A basis for the pathological oscillations in basal ganglia: the crucial role of dopamine.

Introduction Parkinson’s disease is a progressive neurodegenerative movement disorder characterized by reduction and slowness of movement (akinesia and bradykinesia), muscle rigidity, and tremor. The core pathology of the disease is the degeneration of midbrain dopaminergic neurons in the substantia nigra pars compacta that project to the striatum and other basal ganglia nuclei. The striatum is the main input structure of the basal ganglia and receives excitatory projections from many cortical areas and thalamic nuclei. The output neurons of the striatum, named as medium spiny neurons, are g-aminobutyric acidergic (GABAergic) and project to both the globus pallidus internus and externus, and to substantia nigra pars reticulata, which are also GABAergic. The other nucleus within the basal ganglia is the subthalamic nucleus that receives direct cortical inputs and an input from the globus pallidus externus and its glutamatergic neurons project to the globus pallidus internus and substantia nigra pars reticulata (see Fig. 1).