Ketamine “unlocks” the reduced clock-speed effects of cocaine following extended training: Evidence for dopamine–glutamate interactions in timing and time perception

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

“…Moreover, pharmacological tests using dopamine D1/D5 and D2/D3 receptor agonists show that the lack of d-opioid receptors in the Oprd1 2/2 mice modifies the D1/D5-nigral/D2/D3-pallidal balance in the striatum in favour of the nigral output [1]. Hence, the facilitated acquisition of striataldependent tasks observed in Oprd1 2/2 mice is likely the result of potentiated dopaminergic/glutaminergic activity in striatonigral pathways-possibly involving striatal cholinergic interneurons [13,84,90,91]. As a consequence, the inclusion of the Oprd1 2/2 mice in this study strengthens the argument for hippocampal-striatal interactions as the source of the proportional leftward shifts produced by DH lesions.…”

Subjective Duration as a Signature of Coding Efficiency: Emerging Links Among Stimulus Repetition, Predictive Coding, and Cortical GABA Levels

“…The interaction between these two sets of structures supports the specific temporal judgments in a task. In the case of sub-second intervals, the RS and GABA-related effects observed in the cortex are presumably produced by "additive" as opposed to "multiplicative" effects, i.e., changes in the threshold manifold (Mitry et al, 2013) required to initiate timing of the "to-be-timed" stimulus as opposed to the oscillation frequency of the putative clock during the course of the entire stimulus duration (see Cheng et al, 2007;Lake et al, 2014;Lake & Meck, 2013;Matthews, 2011a, b). Future work should be aimed at separating threshold dynamics from speed effects for suband supra-second durations in order to better understand the dynamics of temporal processing and how satellite (i.e., local/peripheral) and core interval-timing mechanisms are integrated with circadian clocks and more general cognitive processes (e.g., Agostino et al, 2011;Boehm, Van Maanen, Forstmann, & Van Rijn, 2014;Bausenhart et al, 2010;Buhusi & Meck, 2005;Gu et al, in press b;Henry & Hermann, 2014;Matthews & Meck, 2014, submitted;Meck et al, 2012;Méndez et al, 2014;Merchant et al, 2013;Polyn & Sederberg, 2014;Shi et al, 2013;Taatgen, Van Rijn & Anderson, 2007;Tucci et al, 2014;Van Rijn et al, 2011, in press).…”

The time–emotion paradox

“…This arousal-induced temporal overestimation has been documented in numerous studies that have manipulated the level of arousal by using click or flicker trains (Treisman et al 1990;Penton-Voak et al 1996;Droit-Volet & Wearden 2002;Ortega & Lopez 2008), by changing body temperature (Wearden & Penton-Voak 1995), or by administrating drugs that modulate arousal by altering the effective level of dopamine in the brain. For example, following the administration of dopanimergic agonists (methamphetamine or cocaine), participants either overestimate the elapsed interval or respond earlier, a phenomenon that is characteristic of an increase in the clock rate (Maricq et al 1981;Cheng et al 2007). By contrast, dopaminergic antagonists, such as haloperidol, produce a temporal underestimation as if the clock were running more slowly (Rammsayer 1989(Rammsayer , 1999Drew et al 2003).…”