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Previous research has shown that extended exposure to delayed reinforcement results in less impulsive choice in a subsequent delay-discounting task. Some work also suggests the opposite effect: extended exposure to immediate reinforcement may result in more impulsive choice behavior in a subsequent delay-discounting task. Understanding the impact that learning histories have on impulsive choice is important and clinically relevant because of the relationship between a strong preference for smaller-sooner over larger-later reinforcement (i.e., impulsive choice) and a myriad of other problematic health behaviors, such as substance misuse. In the present experiment, we exposed 24 rats to an immediate reinforcement intervention and 24 rats to a maturation/handle control group, followed immediately by a delay-discounting task. The procedure was designed as a systematic replication that accounted for several limitations from recent similar work. Results indicated that exposure to immediate reinforcement modestly increased impulsive choice in the delay-discounting task, but the effect was not overwhelming. These findings are consistent with previous work and have implications for understanding how experience-based interventions may affect clinically relevant impulsive choice. [ABSTRACT FROM AUTHOR]

Recently it has been proposed that impairments related to autism spectrum disorder (ASD) may reflect a more fundamental disruption in time perception. Here, we examined whether in utero exposure to valproic acid (VPA) can generate specific behavioral deficits related to ASD and time perception. Pups from control and VPA groups were tested using fixed-interval (FI) temporal bisection, peak interval, and intertemporal choice tasks. In addition, the rats were assessed on motor function, perseverative and exploratory behavior, anxiety, and memory. The VPA group displayed a leftward shift in timing functions. VPA rats displayed no deficits on the motor and memory tasks, but were significantly different from controls on measures of perseveration and anxiety. [ABSTRACT FROM AUTHOR]

Rodent models are commonly used in behavioral research because they offer increased experimental control and findings often generalizable to humans. However, one possible dilemma is that rodents are primarily nocturnal and research tasks often disrupt their light, rest phase. The present study used a within-subjects design to investigate possible effects of light-dark phase on delay discounting, motor coordination, open field, and elevated-plus maze behavior in Wistar rats. Rats spent significantly more time in the closed arms of the elevated plus maze when tested during the light, rest phase compared to the dark, active phase. There were no differences in motor coordination or delay discounting during the two phases. These results suggest possible important differences in certain behavioral tasks when testing in the light, rest versus dark, active phase for rats—researchers should be aware of these possible differences when planning and conducting experiments and when comparing research findings across laboratories. [ABSTRACT FROM AUTHOR]

Highlights • Exposure to delayed rewards increased preference for larger-later rewards. • Exposure to immediate rewards decreased preference for larger-later rewards. • Changes in timing precision were not predictive of changes in choice. • More research is necessary to uncover the underlying mechanism for these effects. Abstract A relatively strong preference for smaller-sooner rewards (SSR) over larger-later rewards (LLR) is associated with a host of maladaptive behavioral patterns. As such, the clinical implications for increasing preference for LLR are profound. There is a growing body of literature that suggests extended exposure to delayed reward may increase preference for LLR in rats. However, questions remain about the underlying mechanism driving this effect and the extent to which extended exposure to immediate rewards may decrease LLR choice. In Experiment 1, we tested effects of a differential-reinforcement-of-low-rates schedule (DRL) to increase LLR choice using a pretest/posttest design with Wistar rats as subjects. We compared this group to a group of rats exposed to a differential-reinforcement-of-high-rates schedule (DRH). The DRH intervention has never been employed in this research context, but explicitly programs an immediate response-reinforcement requirement. In Experiment 2, we tested effects of an intervention with a delay longer than those used in the delay discounting pretest and posttest. No previous research has tested effects of an intervention delay this long, relative to the delay discounting task. We compared this group to a group exposed to a delay that was part of the delay discounting pretest and posttest and to a group exposed to a traditional no-delay, fixed-ratio (FR) 2 control intervention. In both experiments, we found that exposure to delayed rewards in the intervention phase significantly increased LLR choice relative to pretest performance. These findings replicate and extend a growing body of literature showing that delay exposure increases preference for LLR. We also found significant decreases in LLR choice from pretest to posttest in the DRH and no-delay intervention groups in Experiments 1 and 2, respectively. This is the first report of such an effect and has implications for understanding and interpreting effects of delay exposure training in past and future research. Our results also suggested no relationship between improved temporal tracking of reward and increases in LLR choice as a result of delay exposure training. [ABSTRACT FROM AUTHOR]

Models of interval timing typically include a response threshold to account for temporal production. The present study sought to evaluate the dependent concurrent fixed-interval fixed-interval schedule of reinforcement as a tool for selectively isolating the response threshold in rats, pigeons, and humans. In this task, reinforcement is available either at one location after a short delay or at another location at a longer delay. Because the reinforced location is not signaled, subjects normally respond on the first location and, if reinforcement is not delivered, then switch to the second location. The latency to switch between locations served as the primary dependent measure. After training rats, pigeons, and humans with equal reinforcement magnitudes in the short and long delays, the magnitude of reinforcement was increased threefold on the long-delay location. Consistent with model predictions, this biasing procedure decreased estimates of the response threshold of rats and pigeons, but also reduced temporal control in these species and increased response-threshold estimates in humans. Human and pigeon performance also suggested a magnitude-induced increase in the speed of the internal clock. Collectively, these results suggest that differences in reinforcement magnitude between response alternatives appear to modulate the response threshold, but not selectively, and may provide guidance for better isolating response-threshold effects in humans. [ABSTRACT FROM AUTHOR]

• The CNTNAP2 gene is implicated in several neuropsychological disorders. • CNTNAP2 knockout rats and controls were compared on a temporal bisection task. • CNTNAP2 knockout rats exhibited less precise timing at the long cue durations. • Results have implications for understanding role of CNTNAP2 gene in timing. The CNTNAP2 gene has been implicated in several neuropsychological disorders, including autism spectrum disorder (ASD) and schizophrenia. The CNTNAP2 knockout (KO) rat model, rats without the CNTNAP2 gene, exhibits deficits in social interaction and increases in both repetitive and anxiety-like behaviors. However, deficits in time perception that may underlie several of the neuropsychological disorders implicated have not been investigated. The current study investigated timing in CNTNAP2 KO rats compared to control rats using a discrete-trial temporal bisection task. Results suggested deficits in the timing of relatively long durations in the CNTNAP2 KO rats. This finding is consistent with similar findings previously reported in humans diagnosed with ASD, and is promising for understanding the role that the CNTNAP2 gene may play in timing in certain neuropsychological disorders, and for developing targeted clinical therapies. [ABSTRACT FROM AUTHOR]