated with alcohol withdrawal.
  • Targeting the PKA/CREB pathway in the PFC may offer therapeutic strategies for cognitive dysfunction in alcohol withdrawal syndrome.