Neuropsychological mechanisms of interval timing behavior
Read:: - [ ] Matell et al. (2000) - Neuropsychological mechanisms of interval timing behavior 🛫2023-09-27 !!2 rd citation todoist Print::  ❌ Zotero Link:: Zotero Files:: attachment Reading Note:: Web Rip:: url:: https://onlinelibrary.wiley.com/doi/abs/10.1002/%28SICI%291521-1878%28200001%2922%3A1%3C94%3A%3AAID-BIES14%3E3.0.CO%3B2-E
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Interval timing in the seconds-to-minutes range is believed to underlie a variety of complex behaviors in humans and other animals. One of the more interesting problems in interval timing is trying to understand how the brain times events lasting for minutes with millisecond-based neural processes. Timing models proposing the use of coincidence-detection mechanisms (e.g., the detection of simultaneous activity across multiple neural inputs) appear to be the most compatible with known neural mechanisms. From an evolutionary perspective, coincidence detection of neuronal activity may be a fundamental mechanism of timing that is expressed across a wide variety of species. BioEssays 22:94–103, 2000. ©2000 John Wiley & Sons, Inc.
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peak-interval procedure used with humans, participants were instructed to watch as a blue square appeared on a computer screen and to be “aware” of the amount of time that passed (either 8,12, or 21sec) before the square changed color (the criterion duration). After several training trials, participants were instructed that the blue square would appear for an indefinite amount of time, and that they should indicate when in time they expected the square to change by pressing the spacebar. In 25% of the trials, the participants were advised as to whether they were “too early,” “too late,” or “correct.” In all trials, the participants were instructed not to count or subdivide the duration in any fashion.
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Psychological models of interval timing Although a variety of theories on the psychological components of interval timing have been proposed, it has been suggested that all internal-clock models must conform to a common basic structure,(20) in which there is a clock component, a memory component, and a decision/comparison component. In this basic “internal-clock” model shown in Figure 2, the clock component starts upon onset of a signal to be timed, and the output of the clock is compared via a decision mechanism to previously important duration codes held in reference memory.
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The clock component is made up of a repeatable process that can be mapped onto time and is therefore expected to have an isomorphic mapping (e.g., each and every value of the clock is mapped to a specific duration of time).(21) However, recent evidence indicating nonlinearities in time perception(22,23) suggests that such an isomorphic mapping need not be the rule. It is important to note that the clock process is not necessarily periodic, only that it must proceed through a relatively repeatable pattern on each and every occasion it is started. The speed of this clock component is modifiable by drugs, disease, stimulus modality, as well as body temperature.(2,4,24,25) Attentional processes also can influence interval timing and might specifically impact the clock stage.(26)
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The memory component is thought to be a long-term store of previously important, or reinforced, clock output values. The storage, maintenance, and retrieval of these temporal memories are also susceptible to a variety of influences, including
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experimentally altered task constraints,(27–30) drug administration,(3,31,32) and pathologies such as Parkinson’s disease.(1,2)
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The decision or comparison component is described as a mechanism that evaluates how well the current clock value matches previously stored temporal memories, and can be influenced by manipulations in task design.(33)
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A variety of models of this basic “internal clock” exist, in which the formal descriptions of some or all of the components differ. These models can be divided into three classes, based primarily on their clock-stage mechanisms, termed pacemaker-accumulator models, process-decay models, and oscillator/coincidence-detection models. The six primary models of interval timing (two from each class), along with the difficulties in translating their psychological mechanisms into neurobiologically feasible physical mechanisms are summarized in Table 1.
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neuroanatomical and neuropharmacological mechanisms of interval timing are beginning to emerge (reviewed in Gibbon et al.(11) and Meck(34)). The basal ganglia, a set of subcortical brain nuclei traditionally considered important for motor functioning,(35–37) are now also thought to be involved in a variety of cognitive and motivational processes,(38–40) and appear to be critical for interval timing. Excitatory input from the cortex to the basal ganglia comes primarily into the striatum, the input nucleus of the basal ganglia. The striatum also receives modulatory dopaminergic input from the substantia nigra pars compacta (SNPC), a midbrain nucleus involved in reinforcement.
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Finally, the cortex, which provides input to the striatum, and the thalamus, a brain relay nucleus that receives input from the basal ganglia and sends output back to the cortex, are also anatomical areas that influence timing behavior. fMRI and PET brain imaging techniques show that both of these areas are activated in humans during temporal discrimination tasks.(44,45)
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This anatomical arrangement produces a cortico-striatal-thalamic-cortical loop, an anatomical pathway that is proposed to underlie the necessary computations for the timing of behavior (Fig. 3).
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Fig 2
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Table 1 Can we implement these in an RL model and see which is more effective regardless of biological plausibility
