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

Buhusi, Catalin V.; Meck, Warren H.

doi:10.1038/nrn1764

Cited by 1,831 publications

(1,954 citation statements)

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“…Similarly, intrinsic neural oscillations match the temporal scales of perceptual phenomena (Buzsáki and Draguhn, 2004;Roopun et al, 2008;van Wassenhove, 2009;Wang, 2010) and can be entrained to external rhythms (Rees et al, 1986;Regan, 1966). As such, neural oscillations have been hypothesized as natural pacemakers for conscious time estimation (Buhusi and Meck, 2005;Pöppel, 1997;Treisman et al, 1990;Varela et al, 1981). However, within this framework, a major problem for the brain is to determine when events occur with respect to its internal frame of reference.…”

Section: Neural Oscillations As Pacemakers For the Encoding Of Timementioning

confidence: 98%

“…While dedicated neural structures for time perception have been described (Buhusi and Meck, 2005;Coull et al, 2004;Harrington et al, 1998;Ivry and Schlerf, 2008;Morillon et al, 2009;Treisman et al, 1990;van Wassenhove, 2009;Wittmann, 2009Wittmann, , 2013, the encoding of sensory event timing has been proposed to result from the intrinsic dynamics of neural populations not necessarily dedicated to temporal processing (Johnston and Nishida, 2001;Karmarkar and Buonomano, 2007;van Wassenhove, 2009). For instance, the timing of a colored visual patch could be encoded in the dynamics of the neural population dedicated to the analysis of color (Karmarkar and Buonomano, 2007;Moutoussis and Zeki, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Encoding of event timing in the phase of neural oscillations

2014

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a b s t r a c t a r t i c l e i n f oTime perception is a critical component of conscious experience. To be in synchrony with the environment, the brain must deal not only with differences in the speed of light and sound but also with its computational and neural transmission delays. Here, we asked whether the brain could actively compensate for temporal delays by changing its processing time. Specifically, can changes in neural timing or in the phase of neural oscillation index perceived timing? For this, a lag-adaptation paradigm was used to manipulate participants' perceived audiovisual (AV) simultaneity of events while they were recorded with magnetoencephalography (MEG). Desynchronized AV stimuli were presented rhythmically to elicit a robust 1 Hz frequency-tagging of auditory and visual cortical responses. As participants' perception of AV simultaneity shifted, systematic changes in the phase of entrained neural oscillations were observed. This suggests that neural entrainment is not a passive response and that the entrained neural oscillation shifts in time. Crucially, our results indicate that shifts in neural timing in auditory cortices linearly map participants' perceived AV simultaneity. To our knowledge, these results provide the first mechanistic evidence for active neural compensation in the encoding of sensory event timing in support of the emergence of time awareness.

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Section: Neural Oscillations As Pacemakers For the Encoding Of Timementioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Encoding of event timing in the phase of neural oscillations

2014

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“…We were especially interested in whether we would find specific effects of chronic stimulant use depending on the time intervals involved. Different temporal processing mechanisms seem to be involved for different time scales (Buhusi and Meck, 2005;Mauk and Buonomano, 2004;Wittmann, 1999). Temporal integration windows of around 250 to 500 ms (Rammsayer, 1999;Wittmann et al, 2001), of around 1 second (Madison, 2001) and for intervals up to 2 to 3 seconds (Fraisse, 1984;Pöppel, 1997;Wittmann et al, 2007) have been postulated.…”

Section: Introductionmentioning

confidence: 99%

Impaired time perception and motor timing in stimulant-dependent subjects

Wittmann

Leland

Churan

et al. 2007

Drug and Alcohol Dependence

151

152

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Stimulant-dependent individuals (SDI) have abnormal brain metabolism and structural changes involving dopaminergic target areas important for the processing of time. These individuals are also more impulsive and impaired in working memory and attention. The current study tested whether SDI show altered temporal processing in relation to impulsivity or impaired prefrontal cortex functioning. We employed a series of timing tasks aimed to examine time processing from the milliseconds to multiple seconds range and assessed cognitive function in 15 male SDI and 15 stimulant-naïve individuals. A mediation analysis determined the degree to which impulsivity or executive dysfunctions contributed to group differences in time processing. SDI showed several abnormal time processing characteristics. SDI needed larger time differences for effective duration discrimination, particularly for intervals of around 1 sec. SDI also accelerated finger tapping during a continuation period after a 1 Hz pacing stimulus was removed. In addition, SDI overestimated the duration of a relatively long time interval, an effect which was attributable to higher impulsivity. Taken together, these data show for the first time that SDI exhibit altered time processing in several domains, one which can be explained by increased impulsivity. Altered time processing in SDI could explain why SDI have difficulty delaying gratification.

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“…For example, the pacemaker component was shown to be dependent on the dopaminergic (DA) system Maricq and Church, 1983;Meck, 1996), while the long-term memory stage is affected by cholinergic manipulations Church, 1987a, 1987b;Meck et al, 1987). Moreover, lesions of the hippocampal system were shown to interfere with working memory for time (Buhusi and Meck, 2002b;. More importantly for this paper, a recent study (Buhusi and Meck, 2002a) showed that the clock stage and the working-memory stage of the IP model can be dissociated pharmacologically in the PI procedure with gaps, because DA drugs shift the response functions in opposite direction in trials with and without gaps.…”

Section: Introductionmentioning

confidence: 99%

Effect of clozapine on interval timing and working memory for time in the peak-interval procedure with gaps

Buhusi

Meck

2007

Behavioural Processes

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Previous research indicates that dopamine controls both the speed of an internal clock (Maricq and Church, 1983) and sharing of resources between the timer and other cognitive processes (Buhusi, 2003). For example, dopamine agonist methamphetamine increases the speed of an internal clock and resets timing after a gap, while dopamine antagonist haloperidol decreases the speed of an internal clock and stops timing during a gap (Buhusi and Meck, 2002a). Using a 20-s peak-interval procedure with gaps we examined the acute effects of clozapine (2.0 mg/kg i.p.), which exerts differential effects on dopamine and serotonin in the cortex and striatum, two brain areas involved in interval timing and working memory. Relative to saline, clozapine injections shifted the response functions leftward both in trials with and without gaps, suggesting that clozapine increased the speed of an internal clock and facilitated the maintenance of the pre-gap interval in working memory. These results suggest that clozapine exerts effects in different brain areas in a manner that allows for the pharmacological separation of clock speed and working memory as a function of peak trials without and with gaps.

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

Cited by 1,831 publications

References 124 publications

Encoding of event timing in the phase of neural oscillations

Encoding of event timing in the phase of neural oscillations

Impaired time perception and motor timing in stimulant-dependent subjects

Effect of clozapine on interval timing and working memory for time in the peak-interval procedure with gaps

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