Activity-dependent synaptic plasticity occurs in several parts of the basal ganglia. Increasing evidence supports the hypothesis that activity-dependent plasticity underlies the acquisition, maintenance, and extinction of certain types of learning in the basal ganglia. This review focuses on synaptic plasticity in the corticostriatal pathway. As in other systems, both long-term potentiation and long-term depression have been described, and intracellular calcium signalling plays an important role in the induction of plasticity. However, intracellular calcium levels do not appear to be the dominating control factor. Dopamine, via intracellular signalling cascades, also plays a crucial role in determining the magnitude and direction of plasticity, and in modulating the requirements for induction. Endocannabinoids also play an important role in mediating presynaptic expression of synaptic depression. Recent studies have highlighted spike-timing dependent plasticity phenomena, which also involve dopamine and endocannabinoid signalling. Despite significant progress in recent years, many important questions remain unanswered, especially in relation to long-term potentiation. Of particular interest is the question of how to link the molecular and cellular mechanisms of synaptic plasticity to learning operations at the systems level, which are expressed behaviourally as reinforcement-related learning.