The basal ganglia are a group of subcortical nuclei that are involved in a variety of functions including motor, cognitive and mnemonic behaviours. Central to our understanding of basal ganglia function is the relationship between the glutamatergic projection from the cortex to the principal division of the basal ganglia, the striatum, and the dopaminergic innervation of the same region, derived from the substantia nigra pars compacta. Thus excitatory corticostriatal afferents mainly innervate the spines of medium-sized spiny projection neurons and the response of the postsynaptic structure is modulated by the release of dopamine at the neck of the spine. The molecular mechanisms underlying the modulatory role of dopamine are numerous and dependent on a variety of factors including the type of dopamine receptor, but the net outcome is a facilitation or attenuation of the excitatory transmission. In addition to the excitatory input from the cortex, the striatum also receives a major glutamatergic projection from the thalamus, principally the intralaminar nuclei. Extracellular recording and juxtacellular labelling revealed that thalamostriatal neurons in the central lateral and parafascicular nucleus have distinct electrophysiological and morphological properties and have different patterns of connection in the striatum. Although tracing studies have given some indication about the magnitude of the thalamostriatal projection, the discovery that the vesicular glutamate transporters 1 and 2 are markers of cortical and thalamic terminals, respectively, has led to the demonstration that the number of thalamostriatal terminals is of a similar magnitude to the number of corticostriatal terminals. This raises the possibility that glutamatergic thalamostriatal synapses have the same spatial relationship with dopaminergic terminals as has been proposed for corticostriatal synapses and are thus in a position to be equally modulated by released dopamine. Double-immunolabelling of rat striatum to reveal vesicular glutamate transporters 1 and 2, as markers of corticostriatal and thalamostriatal terminals respectively, together with tyrosine hydroxylase to label the dopaminergic axons revealed that indeed, this is the case. Our analysis also revealed that all similarly sized structures within the striatum are equally likely to be apposed by a dopaminergic axon. We conclude that the sub-cortical input to the striatum from the thalamus underlies a rich and diverse complexity of function on a par with that of the corticostriatal projections, that the thalamostriatal terminals are in a position to be equally influenced by dopaminergic axons as corticostriatal terminals are and that the nigrostriatal projection is organised in such a way that every striatal structure has the potential to be influenced by dopamine.