Clocks within clocks: timing by coincidence detection

Abstract

The many existent models of timing rely on vastly different mechanisms to track temporal information. Here we examine these differences, and identify coincidence detection in its most general form as a common mechanism that many apparently different timing models share, as well as a common mechanism of biological circadian, millisecond and interval timing. This view predicts that timing by coincidence detection is a ubiquitous phenomenon at many biological levels, explains the reports of biological timing in many brain areas, explains the role of neural noise at different time scales at both biological and theoretical levels, and provides cohesion within the timing field.

Sex differences in interval timing and attention to time in C57Bl/6J mice

“…However, our recent investigation of the SBF model failed to reveal a neurobiologically-plausible mechanism that would allow the SBF model to flexibly stop, reset, and over-reset in response to distracters [18], suggesting that currently the SBF model cannot flexibly address these phenomena in a neurobiologically-plausible manner. Nevertheless, the observation that males and females differ in regard to attentional processing during timing is compatible with the view that multiple brain regions or neural circuits are involved in the control of an internal clock [17]. …”

“…Moreover, as long the over-reset mode was reported only when the distracter was paired with footshock [13, 14], it was largely ignored by timing theorists, as it could be explained by a non-timing phenomenon: freezing after a stimulus paired with footshock. For example, a description of the neurobiological mechanisms involved in interval timing is currently provided by the Striatal Beat-Frequency (SBF) model, which ascribes a role for detecting event durations to medium spiny neurons within the dorsal striatum [1, 16], which become entrained to fire in response to oscillating, coincident cortical inputs that become active at previously trained event durations [17]. However, our recent investigation of the SBF model failed to reveal a neurobiologically-plausible mechanism that would allow the SBF model to flexibly stop, reset, and over-reset in response to distracters [18], suggesting that currently the SBF model cannot flexibly address these phenomena in a neurobiologically-plausible manner.…”

Deficits in temporal processing correlate with clinical progression in Huntington's disease

“…Indeed, recent findings argue for the involvement of cortico‐striatal circuits, controlled by dopaminergic modulation of oscillatory activity and lateral connectivity. Medium spiny neurons (MSNs) detect the coincident activity of specific beat patterns of cortical oscillations . Manipulations of these dopaminergic systems are able to modify interval timing by altering the speed and other properties of the internal clock .…”

Increased temporal discounting after chronic stress in CHL1-deficient mice is reversed by 5-HT2C agonist Ro 60-0175

“…V. Buhusi & Meck, 2005; C. V. Buhusi et al, 2016; Kim et al, 2013; Matell et al, 2003; Xu et al, 2014).…”