An additional important question is whether the drug-evoked synaptic plasticity in VTA DA neurons is induced uniformly at all excitatory inputs onto a given DA neuron. These arise from many origins including the PFC, the amygdala, the lateral hypothalamus and brain stem nuclei such as the pedunculopontine tegmentum and the basal nucleus of the stria terminalis. Optogenetic approaches involving expression of ChR2 in specific brain regions should help provide an answer to this question in the near future. Identifying both the specific synapses that are subject to drug-evoked plasticity and how the site to which DA cells project influence their synaptic adaptations will be a necessary prerequisite to fully understanding the complex neural circuit adaptations caused by drug experiences.
