More recently, a study observed a gradual increase in the expression of brain-derived neurotrophic factor (BDNF) in the mPFC during acute withdrawal from repetitive cocaine exposure in rats (Lu et al., 2010). This led to a downregulation of GABA-AR-mediated transmission and a subsequent facilitation of activity-induced long-term potentiation (LTP) of excitatory synapses on layer V pyramidal neurons. Taken together, these studies suggest that exposure to addictive drugs also causes glutamate receptor redistribution in PFC neurons, which, given the extensive literature implicating the PFC in drug-related behavior, is not surprising. In the future, direct characterizations of drug-evoked synaptic plasticity in identified synapse will allow for a better understanding of the circuit adaptations in the PFC in response to addictive drugs.
