Synaptic plasticity and addiction: learning mechanisms gone awry

Neuropharmacology. 2011 Dec;61(7):1052-9. doi: 10.1016/j.neuropharm.2011.01.036. Epub 2011 Jan 28.

Abstract

Experience-dependent changes in synaptic strength, or synaptic plasticity, may underlie many learning processes. In the reward circuit for example, synaptic plasticity may serve as a cellular substrate for goal-directed behaviors. Addictive drugs, through a surge of dopamine released from neurons of the ventral tegmental area, induce widespread synaptic adaptations within this neuronal circuit. Such drug-evoked synaptic plasticity may constitute an early cellular mechanism eventually causing compulsive drug-seeking behavior in some drug users. In the present review we will discuss how different classes of addictive drugs cause an increase of dopamine release and describe their effects on synapses within the mesolimbic dopamine system. We will emphasize the early synaptic changes in the ventral tegmental area common to all additive drugs and go on to show how these adaptations may reorganize neuronal circuits, eventually leading to behaviors that define addiction.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cocaine / adverse effects
  • Cocaine-Related Disorders / physiopathology
  • Dopamine / metabolism
  • Dopamine Uptake Inhibitors / adverse effects
  • Drug-Seeking Behavior*
  • Humans
  • Learning*
  • Neuronal Plasticity / drug effects*
  • Neurons / drug effects
  • Neurons / metabolism
  • Substance-Related Disorders / physiopathology*
  • Ventral Tegmental Area / drug effects
  • Ventral Tegmental Area / physiology
  • Ventral Tegmental Area / physiopathology

Substances

  • Dopamine Uptake Inhibitors
  • Cocaine
  • Dopamine