One of the most fascinating and important properties of the mammalian brain is its plasticity:  the ability of an experience, whether it be a stressful event or ingestion of a drug, to modify the functioning of the brain’s complex neural circuits and thereby modify subsequent thoughts, feelings and behavior.  Experience-dependent brain plasticity is in large part due to long-lasting, activity-dependent changes in the strength of communication at excitatory synapses.  The most well understood forms of such synaptic plasticity, termed long-term potentiation (LTP) and long-term depression (LTD), play important roles in several forms of adaptive learning and memory.  After reviewing the basic properties of these intriguing cellular phenomena, I will review evidence demonstrating that drugs of abuse elicit synaptic plasticity in key cells of the brain’s reward circuitry and how these findings led to a more sophisticated understanding of the brain’s circuits that mediate reward and aversion.