Cannabinoid modulation of time estimation in the rat.

Han, C. J.; Robinson, John K.

doi:10.1037/0735-7044.115.1.243

Cited by 57 publications

(29 citation statements)

References 9 publications

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“…Similar observations are observed in preclinical studies. In accordance with Han and Robinson (2001), in the present study we found that treating rodents with the cannabinoid receptor agonist WIN 55 212-2 shortened the response interval in an FI task, effectively leading animals to show a premature acceleration in the temporal response pattern.…”

Section: Discussionsupporting

confidence: 67%

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Cannabinoid Receptor Activation Shifts Temporally Engendered Patterns of Dopamine Release

Oleson

Cachope

Fitoussi

et al. 2013

Neuropsychopharmacol

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The ability to discern temporally pertinent environmental events is essential for the generation of adaptive behavior in conventional tasks, and our overall survival. Cannabinoids are thought to disrupt temporally controlled behaviors by interfering with dedicated brain timing networks. Cannabinoids also increase dopamine release within the mesolimbic system, a neural pathway generally implicated in timing behavior. Timing can be assessed using fixed-interval (FI) schedules, which reinforce behavior on the basis of time. To date, it remains unknown how cannabinoids modulate dopamine release when responding under FI conditions, and for that matter, how subsecond dopamine release is related to time in these tasks. In the present study, we hypothesized that cannabinoids would accelerate timing behavior in an FI task while concurrently augmenting a temporally relevant pattern of dopamine release. To assess this possibility, we measured subsecond dopamine concentrations in the nucleus accumbens while mice responded for food under the influence of the cannabinoid agonist WIN 55 212-2 in an FI task. Our data reveal that accumbal dopamine concentrations decrease proportionally to interval duration-suggesting that dopamine encodes time in FI tasks. We further demonstrate that WIN 55 212-2 dose-dependently increases dopamine release and accelerates a temporal behavioral response pattern in a CB1 receptor-dependent manner-suggesting that cannabinoid receptor activation modifies timing behavior, in part, by augmenting time-engendered patterns of dopamine release. Additional investigation uncovered a specific role for endogenous cannabinoid tone in timing behavior, as elevations in 2-arachidonoylglycerol, but not anandamide, significantly accelerated the temporal response pattern in a manner akin to WIN 55 212-2.

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Section: Discussionsupporting

confidence: 67%

“…Immediately following reinforcement, responding slows before accelerating to a maximal terminal rate at the culmination of the interval (Dews, 1970). Cannabinoids, like other drugs that speed up the internal clock, produce an accelerated temporal response pattern (Cheng et al, 2007;Han and Robinson, 2001).…”

Section: Introductionmentioning

confidence: 99%

Cannabinoid Receptor Activation Shifts Temporally Engendered Patterns of Dopamine Release

Oleson

Cachope

Fitoussi

et al. 2013

Neuropsychopharmacol

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“…High densities of CB 1 receptors are also present in frontal cortical and striatal regions (Egertova and Elphick 2000; Tsou et al 1998), suggesting involvement of the endocannabinoid system in executive functions that appear to be largely controlled by frontal corticostriatal systems (for review, see Miller and Cohen 2001). Indeed, several clinical and preclinical observations have demonstrated that Δ 9 -tetrahydrocannabinol (THC), the principle active cannabinoid of Cannabis sativa and other synthetic cannabimimetics impair selective attention (Arguello and Jentsch 2004; Solowij et al 1995; Verrico et al 2004) and behavioral flexibility (Egerton et al 2005; Hill et al 2006), alter time estimation (Han and Robinson 2001, McDonald et al 2003), and impair working memory (Ilan et al 2004; Jentsch et al 1997). Nonetheless, to date, little is known about the involvement of the endocannabinoid system in other executive functions such as inhibitory control processes subserving impulsivity.…”

Section: Introductionmentioning

confidence: 99%

Effects of the cannabinoid CB1 receptor antagonist rimonabant on distinct measures of impulsive behavior in rats

Pattij¹,

Janssen²,

Schepers³

et al. 2007

Psychopharmacology

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Rationale Pathological impulsivity is a prominent feature in several psychiatric disorders, but detailed understanding of the specific neuronal processes underlying impulsive behavior is as yet lacking. Objectives As recent findings have suggested involvement of the brain cannabinoid system in impulsivity, the present study aimed at further elucidating the role of cannabinoid CB 1 receptor activation in distinct measures of impulsive behavior. Materials and methods The effects of the selective cannabinoid CB 1 receptor antagonist, rimonabant (SR141716A) and agonist WIN55,212-2 were tested in various measures of impulsive behavior, namely, inhibitory control in a fivechoice serial reaction time task (5-CSRTT), impulsive choice in a delayed reward paradigm, and response inhibition in a stop-signal paradigm. Results In the 5-CSRTT, SR141716A dose-dependently improved inhibitory control by decreasing the number of premature responses. Furthermore, SR141716A slightly improved attentional function, increased correct response latency, but did not affect other parameters. The CB 1 receptor agonist WIN55,212-2 did not change inhibitory control in the 5-CSRTT and only increased response latencies and errors of omissions. Coadministration of WIN55,212-2 prevented the effects of SR141716A on inhibitory control in the 5-CSRTT. Impulsive choice and response inhibition were not affected by SR141716A at any dose, whereas WIN55,212-2 slightly impaired response inhibition but did not change impulsive choice. Conclusions The present data suggest that particularly the endocannabinoid system seems involved in some measures of impulsivity and provides further evidence for the existence of distinct forms of impulsivity that can be pharmacologically dissociated.

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“…In accordance with this consequence of the pro posed mechanism, time was shown to flow more slowly for marijuana smokers [65,66]. Rodents treated with cannabinoids also underestimated intervals with dura tions of 10 and 30 s [64,67].…”

Section: Effects Of Opioids and Cannabinoidsmentioning

confidence: 69%

“…The possibility of the alteration of the frequency of the "internal clock" in the presence of cannabinoids has been shown earlier [64]; however, the mechanisms of this effect were not analyzed. We believe that can nabinoids may influence time perception not only via dopamine release but also indirectly via modulation of inputs to neurons of the prefrontal cortex, which has a high density of cannabinoid CB1 receptors [63].…”

Section: Effects Of Opioids and Cannabinoidsmentioning

confidence: 98%

Possible mechanisms for the effects of neuromodulators on the perception of time intervals

Силькис

2012

Neurochem. J.

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We propose possible mechanisms for the effects of neuromodulators on the perception of time on the basis of our hypothesis that estimation of intervals between sensory stimuli depends on the beat frequency of a "internal clock," which is inversely proportional to the latency of reentering excitation of the neocortex. These effects are based on the modification of the efficacy of excitatory inputs to the cortical neurons, as well as inputs from the cortex to the striatum, which are necessary for the disinhibition of thalamic neurons by the basal ganglia and subsequent excitation of the cortex. The character of influence is determined by the con centration of neuromodulators, the types of receptors activated by them on neurons of the striatum and cor tex, and the modulation rules. According to the proposed mechanism, an increase in the frequency of the "internal clock" and overestimation of the duration of intervals may result from treatment with dopaminergic drugs, agonists of dopamine D1 and D2 receptors, and opioids and cannabinoids, which promote an increase in the dopamine concentration, as well as antagonists of adenosine A1 and A2A and muscarinic M2 recep tors, whose activation facilitates disinhibition of the thalamus by the basal ganglia. Antagonists of A1, M2, and D2 receptors, which prevent depression of excitatory inputs to neocortical pyramidal cells, also can increase the frequency of the "internal clock." The activation of a large number of D2 receptors on the cor tical pyramidal cells, which results from a considerable increase in dopamine concentration, like activation of cannabinoid CB1 receptors, should promote a decrease in the frequency of the "internal clock" and the underestimation of interval duration. The activation of D2 and M2 receptors on the GABAergic interneurons of the cortex under conditions of strong inhibition of pyramidal neurons may increase the beat frequency of the "internal clock." The proposed mechanism helps to understand the causes of errors in time perception in neurological diseases and to explain the discrepancies in the results of studies on the effects of neuromodula tors on the estimation of time. The hypothesis may be experimentally examined by treatment of the striatum or neocortex with agonists and antagonists of various types of receptors and measurement of the drug induced changes in the interval between the first and second peaks in the distribution of latencies of responses of cortical neurons to sensory stimulus.

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Cannabinoid modulation of time estimation in the rat.

Cited by 57 publications

References 9 publications

Cannabinoid Receptor Activation Shifts Temporally Engendered Patterns of Dopamine Release

Cannabinoid Receptor Activation Shifts Temporally Engendered Patterns of Dopamine Release

Effects of the cannabinoid CB1 receptor antagonist rimonabant on distinct measures of impulsive behavior in rats

Possible mechanisms for the effects of neuromodulators on the perception of time intervals

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