Molecular basis of alcoholism

Handb Clin Neurol. 2014:125:89-111. doi: 10.1016/B978-0-444-62619-6.00006-9.

Abstract

Acute alcohol intoxication causes cellular changes in the brain that last for hours, while chronic alcohol use induces widespread neuroadaptations in the nervous system that can last a lifetime. Chronic alcohol use and the progression into dependence involve the remodeling of synapses caused by changes in gene expression produced by alcohol. The progression of alcohol use, abuse, and dependence can be divided into stages, which include intoxication, withdrawal, and craving. Each stage is associated with specific changes in gene expression, cellular function, brain circuits, and ultimately behavior. What are the molecular mechanisms underlying the transition from recreational use (acute) to dependence (chronic)? What cellular adaptations result in drug memory retention, leading to the persistence of addictive behaviors, even after prolonged drug abstinence? Research into the neurobiology of alcoholism aims to answer these questions. This chapter will describe the molecular adaptations caused by alcohol use and dependence, and will outline key neurochemical participants in alcoholism at the molecular level, which are also potential targets for therapy.

Keywords: GABA; alcoholism; dependence; dopamine; glutamate; mRNA; microRNA; neuroadaptations; neuroimmune; neurotransmitter.

Publication types

  • Review

MeSH terms

  • Alcoholism / diagnosis
  • Alcoholism / genetics*
  • Alcoholism / metabolism*
  • Animals
  • Brain / metabolism*
  • Brain / pathology*
  • Humans
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • Receptors, GABA / genetics
  • Receptors, GABA / metabolism
  • Signal Transduction / physiology*

Substances

  • MicroRNAs
  • Receptors, GABA