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Prior research suggests that interval timing performance is sensitive to reinforcer devaluation effects and to the rate of competing sources of reinforcement. The present study sought to replicate and account for these findings in rats. A self-paced concurrent fixed-interval (FI) random-ratio (RR) schedule of reinforcement was implemented in which the FI requirement varied across training conditions (12, 24, 48 s). The RR requirement—which imposed an opportunity cost to responding on the FI component—was adjusted so that it took about twice the FI requirement, on average, to complete it. Probe reinforcer devaluation (prefeeding) sessions were conducted at the end of each condition. To assess the effect of contextual reinforcement on timing performance, the RR requirement was removed before the end of the experiment. Consistent with prior findings, performance on the FI component tracked schedule requirement and displayed scalar invariance; the removal of the RR component yielded more premature FI responses. For some rats, prefeeding reduced the number of trials initiated without affecting timing performance; for other rats, prefeeding delayed responding on the FI component but had a weaker effect on trial initiation. These results support the notion that timing and motivational processes are separable, suggesting novel explanations for ostensible motivational effects on timing performance. [ABSTRACT FROM AUTHOR]

Highlights: [•] A sudden change in the timing of reinforcement initiated a transition period. [•] In this period, control of behavior was gradually transferred between schedules. [•] Control was expressed in distinct distributions of responses over time. [•] Schedule discontinuation reduced and displaced the response distribution. [•] Such displacement supports a model of timing based on cascades of behavioral states. [ABSTRACT FROM AUTHOR]

The temporal generalization gradient produced by the peak-interval (PI) procedure reflects behavior under the control of positive reinforcement for responding after the criterial time, but shows negligible discouragement for early responses. The lack of consequences for premature responding may affect estimates of timing accuracy and precision in the PI procedure. In two experiments, we sought to encourage more accurate timing in pigeons by establishing an opportunity cost for such responding. Concurrent ratio and interval schedules of reinforcement reduced the dispersion of keypecking around the target time. A sequence of three response-rate states (low- high-low) characterized performance in individual trials. Opportunity cost substantially reduced the mean and standard deviation of the duration of the middle-high state that typically enveloped the target time, indicating improved temporal acuity. We suggest a model as a first-order approximation to timing with opportunity cost. [ABSTRACT FROM AUTHOR]

Smoking typically begins during adolescence and is largely reinforced by social cues. During adolescence in rats, sensitivity to both social cues and drugs of abuse is enhanced. We have previously demonstrated in adolescent male rats that a low dose of cocaine interacts with social reward to produce an enhanced conditioned place preference (CPP) relative to either reward given alone. The present study further examined the nature of drug–social reward interactions using nicotine. Dose–effect functions for nicotine-CPP were established using two different routes of administration (vehicle, 0.1, 0.3, and 0.6 mg/kg, SC and vehicle, 0.01, 0.03, and 0.06 mg/kg, IV). The effects of nicotine on social reward-CPP and social play behavior were next examined using parameters presumed to be sub-threshold for establishing social reward- and nicotine-CPP. Dose-dependent nicotine-CPP was observed using both routes of administration. Two pairings of the initially non-preferred side of the apparatus with either SC nicotine or another adolescent rat failed to produce CPP when examined alone, but together produced a robust CPP despite nicotine reducing social play. This interaction effect was not observed with the IV nicotine. A final experiment demonstrated that the enhancement of CPP with the combination of rewards was not due to additive effects of weak, sub-threshold conditioning. These findings suggest that nicotine and social rewards interact synergistically in adolescent rats resulting in a greater, perhaps qualitatively different, reward than either reward given alone. Understanding drug–social reward interactions may provide new directions for development of preventions and interventions of adolescent smoking. [ABSTRACT FROM AUTHOR]

Background: The inability to inhibit reinforced responses is a defining feature of ADHD associated with impulsivity. The Spontaneously Hypertensive Rat (SHR) has been extolled as an animal model of ADHD, but there is no clear experimental evidence of inhibition deficits in SHR. Attempts to demonstrate these deficits may have suffered from methodological and analytical limitations. Methods: We provide a rationale for using two complementary response-withholding tasks to doubly dissociate impulsivity from motivational and motor processes. In the lever-holding task (LHT), continual lever depression was required for a minimum interval. Under a differential reinforcement of low rates schedule (DRL), a minimum interval was required between lever presses. Both tasks were studied using SHR and two normotensive control strains, Wistar-Kyoto (WKY) and Long Evans (LE), over an overlapping range of intervals (1 - 5 s for LHT and 5 - 60 s for DRL). Lever-holding and DRL performance was characterized as the output of a mixture of two processes, timing and iterative random responding; we call this account of response inhibition the Temporal Regulation (TR) model. In the context of TR, impulsivity was defined as a bias toward premature termination of the timed intervals. Results: The TR model provided an accurate description of LHT and DRL performance. On the basis of TR parameter estimates, SHRs were more impulsive than LE rats across tasks and target times. WKY rats produced substantially shorter timed responses in the lever-holding task than in DRL, suggesting a motivational or motor deficit. The precision of timing by SHR, as measured by the variance of their timed intervals, was excellent, flouting expectations from ADHD research. Conclusion: This research validates the TR model of response inhibition and supports SHR as an animal model of ADHD-related impulsivity. It indicates, however, that SHR's impulse-control deficit is not caused by imprecise timing. The use of ad hoc impulsivity metrics and of WKY as control strain for SHR impulsivity are called into question. [ABSTRACT FROM AUTHOR]

Abstract: The peak interval (PI) procedure is commonly used to evaluate animals’ ability to produce timed intervals. It consists of presenting fixed interval (FI) schedules in which some of the trials are replaced by extended non-reinforced trials. Responding will often resume (resurge) at the end of the non-reinforced trials unless precautions are taken to prevent it. Response resurgence was replicated in rats and pigeons. Variation of the durations of the FI and the non-reinforced probe trials showed it to be dependent on the time when reinforcement is expected. Timing of both the normal time to reinforcement, and the subsequent time to reinforcement during the probe trials followed Weber''s law. A quantitative model of resurgence is described, suggesting how animals respond to the signaling properties of reinforcement omission. Model results were simulated using a stochastic binary counter. [Copyright &y& Elsevier]

Each of four pigeons was exposed to a single random-ratio schedule of reinforcement in which the probability of reinforcement for a peck on either of two keys was 1/25. Reinforcer amounts were determined by an iterated prisoner's dilemma (IPD) matrix in which the "other player" (a computer) played tit-for-tat. One key served as the cooperation (C) key; the other served as the defection (D) key. If a peck was scheduled to be reinforced and the D-key was pecked, the immediate reinforcer of that peck was always higher than it would have been had the C-key been pecked. However, if the C-key was pecked and the following peck was scheduled to be reinforced, reinforcement amount for pecks on either key were higher than they would have been if the previous peck had been on the D-key. Although immediate reinforcement was always higher for D-pecks, the overall reinforcement rate increased linearly with the proportion of C-pecks. C-pecks thus constituted a form of self-control. All the pigeons initially defected with this procedure. However, when feedback signals were introduced that indicated which key had last been pecked, cooperation (relative rate of C-pecks)—hence, self-control—increased for all the pigeons. [ABSTRACT FROM AUTHOR]

Operant behavior appears to be organized in bouts of responses, whose parameters are differentially sensitive to various manipulations. This study investigated potential differential effects of three forms of operant response disruption—extinction (EXT), non-contingent reinforcement (NCR), and prefeeding (PRE)—on response bouts. In Experiment 1, Wistar Kyoto rats (WKY) were trained on a tandem variable-time (VT) 120 s fixed-ratio (FR) 5 schedule of reinforcement; after stability was established, their responding was disrupted for three sessions with one of the three disrupters (EXT, NCR, or PRE). In Experiment 2, Long Evans (LE) rats were trained on a tandem VT 240 s FR 5 to stability, and their responding disrupted with EXT or NCR. In EXT and NCR, response rates declined significantly and progressively over the course of the session, primarily due to a declining bout-initiation rate in EXT, and to fewer responses per bout in NCR. In contrast, a session-wide drop in response rate was observed in PRE, primarily due to a reduction in bout-initiation rate at the start of the session. These findings suggest that each form of disruption differentially impacts dissociable aspects of behavior. Theories of behavioral persistence should account for these functional relations, which appear to be obscured in response rate measures. [ABSTRACT FROM AUTHOR]

Abstract: Extinction performance is often used to assess underlying psychological processes without the interference of reinforcement. For example, in the extinction/reinstatement paradigm, motivation to seek drug is assessed by measuring responding elicited by drug-associated cues without drug reinforcement. However, extinction performance is governed by several psychological processes that involve motivation, memory, learning, and motoric functions. These processes are confounded when overall response rate is used to measure performance. Based on evidence that operant responding occurs in bouts, this paper proposes an analytic procedure that separates extinction performance into several behavioral components: (1–3) the baseline bout initiation rate, within-bout response rate, and bout length at the onset of extinction; (4–6) their rates of decay during extinction; (7) the time between extinction onset and the decline of responding; (8) the asymptotic response rate at the end of extinction; (9) the refractory period after each response. Data that illustrate the goodness of fit of this analytic model are presented. This paper also describes procedures to isolate behavioral components contributing to extinction performance and make inferences about experimental effects on these components. This microscopic behavioral analysis allows the mapping of different psychological processes to distinct behavioral components implicated in extinction performance, which may further our understanding of the psychological effects of neurobiological treatments. [Copyright &y& Elsevier]

Abstract: Mathematical principles of reinforcement (MPR; Killeen, 1994) is a quantitative model of operant behavior that contains three parameters representing motor capacity (δ), motivation (a), and short term memory (λ). The present study applied MPR to characterize the effects of bilateral infusions of 6-OHDA into the substantia nigra pars compacta in the rat, a model of Parkinson''s disease. Rats were trained to lever press under a 5-component fixed-ratio (5, 15, 30, 60, and 100) schedule of food reinforcement. Rats were tested for 15 days prior to dopamine lesions and again for 15 days post-lesion. To characterize functional loss relative to lesion size, rats were grouped according to the extent and the degree of lateralization of their dopamine loss. Response rates decreased as a function of dopamine depletion, primarily at intermediate ratios. MPR accounted for 98% of variance in pre- and post-lesion response rates. Consistent with reported disruptions in motor behavior induced by dopaminergic lesions, estimates of δ increased when dopamine was severely depleted. There was no support for different estimates of a based on pre- and post-lesion performance of any lesion group, suggesting that dopamine loss has negligible effects on incentive motivation. The present study demonstrates the usefulness of combining operant techniques with a theoretical model to better understand the effects of a neurochemical manipulation. [Copyright &y& Elsevier]