RT Journal Article
SR Electronic
T1 Cocaine Experience Controls Bidirectional Synaptic Plasticity in the Nucleus Accumbens
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 7921
OP 7928
DO 10.1523/JNEUROSCI.1859-07.2007
VO 27
IS 30
A1 Kourrich, Saïd
A1 Rothwell, Patrick E.
A1 Klug, Jason R.
A1 Thomas, Mark J.
YR 2007
UL http://www.jneurosci.org/content/27/30/7921.abstract
AB Plasticity of glutamatergic synapses is a fundamental mechanism through which experience changes neural function to impact future behavior. In animal models of addiction, glutamatergic signaling in the nucleus accumbens (NAc) exerts powerful control over drug-seeking behavior. However, little is known about whether, how or when experience with drugs may trigger synaptic plasticity in this key nucleus. Using whole-cell synaptic physiology in NAc brain slices, we demonstrate that a progression of bidirectional changes in glutamatergic synaptic strength occurs after repeated in vivo exposure to cocaine. During a protracted drug-free period, NAc neurons from cocaine-experienced mice develop a robust potentiation of AMPAR-mediated synaptic transmission. However, a single re-exposure to cocaine during extended withdrawal becomes a potent stimulus for synaptic depression, abruptly reversing the initial potentiation. These enduring modifications in AMPAR-mediated responses and plasticity may provide a neural substrate for disrupted processing of drug-related stimuli in drug-experienced individuals.