Chronic intermittent ethanol exposure and withdrawal leads to adaptations in nucleus accumbens core postsynaptic density proteome and dendritic spines

Addiction Biology
Joachim D UysPatrick J Mulholland

Abstract

Alcohol use disorder is a chronic relapsing brain disease characterized by the loss of ability to control alcohol (ethanol) intake despite knowledge of detrimental health or personal consequences. Clinical and pre-clinical models provide strong evidence for chronic ethanol-associated alterations in glutamatergic signaling and impaired synaptic plasticity in the nucleus accumbens (NAc). However, the neural mechanisms that contribute to aberrant glutamatergic signaling in ethanol-dependent individuals in this critical brain structure remain unknown. Using an unbiased proteomic approach, we investigated the effects of chronic intermittent ethanol (CIE) exposure on neuroadaptations in postsynaptic density (PSD)-enriched proteins in the NAc of ethanol-dependent mice. Compared with controls, CIE exposure significantly changed expression levels of 50 proteins in the PSD-enriched fraction. Systems biology and functional annotation analyses demonstrated that the dysregulated proteins are expressed at tetrapartite synapses and critically regulate cellular morphology. To confirm this latter finding, the density and morphology of dendritic spines were examined in the NAc core of ethanol-dependent mice. We found that CIE exposure and withdr...Continue Reading

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Citations

Jul 3, 2015·Brain Sciences·Joan Y Holgate, Selena E Bartlett
Dec 1, 2015·Frontiers in Cellular Neuroscience·Paolo FollesaGiorgio Gorini
May 14, 2016·Trends in Neurosciences·Patrick J MulhollandPeter W Kalivas
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May 1, 2021·International Journal of Molecular Sciences·Anna K RadkeFrederic W Hopf

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