Journal
PSYCHOPHARMACOLOGY
Volume 201, Issue 1, Pages 67-80Publisher
SPRINGER
DOI: 10.1007/s00213-008-1248-y
Keywords
Interval timing; Time perception; Peak procedure; Dopamine; Cognitive enhancement; Mice; Amphetamine; Atomoxetine; Methamphetamine; Scopolamine
Categories
Ask authors/readers for more resources
Rationale Timing deficits are characteristic of developmental and neurodegenerative disorders that are accompanied by cognitive impairment. A prominent theory of this interval timing posits an internal clock whose pace is modulated by the neurotransmitter dopamine. Objectives We tested two hypotheses about the pharmacology of interval timing in mice: (1) that general cognitive enhancers should increase, and cognitive disruptors should decrease temporal precision and (2) that acutely elevated dopamine should speed this internal clock and produce overestimation of elapsing time. Materials and methods C3H mice were tested in the peak procedure, a timing task, following acute administration of two putative cognitive enhancers (atomoxetine and physostigmine), two cognitive disruptors (scopolamine and chlordiazepoxide [CDP]), or two dopamine agonists (D-amphetamine and methamphetamine). Results The first hypothesis received strong support: temporal precision worsened with both cognitive disruptors, but improved with both cognitive enhancers. The two dopamine agonists also produced underestimation of elapsing time-congruent with the slowing of an internal clock and inconsistent with a dopamine-driven clock. Conclusion Our results suggest that interval timing has potential as an assay for generalized cognitive performance and that the dopamine-clock hypothesis needs further refinement.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available