in the VTA significantly prolongs the persistence of cocaine-evoked plasticity (Mameli et al., 2009). Taken together, these results suggest that mGluR1 triggers an endogenous defense mechanism that ensures the removal of calcium permeable AMPARs, which were inserted in response to drug-exposure. It will be important to determine why such a mechanism does not appear to function following prolonged self-administration of cocaine (Chen et al., 2008).
