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What makes us tick? Functional and neural mechanisms of interval timing

What makes us tick? Functional and neural mechanisms of interval timing Temporal information is crucial for goal reaching, neuroeconomics, and the survival of humans and other animals, and requires multiple biological mechanisms to track time over multiple scales. In mammals, the circadian clock is located in the suprachiasmatic nucleus. Another timer, which is responsible for automatic motor control in the millisecond range, relies on the cerebellum. Finally, a general-purpose, flexible, cognitively-controlled timer that operates in the seconds-to-hours range involves the activation thalamo-cortico-striatal circuits. The hallmark of interval timing is that the error in estimating a duration is proportional to the duration to be timed, a property known as scalar timing. Scalar timing resembles Weber's law, which applies to most sensory modalities. The way that time is perceived, represented and estimated has traditionally been explained using a pacemaker–accumulator model, which is not only straightforward but also surprisingly powerful in explaining behavioural and biological data. Pharmacological studies support a dissociation of the clock stage, which is affected by dopaminergic manipulations, and the memory stage, which is affected by cholinergic manipulations. Despite explaining many findings, the relevance of the pacemaker–accumulator model to the brain mechanisms that are involved in interval timing is unclear. New models will require investigation of recent neurobiological evidence. An impaired ability to process time is found in patients with disorders of the dopamine system, such as Parkinson's disease, Huntington's disease and schizophrenia. By contrast, the failure of a neurological disorder — such as cerebellar injury — to affect interval timing is taken to indicate that the affected structures are not essential for temporal processing in the seconds-to-hours range. Because interval timing depends on the intact striatum, but not on the intact cerebellum, the cerebellum is usually charged with millisecond timing and the basal ganglia with interval timing. Recent findings suggest that separate timing circuits can be dissociated when continuity, motor demands and attentional set are manipulated. The basal ganglia, prefrontal cortex and posterior parietal cortex are activated in both interval-timing tasks, and tasks that require integration of somatosensory signals or quantity/number processing. Electrophysiological data are consistent with the involvement of these structures in number, sequence or magnitude representation as well as in interval timing, thereby supporting a mode-control model of counting and timing in which number and time are processed by the same neural circuits. Functional MRI shows that two clusters of foci are activated during millisecond and interval timing tasks. The 'automatic timing' cluster is activated by tasks that require repetitive movements and involve short timing intervals, and includes the supplementary motor area and primary somatosensory cortex. The 'cognitively controlled timing' cluster is activated when the durations are longer and the amount of movement required is limited, and includes the dorsolateral prefrontal cortex, intraparietal sulcus and premotor cortex. The basal ganglia and the cerebellum are not specific to either cluster. The striatal beat-frequency model describes interval timing as an emergent activity in the thalamo-cortico-striatal loops. In this model, timing is based on the coincidental activation of medium spiny neurons in the basal ganglia by cortical neural oscillators. The activity of the striatal neurons increases before the expected time of reward, and peaks at the criterion interval. The model demonstrates the scalar property, and incorporates features that would allow the integration of a number of lines of evidence into one vision of interval timing in the brain. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Reviews Neuroscience Springer Journals

What makes us tick? Functional and neural mechanisms of interval timing

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References (173)

Publisher
Springer Journals
Copyright
Copyright © 2005 by Nature Publishing Group
Subject
Biomedicine; Biomedicine, general; Neurosciences; Behavioral Sciences; Biological Techniques; Neurobiology; Animal Genetics and Genomics
ISSN
1471-003X
eISSN
1471-0048
DOI
10.1038/nrn1764
Publisher site
See Article on Publisher Site

Abstract

Temporal information is crucial for goal reaching, neuroeconomics, and the survival of humans and other animals, and requires multiple biological mechanisms to track time over multiple scales. In mammals, the circadian clock is located in the suprachiasmatic nucleus. Another timer, which is responsible for automatic motor control in the millisecond range, relies on the cerebellum. Finally, a general-purpose, flexible, cognitively-controlled timer that operates in the seconds-to-hours range involves the activation thalamo-cortico-striatal circuits. The hallmark of interval timing is that the error in estimating a duration is proportional to the duration to be timed, a property known as scalar timing. Scalar timing resembles Weber's law, which applies to most sensory modalities. The way that time is perceived, represented and estimated has traditionally been explained using a pacemaker–accumulator model, which is not only straightforward but also surprisingly powerful in explaining behavioural and biological data. Pharmacological studies support a dissociation of the clock stage, which is affected by dopaminergic manipulations, and the memory stage, which is affected by cholinergic manipulations. Despite explaining many findings, the relevance of the pacemaker–accumulator model to the brain mechanisms that are involved in interval timing is unclear. New models will require investigation of recent neurobiological evidence. An impaired ability to process time is found in patients with disorders of the dopamine system, such as Parkinson's disease, Huntington's disease and schizophrenia. By contrast, the failure of a neurological disorder — such as cerebellar injury — to affect interval timing is taken to indicate that the affected structures are not essential for temporal processing in the seconds-to-hours range. Because interval timing depends on the intact striatum, but not on the intact cerebellum, the cerebellum is usually charged with millisecond timing and the basal ganglia with interval timing. Recent findings suggest that separate timing circuits can be dissociated when continuity, motor demands and attentional set are manipulated. The basal ganglia, prefrontal cortex and posterior parietal cortex are activated in both interval-timing tasks, and tasks that require integration of somatosensory signals or quantity/number processing. Electrophysiological data are consistent with the involvement of these structures in number, sequence or magnitude representation as well as in interval timing, thereby supporting a mode-control model of counting and timing in which number and time are processed by the same neural circuits. Functional MRI shows that two clusters of foci are activated during millisecond and interval timing tasks. The 'automatic timing' cluster is activated by tasks that require repetitive movements and involve short timing intervals, and includes the supplementary motor area and primary somatosensory cortex. The 'cognitively controlled timing' cluster is activated when the durations are longer and the amount of movement required is limited, and includes the dorsolateral prefrontal cortex, intraparietal sulcus and premotor cortex. The basal ganglia and the cerebellum are not specific to either cluster. The striatal beat-frequency model describes interval timing as an emergent activity in the thalamo-cortico-striatal loops. In this model, timing is based on the coincidental activation of medium spiny neurons in the basal ganglia by cortical neural oscillators. The activity of the striatal neurons increases before the expected time of reward, and peaks at the criterion interval. The model demonstrates the scalar property, and incorporates features that would allow the integration of a number of lines of evidence into one vision of interval timing in the brain.

Journal

Nature Reviews NeuroscienceSpringer Journals

Published: Sep 15, 2005

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