Rationale: Previous experiments have shown that d-amphetamine disrupts timi
ng behaviour in rats. It has been proposed that d-amphetamine's effects ref
lect a reduction in the period of the pacemaker of the hypothetical interna
l clock. However, some studies have obtained conflicting results. Objective
: To examine the effects of d-amphetamine (0.2, 0.4, 0.8 mg kg(-1) i.p.) on
performance on two quantitative timing schedules: a free-operant schedule,
in which rats were trained to distribute their responses differentially be
tween two levers during the course of a 50-s trial (free-operant psychophys
ical procedure), and a discrete-trials schedule, in which rats were trained
to discriminate the duration of light stimuli (interval bisection task). M
ethods: In experiment 1, rats were trained under the free-operant psychophy
sical procedure to respond on two levers (A and B) in 50-s trials in which
reinforcement was provided intermittently for responding on A during the fi
rst half and on B during the second half of the trial. For one group, repet
itive switching between levers was permitted; for another group, it was pre
vented. In experiment 2, rats were exposed to press lever A after a 2-s sti
mulus and lever B after an 8-s stimulus, and were then tested with stimuli
of intermediate group, a poke response' (depression duration. For one group
of a central tray flap) was required after stimulus presentation to effect
lever presentation; for the other group, this requirement did not operate.
In both experiments, quantitative indices of timing were derived from the
psychophysical functions (%B responding vs time). Results: In experiment 1,
d-amphetamine increased the Weber fraction and displaced the psychophysica
l curve to the left in both versions of the schedule, as well as producing
rate-dependent suppression of responding. In experiment 2, d-amphetamine in
creased the Weber fraction in both versions of the task without displacing
the curve. Conclusions: These results confirm the disruptive effect of d-am
phetamine on timing. The results of experiment 1 are consistent with the pr
oposal that the drug reduces the period of the hypothetical pacemaker, Howe
ver, the results of experiment 2 do not support this suggestion. Taken toge
ther, the results support the notion that different neural mechanisms may b
e involved in timing tasks involving temporal distribution of responding an
d discrimination of the duration of exteroceptive stimuli.