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Author Notes:

Author for correspondence: Thomas Wichmann, MD, Yerkes National Primate Research Center, 954 Gatewood Road NE, Atlanta, GA, 30329, USA; Phone: 404-727-3511; Fax: 404-727-9294; Email: twichma@emory.edu

We thank Michele Kliem and Yuxian Ma for their expert technical help, and Dr. Robert Bonsall and Milburn Emery for their help with the dopamine assays.

Subjects:

Research Funding:

This work was supported by NIH/NINDS grants NS040432 and NS049474 (TW), and by an institutional NIH grant (RR-000165) to the Yerkes National Primate Research Center.

Keywords:

  • Substantia Nigra Pars Compacta
  • Parkinson’s disease
  • Muscimol
  • Carbachol
  • Ibotenic Acid

Neuronal Activity in the Subthalamic Nucleus Modulates the Release of Dopamine in the Monkey Striatum

Tools:

Journal Title:

European Journal of Neuroscience

Volume:

Volume 29, Number 1

Publisher:

, Pages 104-113

Type of Work:

Article | Post-print: After Peer Review

Abstract:

The primate subthalamic nucleus (STN) is commonly seen as a relay nucleus between the external and internal pallidal segments, and as an input station for cortical and thalamic information into the basal ganglia. In rodents, STN activity is also known to influence neuronal activity in the dopaminergic substantia nigra pars compacta (SNc) through inhibitory and excitatory mono- and polysynaptic pathways. Although the anatomical connections between STN and SNc are not entirely the same in primates as in rodents, the electrophysiologic and microdialysis experiments presented here show directly that this functional interaction can also be demonstrated in primates. In three Rhesus monkeys, extracellular recordings from SNc during microinjections into the STN revealed that transient pharmacologic activation of the subthalamic nucleus by the acetylcholine-receptor agonist carbachol substantially increased burst firing of single nigral neurons. Transient inactivation of the STN with microinjections of the GABA-A-receptor agonist muscimol had the opposite effect. While the firing rates of individual SNc neurons changed in response to the activation or inactivation of the STN, these changes were not consistent across the entire population of SNc cells. Permanent lesions of the STN, produced in two animals with the fiber-sparing neurotoxin ibotenic acid, reduced burst firing and firing rates of SNc neurons, and substantially decreased dopamine levels in the primary recipient area of SNc projections, the striatum, as measured with microdialysis. These results suggest that activity in the primate SNc is prominently influenced by neuronal discharge in the STN, which may thus alter dopamine release in the striatum.

Copyright information:

© The Authors (2008). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd

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