Circuit and Synaptic Plasticity Mechanisms of Drug Relapse

J Neurosci. 2017 Nov 8;37(45):10867-10876. doi: 10.1523/JNEUROSCI.1821-17.2017.

Abstract

High rates of relapse to drug use during abstinence is a defining feature of human drug addiction. This clinical scenario has been studied at the preclinical level using different animal models in which relapse to drug seeking is assessed after cessation of operant drug self-administration in rodents and monkeys. In our Society for Neuroscience (SFN) session entitled "Circuit and Synaptic Plasticity Mechanisms of Drug Relapse," we will discuss new developments of our understanding of circuits and synaptic plasticity mechanisms of drug relapse from studies combining established and novel animal models with state-of-the-art cellular, electrophysiology, anatomical, chemogenetic, and optogenetic methods. We will also discuss the translational implications of these new developments. In the mini-review that introduces our SFN session, we summarize results from our laboratories on behavioral, cellular, and circuit mechanisms of drug relapse within the context of our session.

Keywords: CP-AMPARs; Daun02 inactivation; alcohol; circuit ablation; cocaine; diphtheria toxin receptors; drug cues; homeostatic plasticity; incubation of drug craving; reinstatement; relapse; silent synapse.

Publication types

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

MeSH terms

  • Animals
  • Drug-Seeking Behavior
  • Humans
  • Nerve Net / physiopathology*
  • Neural Pathways
  • Neuronal Plasticity*
  • Recurrence
  • Substance-Related Disorders / physiopathology
  • Substance-Related Disorders / psychology*