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PubMed1999

Comparing the reinforcing efficacy of nicotine containing and de-nicotinized cigarettes: a behavioral economic analysis.

RATIONALE: Smoking-related respiratory stimuli produced by de-nicotinized cigarettes may function as conditioned reinforcers, but behavioral data on such reinforcing effects are limited. OBJECTIVES: The present experiment compared the reinforcing efficacy of cigarettes that provided only smoking-related stimuli (de-nicotinized cigarettes) and cigarettes that provided both smoking-related stimuli and nicotine. METHODS: Eight human subjects responded on a progressive-ratio schedule in which the number of plunger pulls required for standardized cigarette puffs increased across sessions. In one phase, the breakpoints, number of puffs earned per session, peak response rates, ratio producing peak response rates, and the elasticity of demand for cigarette puffs were compared for nicotine-containing and de-nicotinized cigarettes when each cigarette type was the only one available. In another phase, subjects chose between the two cigarette types at some of the prices examined in the previous phase. RESULTS: Nicotine-containing and de-nicotinized cigarettes produced similar measures of reinforcing efficacy when each was presented alone, but there was a strong preference for nicotine-containing cigarettes when subjects were given a choice. CONCLUSIONS: These data support suggestions that smoking-produced sensory stimuli may function as conditioned reinforcers and that the relative reinforcing efficacy of cigarettes is determined by the combined effects of the nicotine/conditioned reinforcing complex provided by smoking.

Adult↗
PubMed1991

Do adenosinergic substrates mediate methylxanthine effects upon reinforcement thresholds for electrical brain stimulation in the rat?

Caffeine and other methylxanthines elevate reinforcement threshold for electrical brain stimulation with an order of potency suggesting that the effect is mediated by antagonism of adenosine A2 receptors. The purpose of this study was to evaluate further the possible mechanism by which caffeine and other methylxanthines elevate reinforcement thresholds for ICSS. Drugs known to affect adenosinergic transmission in predictable ways, adenosine receptor agonists and antagonists and benzodiazepine agonists and inverse agonists, were tested to determine their effect upon reinforcement threshold. Both the selective A1 adenosine agonist, R(-)-PIA, and the non-selective A1/A2 adenosine agonist NECA failed to alter reinforcement thresholds, as did CGS 15943, a potent non-xanthine non-selective adenosine receptor antagonist. Chlordiazepoxide, a benzodiazepine agonist, lowered reinforcement thresholds and FG 7142, a benzodiazepine inverse agonist, elevated reinforcement thresholds, perhaps corresponding to their anxiolytic and anxiogenic subjective effects in humans. However, another benzodiazepine agonist, midazolam and another inverse agonist, beta-CCE, did not alter reinforcement thresholds. These results fail to support a general role for adenosinergic systems in the threshold-elevating effect of methylxanthines.

Adenosine↗
PubMed1985

The conditioned place preference is affected by two independent reinforcement processes.

The conditioned place preference method for measuring the affective properties of reinforcing events was studied using treatments of known affective value. The size of the place aversion observed increased with dose when the reinforcer was injections of lithium chloride. The size of the place preference observed increased with concentration when the reinforcer was drinking sucrose solutions. However, when the reinforcer was solutions of saccharin (that were consumed in the same amounts as the sucrose solutions) no place preferences were observed. This finding was explained in terms of the dual reinforcement hypothesis [20] which postulates that although sucrose and saccharin both have positive affective properties (based on their tastes) only sucrose has memory improving properties (based on its post-ingestive action). It was therefore proposed that conditioned place preferences depend on the activation of both affective and memory improving processes. This hypothesis was confirmed by the observation of place preferences with a saccharin solution as the reinforcer when the pairing trials were followed by non-contingent, post-pairing injections of glucose or amphetamine (both of which are known to improve memory). Therefore, behavior in the place preference method depends upon both the affective and the memory improving properties of the reinforcers under test.

Affect↗
PubMed1987

Factors controlling drug reinforced behavior.

An overview is provided of factors controlling drug reinforced behavior. Drug reinforced behavior is defined, and control procedures for rigorously identifying such behavior are discussed. Factors affecting drug reinforced behavior include the drug itself, animal species, route of administration, current circumstance variables, subject's experimental history, and response consequences. Current circumstance variables concern conditions present during opportunities for drug self-administration and include such factors as stimulus control, food deprivation, drug-access conditions, and brain lesions. Response consequence variables include reinforcement schedule, punishment, drug dose, and competing reinforcers. Drug reinforced behavior is a member of a more general class of behavior, namely operant behavior. Over the last 25 years there has been a rapid increase in understanding drug reinforcement, and this pattern of expanding knowledge suggests that the high rate of progress will continue.

Animals↗
PubMed1996

N-methyl-D-aspartate lesions of the pedunculopontine nucleus block acquisition and impair maintenance of responding reinforced with brain stimulation.

Excitotoxin lesions of the pedunculopontine tegmental nucleus have been found to block the acquisition of a conditioned place preference induced by morphine or amphetamine, and it has been suggested that such lesions may attenuate the primary reinforcing effects of these drugs and, possibly, other reinforcers. The present study examined the effects of pedunculopontine lesions on the reinforcing effects of brain stimulation. N-methyl-D-aspartate-induced lesions of the pedunculopontine nucleus prevented spontaneous acquisition of lever pressing for brain stimulation reinforcement during five daily 1 h sessions of training. The effective lesions damaged the retrorubral fields in addition to the pedunculopontine tegmental nucleus. N-methyl-D-aspartate (25 or 50 nmol) lesions of the retrorubral fields did not block acquisition of self-stimulation, however, controls reached their maximum rate of responding in the first session, responding of rats with retrorubral field lesions gradually increased over five days. When excitotoxin-induced lesions of the pedunculopontine nucleus were made after acquisition of self-stimulation, lesioned rats continued to respond to brain stimulation, but at a lower rate than controls. The results show that pedunculopontine lesions interfere with the learning and expression of a response reinforced by brain stimulation just as they block learning motivated by drugs and natural rewards. They also suggest that collateral damage to the retrorubral fields may contribute to the effects of pedunculopontine lesions on reinforced behaviour. These data support the view that the pedunculopontine tegmental nucleus is involved in the process by which reinforcers control purposive behaviour.

Animals↗
PubMed1993

Orally self-administered cocaine in rhesus monkeys: transition from negative or neutral behavioral effects to positive reinforcing effects.

The establishment of orally delivered cocaine as a reinforcer was examined with nine rhesus monkeys. A 2% ethanol solution served as a reinforcer for all nine monkeys, for it maintained substantially higher response rates than did the concurrently available water vehicle. A test was initially conducted to determine whether cocaine would function as a reinforcer when substituted for 2% ethanol. When an intermediate cocaine concentration (0.2 mg/ml) was substituted for the ethanol solution, the drug maintained behavior at rates less than (seven monkeys), equal to (one monkey), or greater than (one monkey) those maintained by water. Thus, for eight of nine monkeys simple substitution of cocaine for ethanol was not sufficient to establish orally delivered cocaine as a reinforcer. In the next phase a stimulus-fading procedure was used. Blocks of training and testing sessions alternated. Across blocks of training sessions, increasing amounts of cocaine (0.0125, 0.025, 0.05, 0.1 mg/ml) were added to the 2% ethanol solution and subsequently the ethanol concentration was gradually decreased until only the 0.1 mg/ml cocaine solution remained; water was always concurrently available. Between each block of training sessions, a block of test sessions was inserted. Test sessions compared relative rates of responding maintained by two concurrently available drug solutions: (1) a solution containing the combination of ethanol and cocaine used in the prior training block and (2) a solution containing the same concentration of ethanol but with no cocaine. Thus, differences in rates of behavior maintained by the two solutions could be attributed to the presence of cocaine and the existence and degree of any such differences could be monitored at each step in the acquisition procedure. The outcome of the training procedure was that cocaine came to function as a reinforcer for six of the eight monkeys tested (the ninth monkey was not put through the fading procedure, having shown higher cocaine than vehicle rates during the initial substitution procedure). During the phase when ethanol was faded from the drug solution, differences between the combination cocaine-ethanol solution and the ethanol-only solution emerged: for the six monkeys that developed cocaine reinforced behavior, the combination solution maintained higher rates of responding than the ethanol solution alone. The opposite results were obtained with the remaining two monkeys. That cocaine had been established as a reinforcer was confirmed by persistent and orderly responding when dose and fixed-ratio size were subsequently varied.

Administration, Oral↗
PubMed2005

Baclofen-induced reduction of alcohol reinforcement in alcohol-preferring rats.

Recent studies have demonstrated that treatment with the gamma-aminobutyric acid (GABA(B)) receptor agonist, baclofen, reduces alcohol intake in selectively bred Sardinian alcohol-preferring rats tested under the homecage two-bottle "alcohol versus water" choice regimen. This study was designed to investigate whether baclofen also reduces alcohol-reinforcing effects in Sardinian alcohol-preferring rats. To this aim, sP rats were trained to lever press for oral alcohol (15%, vol/vol) or sucrose (0.3%, wt/vol; included as alternative reinforcer to evaluate the specificity of baclofen effect on alcohol reinforcement) under a fixed ratio schedule of 4. Once steady levels of alcohol or sucrose self-administration behavior were established, the effects of acutely administered baclofen (0, 1.7, and 3 mg/kg, intraperitoneal [ip]) and naloxone (0, 1, and 3 mg/kg, ip; included as reference compound) on alcohol- or sucrose-reinforced responding were evaluated. Baclofen administration dose dependently, although not specifically, reduced alcohol-reinforced responding to an extent comparable to that of naloxone. Baclofen also produced a dose-dependent and specific delay in the onset of alcohol-reinforced responding, suggesting that it suppressed the rats' motivation to start drinking alcohol. These data are discussed in terms of adding further support to the hypothesized involvement of the GABA(B) receptor in the neural system mediating alcohol reinforcement. These data are also in agreement with the results of recent preliminary clinical studies suggesting that baclofen may have therapeutic efficacy in the treatment of alcohol dependence.

Alcohol Drinking↗
PubMed2005

Responding for sucrose and wheel-running reinforcement: effect of pre-running.

Six male albino Wistar rats were placed in running wheels and exposed to a fixed interval 30-s schedule that produced either a drop of 15% sucrose solution or the opportunity to run for 15s as reinforcing consequences for lever pressing. Each reinforcer type was signaled by a different stimulus. To assess the effect of pre-running, animals were allowed to run for 1h prior to a session of responding for sucrose and running. Results showed that, after pre-running, response rates in the later segments of the 30-s schedule decreased in the presence of a wheel-running stimulus and increased in the presence of a sucrose stimulus. Wheel-running rates were not affected. Analysis of mean post-reinforcement pauses (PRP) broken down by transitions between successive reinforcers revealed that pre-running lengthened pausing in the presence of the stimulus signaling wheel running and shortened pauses in the presence of the stimulus signaling sucrose. No effect was observed on local response rates. Changes in pausing in the presence of stimuli signaling the two reinforcers were consistent with a decrease in the reinforcing efficacy of wheel running and an increase in the reinforcing efficacy of sucrose. Pre-running decreased motivation to respond for running, but increased motivation to work for food.

Animals↗
PubMed2006

Is extinction the hallmark of operant discrimination? Reinforcement and S(Delta) effects.

Using a successive discrimination procedure with rats, three experiments investigated the contribution of reinforcement rate and amount of S(Delta) exposure on the acquisition of an operant discrimination. S(D) components and were always 2 min in length, while S(Delta) (extinction) components were either 1 min or 4 min in length; responses in S(D) were reinforced on one of four schedules. In Experiment 1, each of eight groups were exposed to one possible combination of rate of reinforcement and S(Delta) component length. At every level of reinforcement, the 4 min S(Delta) groups acquired the discrimination more quickly. However, within each level of reinforcement, the proportions of responding in S(D) as a function cumulative S(Delta) exposure were equivalent, regardless of the number of reinforcers earned in S(D), suggesting that extinction is the "hallmark" of discrimination. Experiment 2 sought to replicate these results in a within-subjects design, and although the 4 min S(Delta) conditions always produced superior discriminations, the lack of discriminated responding in some conditions suggested that stimulus disparity was reduced. Experiment 3 clarified those results and extended the finding that the acquisition of operant discrimination closely parallels extinction of responding in S(Delta). In sum, it appears that higher reinforcement rates and longer S(Delta) exposure facilitate the acquisition of discriminated operant responding.

Animals↗
PubMed2006

Influence of abstinence and conditions of cocaine access on the reinforcing strength of cocaine in nonhuman primates.

The development of addiction is marked by a transition from recreational to uncontrolled drug use. Investigators modeling this phenomenon in rodents observed increases in cocaine self-administration when conditions of drug access were altered as well as after abstinence. The present studies were designed to extend this research to nonhuman primates by examining whether the reinforcing strength of cocaine could be altered by changing conditions of cocaine availability or by introducing abstinence periods. Rhesus monkeys self-administered cocaine (0.03-0.3 mg/kg per injection) under a progressive-ratio (PR) schedule of reinforcement in evening sessions, with the number of injections earned serving as a measure of reinforcing strength. Alterations in the reinforcing strength of cocaine were assessed after additional access to cocaine under a fixed-ratio (FR) schedule was provided in morning sessions and following various periods of abstinence (3, 7 and 14 days) from regimens of self-administration that resulted in a range of cocaine intakes. Under baseline PR conditions, the maximum number of cocaine injections increased dose-dependently, peaking when 0.3 mg/kg per injection cocaine was available. No increases in the reinforcing strength of cocaine were observed under any condition. In contrast, a statistically significant decrease in the reinforcing strength of cocaine was observed following 14 days of abstinence under one condition. These results fail to support the views that increasing access to cocaine or abstinence enhances the reinforcing strength of cocaine.

Animals↗
PubMed1997

A role for D2, but not D1, dopamine receptors in the response-reinstating effects of food reinforcement.

Although the reinforcing properties of food are reduced in the presence of dopamine antagonist drugs, controversy exists about the relative roles of D1 vs D2 receptor subtypes in the actions of these drugs. The current experiment compared the effects of raclopride (a selective D2 receptor antagonist) and SCH 39166 (a selective D1 receptor antagonist) in the response-reinstating effects of food reinforcement. Hungry rats were trained to run a straight-alley for food reinforcement during single daily trials. The operant was then extinguished during consecutive daily non-reinforced trials. Subjects were then injected with one of four doses of raclopride (0.0, 1.0, 0.5, and 0.25 mg/kg, i.p.) or SCH 39166 (0.0, 1.0, 0.5, and 0.1 mg/kg i.p.) 30 min prior to a single reinforced treatment trial. Twenty-four h later, a test trial was conducted in an unbaited runway. The single reinforced trial in the midst of extinction was observed to reinstate operant runway performance. Raclopride, but not SCH 39166, dose-dependently attenuated this reinstatement. Motor control groups ruled out the possibility that these results were due to differential residual motor effects of the drugs. Results suggest that D2, but not D1, dopamine receptors, are involved in the response-reinstating properties of food reinforcement.

Animals↗
PubMed1997

Effects of chlorpromazine on rats' acquisition of lever-press responding with immediate and delayed reinforcement.

The effects of chlorpromazine (0, 2, 6, and 10 mg/kg) on the acquisition of lever-press responding by rats were examined under conditions where reinforcement (water delivery) was immediate or delayed. Under the immediate reinforcement condition, water-deprived rats were exposed during 8-h sessions to a fixed-ratio 1 (FR 1) schedule of water delivery without prior autoshaping or hand shaping. Under the delayed reinforcement condition, similar rats were exposed to a tandem FR 1 fixed-time 8-s schedule of water delivery. A different squad of eight rats was exposed to each delay condition and drug dose. For all subjects, responses on one lever produced water and responses on a second lever had no programmed consequences. Regardless of whether reinforcement was immediate or delayed, chlorpromazine reduced in dose-dependent fashion the mean number of operative-lever responses emitted, which suggests that the drug interfered with learning. At all chlorpromazine doses except 10 mg/kg, substantially more operative-lever than inoperative-lever responding occurred, indicating that the operant response was acquired. Chlorpromazine at 2 and 6 mg/kg disrupted the acquisition of stimulus control by the operative lever when reinforcement was delayed, but not when it was immediate. At 10 mg/kg, most subjects did not acquire lever-pressing regardless of whether they were exposed to the immediate or delayed reinforcement procedure. Procedures similar to those used in the present study appear to provide a reasonable assay for examining how drugs affect the initial behavioral effects of immediate and delayed reinforcement, and may merit further investigation.

Animals↗
PubMed1999

Intraaccumbens raclopride attenuates amphetamine-induced locomotion, but fails to prevent the response-reinstating properties of food reinforcement.

It has been well established that the presentation of a single reinforced trial in the midst of extinction results in a reinstatement of the previously reinforced operant response. In previous experiments, we have shown that systemically applied raclopride (a selective dopamine D2 receptor antagonist) dose dependently blocked the response-reinstating properties of food reinforcement, while SCH39166 (a selective dopamine D1 receptor antagonist) did not (11). The current experiments investigated the possible role of the nucleus accumbens in these actions of raclopride. In the first of two experiments, hungry rats were trained to traverse a straight runway for food reinforcement, a response that was then weakened through a series of extinction trials. On a single treatment trial, subjects were infused with one of three doses of intraaccumbens raclopride (0.0, 2.5, or 5.0 microg/0.5 microl/side) just prior to a reinforced trial. Twenty-four hours later, a single test trial was run in an unbaited runway. The results demonstrate that the prior day's reinforced trial produced a reinstatement of operant runway performance that was unaltered by intraaccumbens applications of raclopride. Two days later, the same animals were tested in a second experiment investigating the effects of intraaccumbens raclopride on amphetamine-induced locomotion. Subjects were pretreated with 1.0 mg/kg s.c. amphetamine prior to a 90-min locomotor activity session. The following day, subjects were again pretreated with amphetamine, but this time with a challenge dose of raclopride. Results demonstrate that the same raclopride doses that produced no effect in the response-reinstating experiment produced, in the same rats, a dose-dependent attenuation in amphetamine-induced locomotion. These data suggest that dopamine D2 receptors in the nucleus accumbens may not, in and of themselves, be necessary for the response-reinstating effects of food reinforcement.

Amphetamine↗
PubMed2003

Reinforcing versus anticonvulsant drugs: effects on intracranial self-stimulation rate-frequency M50 indices.

Drugs of abuse, such as amphetamine and morphine, produce reward-related shifts on intracranial self-stimulation (ICSS) thresholds. The facilitatory effects on ICSS thresholds of drugs that act through the GABAergic system, however, are reported to be attributed to their antiseizure and anticonvulsant effects, rather than their reinforcing effects. Using a rate-frequency ICSS paradigm, we examined the effects of amphetamine (a reinforcing drug of abuse that acts via the catecholaminergic system), pentobarbital (a GABA(A) receptor agonist and reinforcing barbiturate with anticonvulsant properties), and gabapentin (a nonspecific GABAergic agonist and anticonvulsant with low abuse potential) on ICSS M(50) indices. All three doses of amphetamine (0.5, 1.0, and 2.0 mg/kg) and pentobarbital (2.5, 5.0, and 10.0 mg/kg) significantly lowered rate-frequency M(50) values. Gabapentin, on the other hand, significantly raised rate-frequency M(50) values, albeit only at the highest dose administered (30 mg/kg). Our results indicate that shifts in ICSS M(50) values produced by pentobarbital are associated with the reinforcing, not the anticonvulsant, effect of pentobarbital. These results are consistent with the view that there is a common system underlying the reinforcing effects of drugs and ICSS reinforcement, and suggest that the reinforcing and anticonvulsant effects of GABA agonists are dissociable.

Acetates↗
PubMed2003

The relative-reinforcing value of food under differing levels of food deprivation and restriction.

Food deprivation and restriction both increase food consumption. Food deprivation also increases the reinforcing value of food, but it is unknown if food restriction alone or combined with deprivation increases the reinforcing value of food. Forty, normal-weight, college-aged, unrestrained females were randomized to one of four conditions that crossed food deprivation (Dep) and restriction (Res): Dep/Res, Dep/No Res, No Dep/Res, No Dep/No Res. All participants arrived at least 13h food-deprived, and non-deprived participants consumed at least 365cal from a drink during the session. Restriction was manipulated by placing snack food in front of participants, without access for 15min during the session, or having no snack food placed in front of participants. Following the experimental manipulations, participants completed a computer choice task to determine the reinforcing value of food. Repeated measures analysis of variance found a significant main effect of deprivation (p<0.05) and trials (p<0.001) for food points earned. Deprived participants found food to be more reinforcing, and the reinforcing value of food decreased over time. This suggests that while short-term food deprivation increases the relative-reinforcing value of food, short-term food restriction has no effect on the relative-reinforcing value of food in unrestrained eaters.

Adolescent↗
PubMed2000

Cytotoxic lesion of the medial prefrontal cortex abolishes the partial reinforcement extinction effect, attenuates prepulse inhibition of the acoustic startle reflex and induces transient hyperlocomotion, while sparing spontaneous object recognition memory in the rat.

The partial reinforcement extinction effect refers to the increase in resistance to extinction of an operant response acquired under partial reinforcement relative to that acquired under continuous reinforcement. Prepulse inhibition of the acoustic startle response refers to the reduction in startle reactivity towards an intense acoustic pulse stimulus when it is shortly preceded by a weak prepulse stimulus. These two behavioural phenomena appear to be related to different forms of attentional processes. While the prepulse inhibition effect reflects an inherent early attentional gating mechanism, the partial reinforcement extinction effect is believed to involve the development of acquired inattention, i.e. the latter requires the animals to learn about what to and what not to attend. Impairments in prepulse inhibition and the partial reinforcement extinction effect have been independently linked to the neuropsychology of attentional dysfunctions seen in schizophrenia. The proposed neural substrates underlying these behaviourial phenomena also appear to overlap considerably: both focus on the nucleus accumbens and emphasize the functional importance of its limbic afferents, including that originating from the medial prefrontal cortex, on accumbal output/activity. The present study demonstrated that cytotoxic medial prefrontal cortex lesions which typically damaged the prelimbic, the infralimbic and the dorsal anterior cingulate areas could lead to the abolition of the partial reinforcement extinction effect and the attenuation of prepulse inhibition. The lesions also resulted in a transient elevation of spontaneous locomotor activity. In contrast, the same lesions spared performance in a spontaneous object recognition memory test, in which the lesioned animals displayed normal preference for a novel object when the novel object was presented in conjunction with a familiar object seen 10 min earlier within an open field arena. The present results lend support to the hypothesis that medial prefrontal cortex dysfunction might be related to some forms of attentional abnormality central to the symptomatology of schizophrenia. Relevance of the present findings in relation to the neural substrates underlying the partial reinforcement extinction effect and prepulse inhibition is further discussed.

Acoustic Stimulation↗
PubMed2000

Reinforced variability and operant learning.

Reinforcement of variability may help to explain operant learning. Three groups of rats were reinforced, in different phases, whenever the following target sequences of left (L) and right (R) lever presses occurred: LR, RLL, LLR, RRLR, RLLRL, and in Experiment 2, LLRRL. One group (variability [VAR]) was concurrently reinforced once per minute for sequence variations, a second group also once per minute but independently of variations, that is, for any sequences (ANY), and a control group (CON) received no additional reinforcers. The 3 groups learned the easiest targets equally. For the most difficult targets, CON animals' responding extinguished whereas both VAR and ANY responded at high rates. Only the VAR animals learned, however. Thus, concurrent reinforcers--contingent on variability or not--helped to maintain responding when difficult sequences were reinforced, but learning those sequences depended on reinforcement of variations.

Animals↗
PubMed2001

Contextual control of appetitive conditioning: influence of a contextual stimulus generated by a partial reinforcement procedure.

Three experiments with rat subjects examined the effects of a context switch after conditioning treatments in which the conditioned stimulus (CS) was either paired with food on every presentation (continuous reinforcement) or on some of its presentations (partial reinforcement). In each experiment, a target CS was given one of these treatments in Context A, and another CS was given a treatment during sessions that were intermixed in Context B. Final tests of the target CS in Context A and Context B often revealed no loss of responding with the switch to B. However, a loss was observed when partial reinforcement had been associated with Context A and continuous reinforcement had been associated with Context B. Those conditions caused equal decrements in responding to partially reinforced and continuously reinforced targets. The results suggest that under the present conditions partial reinforcement can generate a contextual stimulus that becomes associated with the physical context and controls responding to the CS.

Animals↗