cocaine evoked synaptic potentiation

• We find that cocaine potentiates excitatory transmission in D1-receptor-expressing medium-sized spiny neurons (D1R-MSNs) in mice via ERK signalling with a time course that parallels locomotor sensitization
•  Depotentiation of cortical nucleus accumbens inputs by optogenetic stimulation in vivo efficiently restored normal transmission and abolished cocaine-induced locomotor sensitization. 
• These findings establish synaptic potentiiation selectively in D1R-MSNs as a mechanism underlying a core component of addiction, probably by creating an imbalance between distinct populations of MSNs in the nucleus accumbens. 
• Our data also provide proof of principle that reversal of cocaine-evoke synaptic plasticity can treat behavioural alterations caused by addictive drugs and may inspire novel therapeutic approaches involving deep brain stimulation or transcranial magnetic stimulation.

Nature. 2011 Dec 7;481(7379):71-5. doi: 10.1038/nature10709.

Reversal of cocaine-evoked synaptic potentiation resets drug-induced adaptive behaviour.