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Five experiments were conducted to determine the effects of hippocampal damage on timing and the memory for temporal events. In Experiments 1-3, rats were trained to discriminate between auditory signals that differed in both duration (2 or 8 s) and rate (2 or 16 cycles/s). Half of the rats were trained to discriminate duration, and half were trained to discriminate rate. After rats acquired the relevant discrimination, signals with intermediate durations and rates were presented to obtain psychophysical functions that related signal duration and/or rate to response choice. Rats then received either lesions of the fimbria-fornix or control operations. Postoperatively, the accuracy of duration and rate discriminations as measured by the difference limen (DL) was unaffected by the lesion, but the point of subjective equality (PSE) was shifted to a shorter duration and a slower rate by the lesion in Experiment 1. Both rats with lesions and rats with control operations showed cross-modal transfer of duration and rate from the auditory signals used in training to visual signals used in testing in Experiment 2. A 5-s delay was imposed between the end of a signal and the opportunity to respond in Experiment 3. The delay served as a retention interval for the rats trained in the rate discrimination, and the rats with fimbria-fornix lesions were selectively impaired by the addition of the delay as measured by an increase in the DL. The delay did not serve as a retention interval for rats trained in the duration discrimination because they were able to continue timing through the delay. A peak procedure was employed in Experiment 4. The maximum response rate of control rats was approximately at the time of scheduled reinforcement (20 s), but the maximum response rate of rats with fimbria-fornix lesions was reliably earlier than the time of scheduled reinforcement. When a 5-s gap was imposed in the signal, control rats summed the signal durations before and after the gap, whereas rats with fimbria-fornix lesions showed no retention of the signal duration prior to the gap. Experiment 5 continued the testing of the rats used in Experiments 1-4 and showed that rats with lesions had an impairment in a test of spatial working memory in an eight-arm radial maze. Taken together, these results demonstrate that a fimbria-fornix lesion interferes with temporal and spatial working memory, reduces the remembered time of reinforcement stored in reference memory, and has no effect on the animal's sensitivity to stimulus duration.

The roles that psychostimulant sensitization and tolerance play in temporal perception in the seconds-to-minutes range were assessed in rats. Cocaine (20 mg/kg/day) was administered for 2 weeks either intermittently via daily injections (induces sensitization) or continuously via an osmotic minipump (induces tolerance). Interval timing was evaluated throughout administration and withdrawal. Injections of cocaine caused immediate, proportional, leftward shifts in peak times, indicating an increase in the speed of an internal clock. These shifts grew progressively larger with repeated administration, indicating that stimulant-induced increases in clock speed can be sensitized. Continuous cocaine administration produced no reliable effects. These results suggest that the mechanisms of sensitization may play a considerable role in drug-induced alterations of the perception of time.

The cognitive and emotional effects of amygdala or frontal cortex lesions were compared in rats trained to time both a 50-s visual signal paired with food and an embedded 10- or 20-s auditory signal that was paired with either appetitive (food) or aversive (footshock) outcomes. When both auditory and visual signals were paired with food, control and amygdalar-lesioned rats were able to divide attention and to time both signals simultaneously, whereas when the embedded auditory signal was paired with footshock, control rats were impaired in their ability to divide attention and were able to time only one signal at a time. In contrast, amygdalar inactivation blocked this fear-related impairment and allowed rats to time both signals simultaneously, whereas rats with frontal cortex lesions demonstrated sequential processing under all conditions. These results support the proposal that the frontal cortex exerts executive control over the allocation of attentional resources, but that under stressful conditions the amygdala is crucial for the emergence of fear-evoked increments in selective attention leading to deficits in the ability to time 2 or more signals simultaneously.

Humans and animals process temporal information as if they were using an internal stopwatch that can be stopped and reset, and whose speed is adjustable. Previous data suggest that dopaminergic drugs affect the speed of this internal stopwatch. Using a paradigm in which rats have to filter out the gaps that (sometimes) interrupted timing, the authors found that methamphetamine and haloperidol also affect the stop and reset mechanism of the internal clock, possibly by modulating attentional components that are dependent on the content and salience of the timed events. This is the first report of both clock and attentional effects of dopaminergic drugs on interval timing in the same experimental setting.