Opioid-Induced Neuroplasticity: Insights from Animal Models

Abstract

Synaptic plasticity is defined as the modification of the transmission of synapses. It has been proven to be strongly associated with learning. Thus, drug-evoked synaptic plasticity in brain reward circuits can establish persistent learning of addictive drugs, reflecting the neural basis underlying addiction. The mesolimbic dopamine pathway has been widely indicated to be strongly associated with opioid use disorder (OUD) and other drug addictions. The paper focuses on discussing the drug-evoked neural plasticity underlying two important stages called intoxication and withdrawal which are critical for addiction and reinstatement of drug use respectively. The paper first explores the neural basis of OUD, emphasizing drug-induced plasticity at glutamate and Gamma-aminobutyric acid (GABA) synapses on neurons of key substrates in the pathway and how they influence mesolimbic dopamine (DA) neuron transmission. Then, the review discussed withdrawal-induced neuroplasticity and reorganization of associated neuron circuits, which explain deficits led by withdrawal from opioid administration. An overall understanding of drug-evoked synaptic plasticity in key brain circuits in the development of addiction helps find possible therapeutic methods to prevent the initiation of OUD and reinstatement.