Dopamine (DA) neurons in the ventral midbrain can act as a point of convergence for information arriving from various glutamate and GABA afferents. The synaptic inputs from these afferents to midbrain DA neurons undergo various forms of plasticity. Both excitatory and inhibitory afferents can undergo different forms of long-term potentiation (LTP) and long-term depression (LTD) in response to different experiences such as stress and exposure to drugs, and similar plasticity can be induced in vitro to selectively change currents mediated by AMPA, NMDA, GABA, and DA receptors. Plasticity can also be induced by specific afferents without eliciting changes in other afferents onto the same neuron. This input-specific synaptic plasticity in DA neurons could work with changes in intrinsic plasticity on different dendrites for local coincidence detection. Plasticity in midbrain DA neurons may underlie the association of cues and rewards, which would require the integration of information from separate sources (eg, sensory, motor, cognitive).