Molecular Mechanisms of Drug-Induced Plasticity

Abstract

Substance-use disorders (SUDs) are a significant societal burden. Like many other conditions, SUDs are characterized by chronic relapse after periods without symptoms. Alterations in synaptic plasticity have been documented after acute and addiction-related behavioral exposures to drugs of abuse. These synaptic alterations are persistent and similar to the chronic relapse state of patients with SUDs, suggesting that reversing these synaptic alterations may prevent relapse. Additionally, many of these synaptic features of addiction mirror those found in other forms of learning and memory. These features suggest that the etiology of this disorder stems from persistent modifications in corticolimbic synaptic plasticity mediated by drug-induced alterations in addiction-related gene (ARG) expression. Understanding the regulation of addiction-related genes and their impact on synaptic plasticity and behavior may inform new pharmacological treatments that reverse these aberrant drug-evoked forms of plasticity in favor of remission