This chapter reviews synaptic transmission and plasticity in the basal ganglia (BG). The striatum contains mostly spiny projection neurons (SPNs), which are normally silent and only show brief bursts of activity when activated by a strong excitatory drive. There are also multiple classes of striatal interneurons, which are far fewer in number but still play critical roles in regulating striatal output. Unlike the SPNs, the pallidal projection neurons often show high tonic firing rates, being endowed with membrane properties that permit spontaneous activity even in the absence of synaptic inputs. Both striatal and pallidal projection neurons send axon collaterals to neighboring neurons, forming a lateral inhibition circuit. In the BG, many neuromodulators (e.g. dopamine [DA] and endocannabinoids [eCBs]) activate G-protein–coupled receptors that indirectly modulate both neuronal excitability and synaptic transmission. In addition, long-term synaptic plasticity can change synaptic strength more permanently. Two forms of such plasticity have been extensively studied. Corticostriatal long-term potentiation is a type of heterosynaptic plasticity, in which DA plays an important role in determining the direction of plasticity. On the other hand, striatal long-term depression requires the release of eCBs in the postsynaptic neuron, which act as retrograde messengers to reduce presynaptic transmitter release.