Exposure to cocaine generates silent synapses in the nucleus accumbens (NA c), whose
eventual unsilencing/maturation by recruitment of calcium‐permeable AMPA‐type glutamate …

Cocaine experience generates AMPA receptor (AMPAR)-silent synapses in the nucleus
accumbens (NAc), which are thought to be new synaptic contacts enriched in GluN2B …

In rat models of drug relapse and craving, cue-induced cocaine seeking progressively
increases after withdrawal from the drug. This' incubation of cocaine craving'is partially …

Exposure to cocaine induces addiction-associated behaviors partially through remodeling
neurocircuits in the nucleus accumbens (NAc). The paraventricular nucleus of thalamus …

Exposures to cocaine and morphine produce similar adaptations in nucleus accumbens
(NAc)-based behaviors, yet produce very different adaptations at NAc excitatory synapses …

Following prolonged withdrawal from extended access cocaine self-administration in adult
rats, high conductance Ca2+-permeable AMPA receptors (CP-AMPARs) accumulate in …

Rationale When ad libitum-fed (AL) rats undergo cocaine place preference conditioning
(CPP) but are switched to food restriction (FR) for testing, CPP is enhanced and preference …

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

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 …

Glutamatergic synapses are key cellular sites where cocaine experience creates memory
traces that subsequently promote cocaine craving and seeking. In addition to making across …