SEARCH · Search PubMed

Results for “REINFORCEMENT”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources

PubMed1999

Attenuation of cocaine-induced response-rate increases during repeated administration despite increases in rate of reinforcement.

Repeated administration of cocaine often results in tolerance to its effects on operant behavior. The tolerance is often associated with an initial drug effect that results in loss of reinforcement. Cocaine can also produce effects that result in a gain of reinforcement, and it is not known if tolerance will be observed in such a circumstance. The present experiments investigated whether tolerance would develop when cocaine was administered repeatedly to subjects who experienced an increase in the frequency of reinforcement when cocaine was administered acutely. Pigeons were trained to peck a response key under fixed-ratio schedules of food presentation. The ratio value for each pigeon was chosen such that performance indicated that the ratio was relatively large, and produced "ratio strain.". Cocaine was administered acutely (once per week), and then subsequently a dose was chosen and administered before each session. Once performance under the daily drug regimen was stable, other doses occasionally were substituted for the usual daily dose. Acute administration of cocaine (0.3-10.0 mg/kg) revealed substantial increases of 100% or more in response rate, and therefore equivalent increases in rate of food presentation, at some doses. That finding permitted examination of the role of drug-induced increases in rate of reinforcement during repeated administration of a response-rate-increasing dose. Repeated, daily administration of a rate-increasing dose resulted in attenuation of the effects of that dose, and subsequent administration of other doses that previously had increased response rates revealed that these doses, too, had lost their ability to increase rates. That is, "tolerance" developed to the rate-increasing effects, even though the rate increases were associated with more frequent access to food. These findings suggest that "reinforcement gain" may not be sufficient to prevent tolerance from developing to effects of cocaine on operant behavior.

Animals↗

PubMed2007

Can reinforcement induce children to falsely incriminate themselves?

This study examined whether reinforcement can induce children to falsely incriminate themselves. Ninety-nine children in kindergarten through third grade were questioned regarding the staged theft of a toy. Half received reinforcement for self-incriminating responses. Within 4 min reinforced children made 52% false admissions of guilty knowledge concerning the theft, and 30% false admissions of having witnessed it. Corresponding figures for controls were 36 and 10%. Twelve percent of children admitted to participating in the theft, but the effect of reinforcement was only marginally significant. The findings indicate that reinforcement can induce children to falsely implicate themselves in wrongdoing.

Child↗

PubMed1984

An effect of immediate reinforcement and delayed punishment, with possible implications for self-control.

Behavior said to show self-control occurs virtually always as an alternative to behavior that produces conflicting consequences. One class of such consequences, immediate reinforcement and delayed punishment, is especially pervasive. Three experiments are described in which an effect of immediate reinforcement and delayed punishment is demonstrated. The results suggest that when immediate reinforcement and delayed punishment are imminent, the reinforcer alone controls the organism's behavior (in other words the organism behaves "impulsively"). The key to self-control, therefore, may be the acquisition of a large number of avoidance behaviors relevant to reinforcers that are correlated with delayed punishment. Human self-control may indeed involve such a process but undoubtedly involves others as well.

Animals↗

PubMed1986

The influence on patients' pain intensity ratings of antecedent reinforcement of pain talk or well talk.

This study sought to determine whether positive verbal reinforcement for pain talk or well talk could effectively influence chronic pain patients' subsequent ratings of pain intensity. Four female chronic pain inpatients were each exposed over seven consecutive days to two conditions within an alternating treatments design. Inter-rater reliability analysis from the audiotapes on occurrences of pain and well talk, verbal reinforcement and appropriate reinforcement of verbal behavior across conditions resulted in agreement values from 91 to 100%. Findings revealed that subjects' pain intensity ratings were consistently and significantly lower after verbally reinforcing well talk compared with verbally reinforcing pain talk.

Adult↗

PubMed1987

Treatment of pica in an adult disabled by autism by differential reinforcement of incompatible behavior.

The usefulness of differential reinforcement of incompatible behavior was examined in the treatment of pica in a young man severely disabled by autism in a nonsheltered place of employment. The results indicated that a reduction in pica could be achieved by differential reinforcement of other behavior (DRO). Behaviors which were reinforced included remaining in this assigned location, keeping his hands on his work, working quickly and keeping his mouth clear. Reinforcements included favorite drinks, snacks, activities and praise. Treatment procedures were implemented by direct care paraprofessional staff. Withdrawal of treatment resulted in an increase in pica, with renewed reduction on reinstatement of the reinforcement schedule.

Adult↗

PubMed1982

Covert positive reinforcement and pain modification: a test of efficacy and theory.

The effects of covert positive reinforcement, covert positive reinforcement plus positive expectancy, covert positive reinforcement plus negative expectancy, covert positive reinforcement of pain, attention placebo and no treatment on control of headache and finger pressure pain were examined. Self-report, behavioural and physiological measures were taken. Groups did not differ on any measures except for validity checks of the expectancy manipulation. The results provide little support for the efficacy of covert positive reinforcement in modifying pain. Additionally, the data failed to substantiate the theoretical basis of the procedure.

Adolescent↗

PubMed1989

Behaviour in rats maintained by low differential reinforcement rate: effects of delta 1-tetrahydrocannabinol, cannabinol and cannabidiol, alone and in combination.

Rats were trained to respond according to a low rate differential reinforcement (DRL) 72 sec schedule of operant behaviour. The animals were then tested with delta 1-tetrahydrocannabinol (delta 1-THC), cannabinol, and cannabidiol alone and in combination. Tests with single doses of delta 1-THC (dose-range: 0.3-5.6 mg/kg) and cannabinol (dose-range: 1-56 mg/kg) but not cannabidiol (dose-range 3-100 mg/kg), yielded a dose-related biphasic effect on the response rate. Small doses of delta 1-THC and cannabinol increased the rate of responding, large doses of these agents decreased it. Cannabidiol alone only decreased the rate of responding (occurring at large doses). The rate of reinforcement generally was decreased when response rates increased and vice versa. Cannabidiol (10 and 30 kg/kg), together with delta 1-THC (1 and 3 mg/kg), decreased the response output and increased the rate of reinforcement. Similar results were observed with combinations of cannabinol (10 and 30 mg/kg) and cannabidiol (10 and 30 mg/kg). Combinations of delta 1-THC (0.3 and 1 mg/kg) and cannabinol (1 and 3 mg/kg) also reduced the response rate and there were no significant changes in the rate of reinforcement. Hence the actions of delta 1-THC and cannabinol on behaviour in rats maintained by low rate differential reinforcement were similar (approximate difference in potency 1:10), whereas no stimulation of response rate was demonstrated with cannabidiol. Vehicle and day of testing (Tuesday or Friday) variables were found not to affect the results.

Animals↗

PubMed1980

Differential effects of methylphenidate on signalled and non-signalled reinforcement.

Rats were trained to press a bar with water reinforcement under a variable interval 15-sec (VI 15), variable interval 15-sec signalled-reinforcement (VI SD), or a differential-reinforcement-of-low-rate 10-sec (DRL 10) schedule. Methylphenidate (MP) had little effect on response rates or reinforcements-earned in the VI 15 group. However, MP increased response rates in a dose-related manner in the VI SD and the DRL 10 groups. These findings and additional results reported in the literature suggest that signalled reinforcement does not necessarily antagonize the rate-increasing effects of the amphetamine-type drugs.

Animals↗

PubMed1982

Effects of reinforcement-blocking doses of pimozide on neural systems driven by rewarding stimulation of the MFB: a 14C-2-deoxyglucose analysis.

An analysis by means of 14C-2-deoxyglucose autoradiography of the neural systems unilaterally activated by the reinforcing stimulation used in the two accompanying papers revealed strong and reliable effects in the nucleus of the diagonal band of Broca, in the medial forebrain bundle (MFB) and/or the fornix throughout the diencephalon, and in the part of the anterior ventral tegmentum where the dopaminergic projection to the lateral habenula originates. The terminal fields of the dopaminergic forebrain projections were not affected, but there was bilateral suppression of lateral habenular activity. A second experiment found that the same systems are still activated by (automatically administered) reinforcing stimulation in rats treated with reinforcement blocking doses of pimozide. The only clear effect of pimozide was to reverse the bilateral suppressive effect of the stimulation on lateral habenular activity. Animals treated with pimozide show greatly elevated activity in the lateral habenula, whether or not they receive reinforcing stimulation. The results suggest that pimozide's effect on reinforcement is mediated by the circuitry interconnecting the lateral habenula with the nucleus of the diagonal band of Broca and/or the anterior ventral tegmentum.

Animals↗

PubMed1987

Reinforcement reduces behavioural impairment under an acute dose of alcohol.

Two experiments employed a total of 25 male social drinkers who learned a complex psychomotor task (Tracometer) and subsequently performed it 20 times under alcohol (0.60 g absolute alcohol/kg) while blood alcohol concentrations (BAC) rose and fell. In each experiment, one group received reinforcement for drug-compensatory performance (RP) and one received no reinforcement (P). The BACs associated with the onset and offset of behavioral impairment under the dose were measured, and these thresholds were significantly higher in RP than P groups; reinforcement delayed the onset and also hastened the offset of drug effects. The accelerated recovery from impairment was considered to imply that reinforcement may facilitate the adaptive process involved in acute tolerance. Since this same reinforcement treatment accelerates the development of tolerance to repeated doses of alcohol, the results of the present research suggest that the behavioural effect of acute and chronic doses may both be similarly influenced by environmental learning factors.

Adult↗

PubMed1988

Reinforcing properties of caffeine: studies in humans and laboratory animals.

Three types of experimental studies are reviewed: (1) intravenous and oral caffeine self-administration by laboratory animals, (2) oral caffeine self-administration by humans, and (3) human subjective effects of caffeine relevant to reinforcing effects. These studies show that, under appropriate conditions, caffeine can serve as a reinforcer and can produce elevations in subjective drug liking and/or euphoria. In this regard, caffeine can be distinguished from a wide range of behaviorally active compounds, such as the amphetamine analog fenfluramine and the major tranquilizer chlorpromazine, which do not produce such effects. Caffeine can also be distinguished from classic drugs of abuse such as cocaine, d-amphetamine or pentobarbital which generally maintain high levels of self-administration (or liking) in contrast to caffeine which tends to maintain lower levels of self-administration (or liking) or maintain self-administration under a more narrow range of parametric conditions. Several human studies and one animal experiment suggest that physical dependence substantially potentiates the reinforcing effects of caffeine. Other human and animal studies indicate that there may be substantial differences between individual subjects in the reinforcing effects of caffeine. An important challenge for future human and animal drug self-administration research will be to delineate more precisely the conditions under which caffeine does and does not serve reliably as a reinforcer.

Animals↗

PubMed1988

Reinforcing effects of nicotine in humans and experimental animals responding under intermittent schedules of i.v. drug injection.

The self-administration paradigm is an experimental model of drug dependence in which the reinforcing properties of drugs can be directly assessed. This paradigm avoids the possible confounding influence of nonpharmacologic factors which may contribute to drug taking in the nonlaboratory environment. When animals serve as subjects, social and cultural factors unique to humans may also be eliminated as confounding influences. Most drugs of abuse are self-administered by animals and humans under such conditions. Until 1981, laboratory studies of nicotine self-administration suggested that nicotine, in its own right, was only a marginally effective reinforcer. As will be shown in the present review, a study by Goldberg and his co-workers in 1981 [13] demonstrated clearly that nicotine could serve as a highly efficacious reinforcer in laboratory animals. There are several parameters which can function to substantially strengthen the behavior which leads to nicotine ingestion. These include the following: (1) intermittent availability of nicotine, (2) intermittent presentation of nicotine-paired stimuli, and (3) concurrent schedules of food reinforcement. Initial findings from a human IV nicotine self-administration study were consistent with those from the animal studies. Together these results confirm that nicotine can function to control behavior by serving as a reinforcer for animals and humans. The results also suggest that commonly used tobacco products function as ideal nicotine delivery systems for controlling behavior since they provide discrete nicotine-paired stimuli and lend themselves to intermittent nicotine delivery.

Animals↗

PubMed1992

Reinforced responding of the 11-day-old rat pup: synergistic interaction of D1 and D2 dopamine receptors.

Reinforced responding of 11-day-old rat pups was assessed after blockade of D1 and D2 dopamine receptors. Initially, rat pups were trained to traverse a straight alley for nipple attachment reward. Rat pups were than injected IP with either the D1 antagonist SCH 23390 (0.01, 0.015, 0.03, or 0.1 mg/kg), the D2 antagonist sulpiride (15 or 50 mg/kg), or a combination of SCH 23390 (0.015 mg/kg) and sulpiride (15 mg/kg). The approach performance of drug-treated pups was then compared to vehicle-treated pups on both reinforcement and extinction trials. Sulpiride (15 mg/kg) did not affect either the extinction or reinforced responding of 11-day-old rat pups. In contrast, SCH 23390-treated pups showed significantly longer response latencies than the vehicle controls in both extinction and reinforcement conditions. Combined treatment with SCH 23390 and sulpiride produced the longest response latencies. Analyses of "best score" and frequency data indicated that the drug-induced decline in responding was due to effects on both reward processes and motor capability. The combined results indicate that D1 and D2 receptors interact complexly to affect reinforced responding.

Animals↗

PubMed1992

Microinjections of dopamine agonists in the nucleus accumbens increase ethanol-reinforced responding.

Long-Evans rats (N = 3) were trained to lever press on a fixed-ratio 4 (FR 4) schedule with ethanol (10% v/v) presented as the reinforcer. Each rat received a total of six bilateral nucleus accumbens microinjections, one per week. They were tested with one physiological saline control, three 20.0-microgram/brain d-amphetamine, and two 6.0-microgram/brain quinpirole injections given 10 min prior to operant sessions. Ethanol-reinforced responding terminated after approximately 10 min during control sessions. Microinjections of the D2 agonist quinpirole and the nonspecific dopamine (DA) agonist d-amphetamine increased total responding but produced slowed response rates that continued for 45-60 min. The slowed response rate produced by d-amphetamine resulted in a peak increase in interresponse times (IRTs) between 8-10 s, whereas quinpirole increased IRTs in the 14- to 16-s range, indicating that nonspecific DA activation resulted in higher rates of ethanol-reinforced responding than specific D2 activation although both drugs decreased local response rates. These data indicate that the amount and temporal extent of ethanol-reinforced responding are increased by microinjections of DA agonists in the nucleus accumbens and support the hypothesis that DA activity in this region is involved in the regulation of ethanol-reinforced responding.

Animals↗

PubMed1995

Strain differences in the analgesic and reinforcing action of morphine in mice.

The analgesic and reinforcing effects of morphine were compared in four strains of mice (C57BL/6, BALB/c, DBA, CBA). The analgesic action of morphine was measured in tail immersion (49 degrees C), hot plate (60 degrees C), and tail clip (four-point scale of nociceptive response) tests. The reinforcing action of morphine was studied in i.v. self-administration and conditioned place preference techniques. The results demonstrate strain differences in the analgesic and reinforcing action of morphine in mice. The relative rank order of the strains varied for the several tests as well as for the morphine effects. The lack of correlation between analgesic and reinforcing action of morphine in inbred strains supports the conclusion that analgesia and reinforcement are separate processes with different genetic control.

Analgesics↗

PubMed1991

Septal lesions lower responding under fixed-ratio schedules of reinforcement.

Albino Sprague-Dawley rats with complete septal lesions and rats with control operations were studied under fixed-ratio (FR) schedules of reinforcement. Both groups were trained for 10 sessions each under FR 10, 20, 40, 60, 80, and 100. In contrast to findings from progressive FR studies and some simple FR studies, septal lesions resulted in lower overall and local response rates along with longer postreinforcement pauses. These effects were especially evident during the FR 100 schedule of reinforcement. A comparison of reinforcement rate as a function of FR size within the context of behavioral economics (i.e., a demand function) indicated that septal lesions did not alter the reward value of food. These findings suggest that responding on FR schedules of reinforcement can be altered by the various procedures used to train rats to reach the terminal value of a reinforcement schedule.

Analysis of Variance↗

PubMed1995

The ascending neuromodulatory systems in learning by reinforcement: comparing computational conjectures with experimental findings.

A central problem in cognitive neuroscience is how animals can manage to rapidly master complex sensorimotor tasks when the only sensory feedback they use to improve their performance is a simple reinforcing stimulus. Neural network theorists have constructed algorithms for reinforcement learning that can be used to solve a variety of biological problems and do not violate basic neurophysiological principles, in contrast to the back-propagation algorithm. A key assumption in these models is the existence of a reinforcement signal, which would be diffusively broadcast throughout one or several brain areas engaged in learning. This signal is further assumed to mediate up- and downward changes in synaptic efficacy by acting as a multiplicative factor in learning rules. The biological plausibility of these algorithms has been defended by the conjecture that the neuromodulators noradrenaline, acetylcholine or dopamine may form the neurochemical substrate of reinforcement signals. In this commentary, the predictions raised by this hypothesis are compared to anatomical, electrophysiological and behavioural findings. The experimental evidence does not support, and often argues against, a general reinforcement-encoding function of these neuromodulatory systems. Nevertheless, the broader concept of evaluative signalling between brain structures implied in learning appears to be reasonable and the available algorithms may open new avenues for constructing more realistic network architectures.

Adaptation, Psychological↗

PubMed1993

Differential effects of excitotoxic lesions of the basolateral amygdala, ventral subiculum and medial prefrontal cortex on responding with conditioned reinforcement and locomotor activity potentiated by intra-accumbens infusions of D-amphetamine.

The experiments reported here have investigated the impact on reward-related processes of lesioning the basolateral amygdala, ventral subiculum and prelimbic cortex which represent the major limbic sources of afferents to the ventral striatum. The results showed that, while lesions of the prelimbic cortex were without effect on the approach to a CS predictive of sucrose reinforcement and the acquisition of a new response with conditioned reinforcement, lesions of the other two structures significantly impaired both responses. However, there were important differences between the effects of basolateral amygdala and ventral subiculum lesions. Thus, lesions of the ventral subiculum completely abolished the locomotor response to intra-accumbens infusions of D-amphetamine, in addition to blocking the potentiative effect of the same treatment on responding with conditioned reinforcement. Lesions of the basolateral amygdala, by contrast, reduced the control over behaviour by a conditioned reinforcer, but not the potentiation of that control by intra-accumbens D-amphetamine except at the highest dose. Moreover, the locomotor response to D-amphetamine-induced increases in dopamine in the nucleus accumbens was unaffected by amygdala lesions over the dose range blocked by ventral subiculum lesions. The results suggest a rather selective effect of amygdala-ventral striatal interactions on processes subserving conditioned reinforcement and a more fundamental influence of ventral subiculum-ventral striatal interactions in mediating the psychomotor stimulant effects of D-amphetamine.

Afferent Pathways↗