The "basal ganglia" refers to a group of subcortical nuclei responsible primarily for motor control, as well as other roles such as motor learning, executive functions and behaviors, and emotions. Proposed more than two decades ago, the classical basal ganglia model shows how information flows through the basal ganglia back to the cortex through two pathways with opposing effects for the proper execution of movement. Although much of the model has remained, the model has been modified and amplified with the emergence of new data. Furthermore, parallel circuits subserve the other functions of the basal ganglia engaging associative and limbic territories. Disruption of the basal ganglia network forms the basis for several movement disorders. This article provides a comprehensive account of basal ganglia functional anatomy and chemistry and the major pathophysiological changes underlying disorders of movement. We try to answer three key questions related to the basal ganglia, as follows: What are the basal ganglia? What are they made of? How do they work? Some insight on the canonical basal ganglia model is provided, together with a selection of paradoxes and some views over the horizon in the field.T he basal ganglia and related nuclei consist of a variety of subcortical cell groups engaged primarily in motor control, together with a wider variety of roles such as motor learning, executive functions and behavior, and emotions. The term basal ganglia in the strictest sense refers to nuclei embedded deep in the brain hemispheres (striatum or caudate-putamen and globus pallidus), whereas related nuclei consist of structures located in the diencephalon (subthalamic nucleus), mesencephalon (substantia nigra), and pons ( pedunculopontine nucleus). Ideas and concepts regarding the functions of the basal ganglia were strongly influenced by clinical observations during the 20th century, which showed that lesions of the lenticular nucleus ( putamen and globus pallidus) and the subthalamic nucleus (STN) were associated with parkinsonian signs, dystonia, and hemiballismus (Wilson 1925;Purdon-Martin 1927). Thus, the terms extra-pyramidal system and extra-pyramidal syndrome were frequently used in the past to refer to the pathological basis of movement disorders in an attempt to make a clear distinction from the pyramidal system (corticofugal neurons that give rise to corticospinal projections). At present, these terms and distinctions are considered obsolete and misleading and, therefore, will not be used in

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Although type 1 cannabinoid receptors (CB1Rs) are expressed abundantly throughout the brain, the presence of type 2 cannabinoid receptors (CB2Rs) in neurons is still somewhat controversial. Taking advantage of newly designed CB1R and CB2R mRNA riboprobes, we demonstrate by PCR and in situ hybridization that transcripts for both cannabinoid receptors are present within labeled pallidothalamic-projecting neurons of control and MPTP-treated macaques, whereas the expression is markedly reduced in dyskinetic animals. Moreover, an in situ proximity ligation assay was used to qualitatively assess the presence of CB1Rs and CB2Rs, as well as CB1R–CB2R heteromers within basal ganglia output neurons in all animal groups (control, parkinsonian and dyskinetic macaques). A marked reduction in the number of CB1Rs, CB2Rs and CB1R–CB2R heteromers was found in dyskinetic animals, mimicking the observed reduction in CB1R and CB2R mRNA expression levels. The fact that chronic levodopa treatment disrupted CB1R–CB2R heteromeric complexes should be taken into consideration when designing new drugs acting on cannabinoid receptor heteromers.