Acquisition of “Start” and “Stop” response thresholds in peak-interval timing is differentially sensitive to protein synthesis inhibition in the dorsal and ventral striatum

MacDonald, Christopher J.; Cheng, Ruey‐Kuang; Meck, Warren H.

doi:10.3389/fnint.2012.00010

Cited by 57 publications

(49 citation statements)

References 192 publications

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“…Thus, the LTD-like plasticity we observed might also reflect LTD mechanisms, rather than depotentiation, enabling behavioural adaptation to the new CS–US interval. It is worth mentioning a recent study showing that infusion of anisomycin, a protein synthesis inhibitor, into the dorsal striatum of rats did not prevent the rapid learning of a new time of reinforcement arrival in an appetitive instrumental peak interval paradigm46. Since both pre- and postsynaptic LTD co-exist at cortico-striatal synapses4748495051, one possibility is that learning of a new duration also involves presynaptic LTD mechanisms, which may be independent of protein synthesis48.…”

Section: Discussionmentioning

confidence: 99%

Updating temporal expectancy of an aversive event engages striatal plasticity under amygdala control

et al. 2017

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Pavlovian aversive conditioning requires learning of the association between a conditioned stimulus (CS) and an unconditioned, aversive stimulus (US) but also involves encoding the time interval between the two stimuli. The neurobiological bases of this time interval learning are unknown. Here, we show that in rats, the dorsal striatum and basal amygdala belong to a common functional network underlying temporal expectancy and learning of a CS–US interval. Importantly, changes in coherence between striatum and amygdala local field potentials (LFPs) were found to couple these structures during interval estimation within the lower range of the theta rhythm (3–6 Hz). Strikingly, we also show that a change to the CS–US time interval results in long-term changes in cortico-striatal synaptic efficacy under the control of the amygdala. Collectively, this study reveals physiological correlates of plasticity mechanisms of interval timing that take place in the striatum and are regulated by the amygdala.

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Section: Discussionmentioning

confidence: 99%

Updating temporal expectancy of an aversive event engages striatal plasticity under amygdala control

et al. 2017

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“…While phasic dopaminergic firing is thought to play a role in the 'start gun' process (Kononowicz, 2015;MacDonald et al, 2012MacDonald et al, , 2014, such phasic dopamine bursts may also mediate the transient physiological arousal component of temporal distortion induced by emotional stimuli (Droit-Volet & Meck, 2007;Lake et al, 2016;Schirmer, 2014). The input pathway inducing phasic bursting of dopaminergic midbrain neurons could influence the latency after stimulus onset that these neurons fire, with earlier bursting resulting in increases in temporal estimates.…”

Section: Striatal Beat Frequency Model and Dopamine Activitymentioning

confidence: 99%

Clock Speed as a Window into Dopaminergic Control of Emotion and Time Perception

Cheng

Tipples

Narayanan

et al. 2016

Timing Time Percept

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Although fear-producing treatments (e.g., electric shock) and pleasure-inducing treatments (e.g., methamphetamine) have different emotional valences, they both produce physiological arousal and lead to effects on timing and time perception that have been interpreted as reflecting an increase in speed of an internal clock. In this commentary, we review the results reported by Fayolle et al. (2015): Behav. Process., 120, 135-140) and Meck (1983: J. Exp. Psychol. Anim. Behav. Process., 9, 171-201) using electric shock and by Maricq et al. (1981: J. Exp. Psychol. Anim. Behav. Process., 7, 18-30) using methamphetamine in a duration-bisection procedure across multiple duration ranges. The psychometric functions obtained from this procedure relate the proportion 'long' responses to signal durations spaced between a pair of 'short' and 'long' anchor durations. Horizontal shifts in these functions can be described in terms of attention or arousal processes depending upon whether they are a fixed number of seconds independent of the timed durations (additive) or proportional to the durations being timed (multiplicative). Multiplicative effects are thought to result from a change in clock speed that is regulated by dopamine activity in the medial prefrontal cortex. These dopaminergic effects are discussed within the context of the striatal beat frequency model of interval timing (Matell & Meck, 2004: Cogn. Brain Res., 21, 139-170) and clinical implications for the effects of emotional reactivity on temporal cognition (Parker et al., 2013: Front. Integr. Neurosci., 7, 75).

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“…Response states defined by 'start' (S1) and 'stop' (S2) response thresholds were identified on individual trials that contained at least five lever presses as previously described [57][58][59][60]. Briefly, in a single trial, the location of a 'high, relatively continuous' state of lever pressing during a trial is determined by fitting three contiguous, but non-overlapping horizontal lines to the response series over time during a single unreinforced probe trial.…”

Section: (K) Single-trials Analysismentioning

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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Acquisition of “Start” and “Stop” response thresholds in peak-interval timing is differentially sensitive to protein synthesis inhibition in the dorsal and ventral striatum

Cited by 57 publications

References 192 publications

Updating temporal expectancy of an aversive event engages striatal plasticity under amygdala control

Updating temporal expectancy of an aversive event engages striatal plasticity under amygdala control

Clock Speed as a Window into Dopaminergic Control of Emotion and Time Perception

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

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