Synaptic and intrinsic plasticity in the ventral tegmental area after chronic cocaine

Curr Opin Neurobiol. 2019 Feb:54:66-72. doi: 10.1016/j.conb.2018.08.013. Epub 2018 Sep 17.

Abstract

Cocaine exposure induces persistent changes in synaptic transmission and intrinsic properties of ventral tegmental area (VTA) dopamine neurons. Despite significant progress in understanding cocaine-induced plasticity, an effective treatment of cocaine addiction is lacking. Chronic cocaine potentiates excitatory and alters inhibitory transmission to dopamine neurons, induces dopamine neuron hyperexcitability, and reduces dopamine release in projection areas. Understanding how intrinsic and synaptic plasticity interact to control dopamine neuron firing and dopamine release could prove useful in the development of new therapeutics. In this review, we examine recent literature discussing cocaine-induced plasticity in the VTA and highlight potential therapeutic interventions.

Publication types

  • Research Support, N.I.H., Intramural
  • Review

MeSH terms

  • Animals
  • Cocaine / pharmacology*
  • Cocaine-Related Disorders / pathology
  • Dopamine / metabolism
  • Dopamine Uptake Inhibitors / pharmacology*
  • Dopaminergic Neurons / drug effects*
  • Dopaminergic Neurons / physiology
  • Humans
  • Neuronal Plasticity / drug effects*
  • Neurotransmitter Agents / metabolism
  • Synapses / drug effects*
  • Ventral Tegmental Area / cytology*
  • Ventral Tegmental Area / drug effects
  • Ventral Tegmental Area / metabolism

Substances

  • Dopamine Uptake Inhibitors
  • Neurotransmitter Agents
  • Cocaine
  • Dopamine