Open AccessModeling facilitation and inhibition of competing motor programs in basal ganglia subthalamic nucleus–pallidal circuits
Author(s) -
Leonid L. Rubchinsky,
Nancy Kopell,
Karen A. Sigvardt
Publication year - 2003
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2036283100
Subject(s) - neuroscience , subthalamic nucleus , basal ganglia , indirect pathway of movement , striatum , motor cortex , globus pallidus , motor control , putamen , hypokinesia , parkinson's disease , psychology , motor system , direct pathway of movement , facilitation , biology , deep brain stimulation , medicine , central nervous system , disease , pathology , stimulation , dopamine , endocrinology
The motor symptoms of Parkinson's disease (PD) implicate the basal ganglia (BG) in some aspect of motor control, although the role the BG play in regulation of motor behavior is not completely understood. The modeling study presented here takes advantage of available cellular, systems, and clinical data on BG and PD to begin to build a biophysically based network model of pallidosubthalamic circuits of BG, to integrate this information and better understand the physiology of the normal BG and PD pathophysiology. The model reflects the experimentally supported hypothesis that the BG are involved in facilitation of the desired motor program and inhibition of competing motor programs that interfere with the desired movement. Our model network consists of subthalamic and pallidal (both external and internal segments) neural assemblies, with inputs from cortex and striatum. Functional subsets within each of the BG nuclei correspond to the desired motor program and the unwanted motor programs. A single compartment conductance-based model represents each subset. This network can discriminate between competing signals for motor program initiation, thus facilitating a single motor program. This ability depends on metabotropic gamma-aminobutyric acid B projections from the external pallidum to subthalamic nucleus and rebound properties of subthalamic cells, as well as on the structure of projections between pallidum and subthalamus. The loss of this ability leads to hypokinesia, known PD motor deficits characterized by a slowness or inability to switch between motor programs.