Addiction is a behavioral disease, of which core components can be modeled in rodents.
Much evidence implicates drug-evoked synaptic plasticity in cocaine-evoked locomotor …

Drug-evoked synaptic plasticity in the mesolimbic dopamine (DA) system reorganizes neural
circuits that may lead to addictive behavior. The first cocaine exposure potentiates AMPAR …

Drugs of abuse induce long-lasting changes in neural circuits that may underlie core
components of addiction. Here we focus on glutamatergic synapses onto dopamine (DA) …

Background Addictive drugs have in common that they cause surges in dopamine (DA)
concentration in the mesolimbic reward system and elicit synaptic plasticity in DA neurons of …

Cocaine strengthens excitatory synapses onto midbrain dopamine neurons through the
synaptic delivery of GluR1-containing AMPA receptors. This cocaine-evoked plasticity …

Repeated exposure to psychostimulant drugs such as cocaine or amphetamine can promote
drug-seeking and-taking behavior. In rodent addiction models, persistent changes in …

Plasticity of glutamatergic synapses is a fundamental mechanism through which experience
changes neural function to impact future behavior. In animal models of addiction …

AMPA receptor (AMPAR) plasticity at glutamatergic synapses in the mesoaccumbal
dopaminergic pathway has been implicated in persistent cocaine-induced behavioral …

Chronic cocaine use reduces glutamate levels in the nucleus accumbens (NAc), and is
associated with experience‐dependent changes in (±)‐α‐amino‐3‐hydroxy‐5 …

Understanding the neurobiological processes that incite drug craving and drive relapse has
the potential to help target efforts to treat addiction. The NAc serves as a critical substrate for …