Using viral vectors, we express light-activatable ion channels in neurons such that their activity can be controlled in freely moving animals. With this approach we have observed that mice will self-stimulate for light activating midbrain dopamine neurons and will avoid situations where these neurons are inhibited. Strong stimulation of dopamine neurons mimics synaptic traces left by addictive drugs such as cocaine. We are developing strategies using optogenetic manipulation to reverse drug-evoked synaptic plasticity to restore normal behavior.