Abstract
Since the pioneering work of Whittier and Mettler (1949) showing that small electrolytic lesion of the subthalamic nucleus (STN) induces violent involuntary movements of the contralateral limbs in non-human primates, the exact mechanisms by which the STN plays such a powerful role in the control of motor behaviors have been the subject of intensive research. In the 1980’s, the introduction of sensitive immunocytochemical and tract-tracing techniques, combined with single-unit recording in normal and parkinsonian monkeys, led to major breakthroughs in our knowledge of the critical role of this nucleus in the functional circuitry of the basal ganglia (Albin et al., 1989; Bergman et al., 1990; Wichmann and DeLong, 1996). The STN, which is the only excitatory glutamatergic structure of the basal ganglia (Smith and Parent, 1988), is now considered to be a major source of excitatory drive to basal ganglia output nuclei (Kitai and Kita, 1987). Observations in l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP)-treated monkeys showing that the STN activity is increased after dopamine depletion led to the development of novel surgical therapies aimed at silencing STN outflow to basal ganglia output nuclei (Bergman et al., 1990; Aziz et al., 1991). Such therapies are currently used worldwide as efficient treatment for Parkinson’s disease in humans (Starr et al., 1998). The recent demonstration that the interconnections between the globus pallidus (GP) and the STN act as a pacemaker of neuronal oscillations observed in various basal ganglia structures after dopamine depletion is further evidence that the STN plays a critical role in mediating basal ganglia functions in both normal and pathological conditions (Plenz and Kitai, 1999).
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Smith, Y., Charara, A., Hanson, J.E., Hubert, G.W., Kuwajima, M. (2001). Chemical Anatomy and Synaptic Connectivity of the Globus Pallidus and Subthalamic Nucleus. In: Kultas-Ilinsky, K., Ilinsky, I.A. (eds) Basal Ganglia and Thalamus in Health and Movement Disorders. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1235-6_10
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DOI: https://doi.org/10.1007/978-1-4615-1235-6_10
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-5454-3
Online ISBN: 978-1-4615-1235-6
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