Prenatal choline supplementation increases sensitivity to time by reducing non-scalar sources of variance in adult temporal processing

Cheng, Ruey‐Kuang; Meck, Warren H.

doi:10.1016/j.brainres.2007.10.025

Cited by 54 publications

(67 citation statements)

References 99 publications

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“…If this ratio was greater than 0.8, the animal's data for that criterion duration was not used. The S1 and S2 rate indexes were determined as previously described (Cheng and Meck, 2007). In the present work, the S1 rate index for the PI 24-s procedure was defined by the response rate occurring during the 3-s period just prior to the observed peak time (i.e., seconds 22-24) divided by the overall response rate for the first 24-s of the trial (i.e., seconds 0-24).…”

Section: Discussionmentioning

confidence: 99%

“…For the FI and PI training, the stimulus was a 50-lux house light mounted at the center-top of the front wall. Animals were trained following the peak-interval (PI) procedure in three consecutive phases -lever press training, fixed interval training and peak interval training (Cheng and Meck, 2007;Drew et al, 2007). In all segments of the experiment, sessions occurred once per day, 5 days per week.…”

Section: 5mentioning

confidence: 99%

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Circadian modulation of interval timing in mice

et al. 2011

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Temporal perception is fundamental to environmental adaptation in humans and other animals. To deal with timing and time perception, organisms have developed multiple systems that are active over a broad range of order of magnitude, the most important being circadian timing, interval timing and millisecond timing. The circadian pacemaker is located in the suprachiasmatic nuclei (SCN) of the hypothalamus, and is driven by a selfsustaining oscillator with a period close to 24 h. Time estimation in the second-to-minutes range -known as interval timing -involves the interaction of the basal ganglia and the prefrontal cortex. In this work we tested the hypothesis that interval timing in mice is sensitive to circadian modulations. Animals were trained following the peak-interval (PI) procedure. Results show significant differences in the estimation of 24-second intervals at different times of day, with a higher accuracy in the group trained at night, which were maintained under constant dark (DD) conditions. Interval timing was also studied in animals under constant light (LL) conditions, which abolish circadian rhythmicity. Mice under LL conditions were unable to acquire temporal control in the peak interval procedure.Moreover, short time estimation in animals subjected to circadian desynchronizations (modeling jet lag-like situations) was also affected. Taken together, our results indicate that short-time estimation is modulated by the circadian clock.© 2010 Elsevier B.V. All rights reserved. Keywords:Circadian rhythms Interval timingBasal ganglia Suprachiasmatic nuclei IntroductionTiming and time perception are fundamental to survival and goal reaching in humans and other animals. Organisms have developed diverse mechanisms for timing across different scales, the most important being circadian timing, interval timing and millisecond timing . The circadian pacemaker -which is driven by a self-sustaining oscillator with a period close to 24 h -is located in the suprachiasmatic nuclei (SCN) of the hypothalamus (Dunlap et al., 2004), and the principal signal that adjusts its activity is the light-dark cycle (Morin and Allen, 2006;Golombek and Rosenstein, 2010). The molecular mechanism of the endogenous circadian clock is comprised by interlocked transcription-translation feedback loops (Reppert and Weaver, 2002). On the other hand, the perception of shorter durations in the seconds-to-minutes range, known as interval timing, is crucial to learning, memory, decision making and other cognitive

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Section: Discussionmentioning

confidence: 99%

Section: 5mentioning

confidence: 99%

Circadian modulation of interval timing in mice

et al. 2011

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“…The high-degree of overlap among all four functions indicates excellent superimposition, a feature of the scalar property of interval timing indicating that timing variability (e.g. standard deviation or spread of response functions) increases in proportion to the duration of the interval being timed [47,57,63]. Interestingly, the only systematic deviation from superimposition is observed on the right-hand tail of the response functions which is thought to reflect a level of impulsive responding uncontrolled by the timing of the target duration [66,67].…”

Section: (F ) Histologymentioning

confidence: 99%

“…A bi-peak procedure was used in order to evaluate changes in accuracy and precision as a function of multiple target durations [5,47,48].…”

Section: Introductionmentioning

confidence: 99%

Comparison of interval timing behaviour in mice following dorsal or ventral hippocampal lesions with mice having δ -opioid receptor gene deletion

Yin

Meck

2014

Phil. Trans. R. Soc. B

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Mice with cytotoxic lesions of the dorsal hippocampus (DH) underestimated 15 s and 45 s target durations in a bi-peak procedure as evidenced by proportional leftward shifts of the peak functions that emerged during training as a result of decreases in both ‘start’ and ‘stop’ times. In contrast, mice with lesions of the ventral hippocampus (VH) displayed rightward shifts that were immediately present and were largely limited to increases in the ‘stop’ time for the 45 s target duration. Moreover, the effects of the DH lesions were congruent with the scalar property of interval timing in that the 15 s and 45 s functions superimposed when plotted on a relative timescale, whereas the effects of the VH lesions violated the scalar property. Mice with DH lesions also showed enhanced reversal learning in comparison to control and VH lesioned mice. These results are compared with the timing distortions observed in mice lacking δ -opioid receptors (Oprd1 −/− ) which were similar to mice with DH lesions. Taken together, these results suggest a balance between hippocampal–striatal interactions for interval timing and demonstrate possible functional dissociations along the septotemporal axis of the hippocampus in terms of motivation, timed response thresholds and encoding in temporal memory.

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“…In contrast, the distribution of Stop times is much more precise and symmetrical (e.g., Cheng and Meck, 2007;Gallistel et al, 2004;Matell et al, 2006). The distribution of Stop times is where one typically finds the scalar property to be the most robust, yielding a constant CV across a variety of target times.…”

Section: Analysis Of Stop Cv-precisionmentioning

confidence: 99%

Intact interval timing in circadian CLOCK mutants

Cordes

Gallistel

2008

Brain Research

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While progress has been made in determining the molecular basis for the circadian clock, the mechanism by which mammalian brains time intervals measured in seconds to minutes remains a mystery. An obvious question is whether the interval timing mechanism shares molecular machinery with the circadian timing mechanism. In the current study, we trained circadian CLOCK +/− and −/ − mutant male mice in a peak-interval procedure with 10 and 20-s criteria. The mutant mice were more active than their wild-type littermates, but there were no reliable deficits in the accuracy or precision of their timing as compared with wild-type littermates. This suggests that expression of the CLOCK protein is not necessary for normal interval timing.

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Prenatal choline supplementation increases sensitivity to time by reducing non-scalar sources of variance in adult temporal processing

Cited by 54 publications

References 99 publications

Circadian modulation of interval timing in mice

Circadian modulation of interval timing in mice

Comparison of interval timing behaviour in mice following dorsal or ventral hippocampal lesions with mice having δ -opioid receptor gene deletion

Intact interval timing in circadian CLOCK mutants

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