Action, time and the basal ganglia

The ability to control the speed of movement is compromised in neurological disorders involving the basal ganglia, a set of subcortical cerebral nuclei that receive prominent dopaminergic projections from the midbrain. For example, bradykinesia, slowness of movement, is a major symptom of Parkinson&...

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Bibliographic Details
Published in:Philosophical transactions of the Royal Society of London. Series B. Biological sciences 2014-03, Vol.369 (1637), p.20120473-20120473
Main Author: Yin, Henry H.
Format: Article
Language:English
Subjects:
Action
Basal Ganglia
Basal Ganglia - physiology
Bradykinesia
Dopamine
Dopamine - metabolism
Feedback, Physiological - physiology
Humans
Hypokinesia - physiopathology
Models, Neurological
Movement - physiology
Review
Striatum
Substantia Nigra
Time Factors
Time Perception - physiology
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Summary:The ability to control the speed of movement is compromised in neurological disorders involving the basal ganglia, a set of subcortical cerebral nuclei that receive prominent dopaminergic projections from the midbrain. For example, bradykinesia, slowness of movement, is a major symptom of Parkinson's disease, whereas rapid tics are observed in patients with Tourette syndrome. Recent experimental work has also implicated dopamine (DA) and the basal ganglia in action timing. Here, I advance the hypothesis that the basal ganglia control the rate of change in kinaesthetic perceptual variables. In particular, the sensorimotor cortico-basal ganglia network implements a feedback circuit for the control of movement velocity. By modulating activity in this network, DA can change the gain of velocity reference signals. The lack of DA thus reduces the output of the velocity control system which specifies the rate of change in body configurations, slowing the transition from one body configuration to another.
ISSN:0962-8436
1471-2970
DOI:10.1098/rstb.2012.0473