Abstract
Accurate and reliable timing is an essential component of nearly every purposeful behavior. Just as the brain contains mechanisms to track and orient the body in space, so too must it be able to orient itself in time. Coincidence detection – the integration of simultaneous activation of multiple inputs – is a proposed solution to the question of how the brain tracks the duration of events in the seconds-to-minutes range using millisecond-scale neural processes (Matell and Meck, 2000). The striatal beat-frequency (SBF) model is one of the most successful attempts at explaining the neural basis of interval timing in terms of coincidence detection of oscillatory processes (Matell and Meck, 2004; Lustig et al., 2005; Harrington et al., 2010; Oprisan and Buhusi, 2011, submitted). The SBF model involves a set of cortical timekeeper neurons that oscillate at regular, but distinct frequencies, allowing a unique pattern of activation to occur at each point in time. These activation patterns project onto striatal integrators that combine their information with feedback (e.g., reward input) and form the basis of interval timing.
Highlights
These neural structures contained within cortico-striatal circuits may not be the only ones involved in interval timing
Numerous studies have demonstrated reliable changes in the accuracy and precision of interval timing following a variety of techniques impacting hippocampal function
The primary goal of this opinion article is to outline mechanisms by which the hippocampus could have specific effects on the modulation of the neural circuits specified by the striatal beat-frequency (SBF) model of interval timing
Summary
These neural structures contained within cortico-striatal circuits may not be the only ones involved in interval timing, . Numerous studies have demonstrated reliable changes in the accuracy and precision of interval timing following a variety of techniques impacting hippocampal function (e.g., transection of the fimbria fornix, lesions of the medial septal area, resection of the temporal lobe, selective lesions of the dorsal hippocampus, and destruction of the entire hippocampus – see Balci et al, 2009 for a review).
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