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PubMed2005

Rewarding properties of visual stimuli.

The behavioral functions of rewards comprise the induction of learning and approach behavior. Rewards are not only related to vegetative states of hunger, thirst and reproduction but may also consist of visual stimuli. The present experiment tested the reward potential of different types of still and moving pictures in three operant tasks involving key press, touch of computer monitor and choice behavior in a laboratory environment. We found that all tested visual stimuli induced approach behavior in all three tasks, and that action movies sustained consistently higher rates of responding compared to changing still pictures, which were more effective than constant still pictures. These results demonstrate that visual stimuli can serve as positive reinforcers for operant reactions of animals in controlled laboratory settings. In particular, the coherently animated visual stimuli of movies have considerable reward potential. These observations would allow similar forms of visual rewards to be used for neurophysiological investigations of mechanisms related to non-vegetative rewards.

Animals↗
PubMed1985

Integrated lateral hypothalamic neural responses to natural and artificial rewards and cue signals in the rat.

Effects of natural and intracranial electrical rewarding stimuli and cue signals were investigated while recording from single neurons in the rat lateral hypothalamus. The rat obtained both rewards using identical behavior, viz. licking. When both rewarding stimuli influenced a neuron, the responses were usually similar, i.e. both excitatory or both inhibitory. Only neurons that responded to either or both rewards acquired responses to tone cues, and these acquired responses were in the same direction as reward responses. The data indicate that the same single neuron in the lateral hypothalamus might be implicated in reward processes and learning.

Acoustic Stimulation↗
PubMed1989

Forebrain neurons driven by rewarding stimulation of the medial forebrain bundle in the rat: comparison of psychophysical and electrophysiological estimates of refractory periods.

Psychophysically derived estimates of recovery from refractoriness were obtained at self-stimulation sites in the lateral hypothalamus and ventral tegmental area. The refractory periods of single units driven by the same stimulation electrodes and stimulation fields were then measured electrophysiologically. Antidromically driven units with refractory periods longer than those of the neurons responsible for the rewarding effect were concentrated in the septal complex. Units with refractory periods that overlapped the estimates for the reward-related neurons were found in this region as well but were also encountered in neighboring structures lateral, ventral, and/or caudal to the septal nuclei. It is argued that this latter class of units should be considered as possible constituents of the directly stimulated substrate for the rewarding effect because they are driven by rewarding stimulation, have refractory periods similar to those of the reward-related neurons and arise in or near regions in which lesions have been effective in decreasing the rewarding effect of stimulating the medial forebrain bundle.

Animals↗
PubMed1993

Lack of sensitization or tolerance to the facilitating effect of ventral tegmental area morphine on lateral hypothalamic brain stimulation reward.

Unilateral microinjections of morphine (2.5 micrograms/0.5 microliter) into the ventral tegmental area potentiated the rewarding effects of lateral hypothalamic brain stimulation, causing parallel leftward shifts of the functions relating response rate to stimulation frequency. Testing was repeated eight times with no evidence of reliable day-to-day changes either in the direction of sensitization or in the direction of tolerance to the reward-facilitating effects of the drug. The injection dose was sufficient to cause contraversive circling that continued long after the period of reward testing; as with the reward-facilitation, there was neither tolerance nor sensitization to this locomotor effect of the drug. The same dose given to control animals that were not tested for self-stimulation caused progressively stronger circling with repeated testing. Lack of sensitization of the reward-facilitating effects of ventral tegmental morphine raises the possibility of some degree of independence of the brain mechanisms of drug-induced locomotion and of reward-facilitation.

Animals↗
PubMed1994

N-methyl-D-aspartic acid-induced lesions of the nucleus accumbens and/or ventral pallidum fail to attenuate lateral hypothalamic self-stimulation reward.

The role of ventral striatum in the maintenance and transmission of a hypothalamic intracranial self-stimulation (ICSS) reward signal was investigated using the rate-frequency multiple-curve shift paradigm. The excitotoxin N-methyl-D-aspartic acid (NMDA) was bilaterally administered into the nucleus accumbens (15 micrograms per side), the ventral pallidum (15 micrograms per side) or the juncture between the two structures (20 micrograms per side) creating three lesion groups. Both the nucleus accumbens (NAC) lesion group and the ventral pallidum (VP) lesion group displayed substantial NMDA-induced damage which was generally restricted to the intended limbic structure. The NMDA lesions in the third group displayed extensive damage to both the NAC and VP, as intended, but also typically diffused into adjacent medial structures. NMDA-induced lesions in all groups caused a suppression in motor/performance activity at all currents tested. Contrary to motor effects, reward efficacy was relatively unaffected for the NAC and VP groups. The lack of reward effects may be due to plasticity of neuronal systems and redundancy of circuit connections. However, this explanation is questionable given the fact that NMDA lesions which encompassed both the NAC and VP had little effect on reward efficacy. The above data suggests that the nucleus accumbens and the ventral pallidum are not critical for ICSS rewards stimulation and that hypothalamic ICSS reward signals are processed downstream from these limbic structures.

Animals↗
PubMed1983

The effects of reward on tutor's behaviors in a cross-age tutoring context.

Utilizing a cross-age tutoring context, this study examined the effects of reward on the teaching behaviors of the tutor, the tutor's subsequent motivation to continue to teach during a free choice period, and the social interaction between a tutor and a tutee. Third-grade boys and girls (n = 96) who exhibited a positive reinforcement style were asked to teach six addition problems to a first-grade boy or girl (n = 96). The children were randomly assigned to pairs and to one of the three reward conditions. In the performance-contingent reward condition, the tutors were promised a toy if the first-grader learned all of the arithmetic problems. In the noncontingent reward condition, the tutors were promised a toy for teaching the first-grader. In the no reward condition, the tutors taught the first-grader without promise of a toy. The results indicated that the social interaction was rated lower for the children in the performance-contigent group and that the tutors in this group spent less time teaching during the free choice period. However, neither the tutor's teaching style nor the tutee's post-test performance was adversely affected by the reward.

Achievement↗
PubMed1996

Genetic differences in delta 9-tetrahydrocannabinol-induced facilitation of brain stimulation reward as measured by a rate-frequency curve-shift electrical brain stimulation paradigm in three different rat strains.

Lewis, Fischer 344, and Sprague-Dawley rats were implanted with electrodes in the medial forebrain bundle and trained to lever press for brain stimulation reward using a rate-frequency curve-shift electrical brain stimulation paradigm based on a series of 16 pulse frequencies ranging from 25 to 141 Hz in descending order. Once reward thresholds were stable, rats were given 1.0 mg/kg delta 9-tetrahydrocannabinol (delta 9-THC), the psychoactive constituent in marijuana and hashish, or vehicle, by intraperitoneal injection. Lewis rats showed the most pronounced delta 9-THC-induced enhancement of brain reward functions. Sprague-Dawley rats showed an enhancement of brain reward functions that was approximately half that seen in Lewis rats. Brain reward functions in Fischer 344 rats were unaffected by delta 9-THC at the dose tested. These results are consistent with previous work showing Lewis rats to be highly sensitive to the rewarding properties of a variety of drugs of abuse, including opiates, cocaine, and alcohol, while Fischer 344 rats are relatively less sensitive. They extend such previous findings to cannabinoids, and further suggest that genetic variations to other cannabinoid effects may also exist.

Animals↗
PubMed1993

Regional reward differences within the ventral pallidum are revealed by microinjections of a mu opiate receptor agonist.

The ventral pallidum receives a major projection from the nucleus accumbens, a heavily studied terminus of the mesolimbic dopamine system that is known to be involved in a variety of reward and behavioral functions. Recently, ventral pallidum microinjections of the mu opiate receptor agonist Tyr-D-Ala-Gly-NMe-Phe-Gly-ol-enkephalin (DAMGO) have been shown to increase motor activity while ventral pallidum lesions have been shown to reduce opiate and cocaine self-administration behaviors. These results suggest a possible continuation of the mesolimbic reward/motor circuit from the nucleus accumbens into the ventral pallidum. This study investigated the effects of ventral pallidum DAMGO microinjections on reward and motor/performance through the use of the intracranial self-stimulation rate-frequency curve-shift paradigm. Microinjections of DAMGO (vehicle, 0.03 nmol, and 0.33 nmol) were administered bilaterally in a random dose order with a minimum of 3 days between injections. Rats were tested over three consecutive rate-frequency curves immediately following the opiate microinjections to investigate the time course of drug effects. DAMGO microinjections in the rostral ventral pallidum produced decreases in reward and motor/performance when compared to normal baseline activity or vehicle microinjections. In contrast, DAMGO microinjections into the caudal ventral pallidum produced increases in reward and motor/performance. These data confirm a role for the ventral pallidum in limbic function and extend it to intracranial self-stimulation reward. They also suggest reward modulation in the ventral pallidum is a regionally heterogeneous function and that the rostral ventral pallidum may be a transition area between the nucleus accumbens and the ventral pallidum.

Analgesics↗
PubMed1984

Self-deprivation: a test of the reward hypothesis.

Self-deprivation refers to the observation that despite severe levels of water and food deprivation some rats dramatically reduce food and water intake when brain stimulation reward and the alternative reward are placed in competition. In order to determine if the rewarding properties of brain stimulation are responsible for self-deprivation, rats were implanted bilaterally with stimulating electrodes and subsequently tested for self-deprivation and preferences among various electrode locus/stimulation current combinations. According to the reward hypothesis, the relative degree of self-deprivation observed for each electrode/current pair should predict the order of preference for each combination when different electrode/current pairs are placed in competition. Likewise, across all combinations of electrodes and intensities, increasing preferences should be associated with increasing self-deprivation. The findings of the study provide support for the reward hypothesis of self-deprivation. The correlation between the self-deprivation and the preference measure was r = 0.62 (p less than 0.001), which rose to r = 0.80 (p less than 0.001) when floor and ceiling effects were taken into account. It was concluded that the rewarding aspects of brain stimulation are responsible for the self-deprivation phenomenon.

Animals↗
PubMed1987

Summation and saturation properties in the rewarding effect of brain stimulation.

We used a two-lever self-stimulation chamber and rats with central grey and hypothalamic electrodes to obtain a choice-frequency (C/F) function, which plots the relative choice of an electrical stimulus of fixed pulse frequency (the standard stimulus) as a function of the frequency of a second competing stimulus (the alternative stimulus). A family of C/F functions was obtained using increasing frequencies for the standard. A choice index, varying from -1.0 (exclusive choice of the fixed stimulus) to 1.0 (exclusive choice of the alternative stimulus) was computed by using the barpressing rates on the two levers. Reward saturation was assumed to occur when the C/F function obtained with the largest standard reached an asymptote below the value of 1.0. For the hypothalamic subjects, the pulse frequency at the point of reward saturation was twice as high as the frequency required for the maximum rate of self-stimulation in the usual single-lever chamber. Decreasing the pulse intensity always increased the saturation frequency, indicating that the saturation was not due to a frequency blocking effect in the directly activated neurons. Reward saturation occurred with a considerably higher frequency in the central grey than in the hypothalamus. Thus, the asymptotic rate of self-stimulation in the usual single-lever chamber is not conditioned by the processes that summate the central grey and hypothalamic rewarding effects. From the central grey data we obtained the relation between the slope and the position of the C/F function on the frequency axis. We used the slope/frequency profile to delimit the most probable profile of summation rate in the rewarding process. We found that the slope/frequency function has an early plateau followed by a rapidly decelerating phase. We proposed that these two distinct phases reflect an early accelerating rate of summation, followed by a decelerating rate of summation. In other words, reward summation would be predicted by a sigmoid growth model.

Animals↗
PubMed1990

Prenatal protein malnutrition alters response to reward in adult rats.

Developing rats were either malnourished or adequately nourished during the prenatal period by feeding their dams diets of 6% (low) or 25% (adequate) casein content 5 weeks prior to mating and throughout pregnancy. All pups received adequate nutrition from the day of birth onwards. In Experiment 1, male offspring aged 125 days were tested in a food-rewarded variable interval 2-min (VI 2') operant paradigm under three levels of body weight reduction (90%, 85% and 80% of their ad lib feeding weight). Previously malnourished rats showed significantly higher response rates than well-nourished controls at the 90% and 85% levels but not at the 80% level. In Experiment 2, behaviorally native male littermates aged 225 days were tested in a saccharin-solution-rewarded VI 2' operant task. The rate of receipt of reward within each daily session was found to differ in the two nutritional groups. Previously malnourished rats maintained a stable rate of reward throughout the session while the controls showed a rapid decline over the first 15-20 min. The higher rate of reward late in the session in Experiment 2 and the elevated response rate in the first two phases of Experiment 1 suggests that prenatal protein malnutrition increases subsequent responsiveness to reward.

Animals↗
PubMed1983

Effects of peripheral and central dopamine blockade on lateral hypothalamic self-stimulation: evidence for both reward and motor deficits.

The effects of dopamine receptor antagonists on lateral hypothalamic self-stimulation were analyzed using a reward summation function (RSF) technique. This paradigm relates running speed in a runway to the number of stimulation pulses received as a reward, and it is able to separately characterize changes in reward pulse effectiveness and motor performance. Pimozide, administered peripherally (0.125, 0.25, 0.5 mg/kg, IP), dose-dependently shifted the RSF toward higher values of number of pulses indicating reduced reward. Pimozide also reduced the asymptotic running speed of the RSF, indicating a deficit in motor performance. In a second experiment, alpha-flupenthixol infused directly into the nucleus accumbens (0.5 micrograms-0.5 micrograms, bilaterally) induced changes in the RSF similar to those obtained with peripheral neuroleptic treatment. These findings are discussed from the perspective that dopamine is involved both in the perception of reward value and in the performance of the response to obtain reward.

Animals↗
PubMed1988

Catecholamines and endogenous opioids in ventral tegmental self-stimulation reward.

Midbrain dopaminergic pathways and opioid receptor systems have been implicated in the reward experienced in electrical intracranial self-stimulation behavior. In the present experiment, the influence of graded doses of the dopamine antagonist haloperidol and of the agonist cocaine were investigated on electrical self-stimulation reward, elicited by electrodes located in the ventral tegmental area. A threshold method, which is rather insensitive for aspecific motor effects, was applied to determine the reward of self-stimulation. The method allowed to determine simultaneously the rate of lever pressing for self-stimulation. All doses of haloperidol and cocaine were administered with and without the opioid antagonist naloxone, in order to investigate the interaction between dopaminergic and opioid modulation of reward. Haloperidol lowered and cocaine tended to increase the response rate, whereas cocaine but also haloperidol lowered the self-stimulation threshold. The effects appear to be dose-dependent. Naloxone did not interact with the effect of the drugs on threshold and it lowered the response rate, but in the haloperidol-treated rats only. It is concluded that dopamine is involved in the reward of electrical self-stimulation elicited from the ventral tegmental area and that this involvement is independent of endorphin systems, suggesting the existence of separate catecholamine and opioid mechanisms modulating brain reward.

Animals↗
PubMed1990

Haloperidol prevents the reinstatement of amphetamine-rewarded runway responding in rats.

Animals were trained to traverse a straight-alley once each day for a reward of 1.0 mg/kg SC d-amphetamine sulfate. After 14 days of acquisition, extinction trials were initiated in which the amphetamine reward was replaced by injections of physiological saline. After running speeds had decreased to less than one third those of preextinction values, rats received a single amphetamine-rewarded trial either in the absence or presence of haloperidol (0.075, 0.15 or 0.3 mg/kg IP). Twenty-four hours later, animals were tested for reinstatement of operant running in a single drug-free Test trial. Animals that were nondrugged during the amphetamine-rewarded trial demonstrated a statistically reliable increase in running speed on the Test trial relative to extinction baseline speeds. In contrast, animals that were under the influence of medium or high doses of haloperidol during the amphetamine-rewarded trial failed to show Test day increases in running speed. This result did not stem from some residual sedative or performance impairing quality of the drug since a "motor control group" administered a high dose of haloperidol shortly after a rewarded trial, was able to demonstrate unimpaired reinstatement of operant running on Test day (i.e., 24 hr later). These findings support the view that dopamine systems play a role in the neural substrates underlying the incentive motivational properties of amphetamine reinforcement.

Animals↗
PubMed1992

Chronic morphine fails to enhance the reward value of prefrontal cortex self-stimulation.

Dopamine (DA) plays an important role in the rewarding effects of drugs of abuse and intracranial self-stimulation (ICSS). We previously reported that ICSS derived from the prefrontal cortex appears insensitive to the reward-enhancing effects of amphetamine, a drug that increases DA release and reward at other ICSS sites. In the present study, rats with prefrontal electrodes were tested to see if morphine (7.5 or 10.0 mg/kg, IP) given once per day for 10 days enhanced prefrontal reward as assessed with the curve-shift method. Morphine initially produced sedation; however, after 3-4 days response rates increased sharply while frequency thresholds were unaffected. These results demonstrate that morphine does not enhance prefrontal ICSS reward and provide further evidence that prefrontal brain stimulation reward does not display the same characteristics as other ICSS sites.

Animals↗
PubMed1992

Effects of nicotine on the threshold for rewarding brain stimulation in rats.

The rewarding effects of nicotine alone and nicotine challenged with mecamylamine, a nicotine receptor blocker, or naloxone were determined using a rate-independent discrete-trial threshold measure of brain-stimulation reward in rats. If nicotine acts as other drugs of abuse, it would be expected to lower the reward threshold, that is, increase an animal's sensitivity to rewarding brain stimulation, and naloxone would be expected to block this effect, as it does other stimulants in this paradigm. Nicotine was found to significantly lower the reward threshold and mecamylamine blocked this effect. However, although naloxone increased the variability of nicotine's effect on the reward threshold, it failed to dose dependently block nicotine's threshold-lowering effect.

Animals↗
PubMed1996

Anabolic-androgenic steroids and brain reward.

Anabolic-androgenic steroid (AAS) effects on brain reward were investigated in male rats with electrodes implanted in the lateral hypothalamus using the rate-frequency curve shift paradigm of brain stimulation reward. In the first experiment, treatment for 2 weeks with the AAS methandrostenolone had no effect on either the reward or performance components of intracranial self-stimulation. In the second experiment, treatment for 15 weeks with an AAS "cocktail" consisting of testosterone cypionate, nandrolone decanoate, and boldenone undecylenate did not alter brain reward but did produce a slight but significant change in bar press rate. In addition to the AAS treatment, animals in the second study were administered a single injection of d-amphetamine before and after 15 weeks of AAS exposure. The rate-frequency curve shift observed in response to a systemic injection of amphetamine was significantly greater in animals after 15 weeks of treatment with the AAS cocktail. Although AAS do not appear to alter the rewarding properties of brain stimulation, AAS may influence the sensitivity of brain reward systems.

Amphetamine↗
PubMed1995

Rewarding drugs produce taste avoidance, but not taste aversion.

Paradoxically, drugs that animals will self-administer also produce conditioned taste avoidance at similar dosage levels. The present review presents evidence that the taste avoidance produced by these rewarding drugs differs qualitatively from the taste avoidance produced by the nonrewarding, emetic drug, lithium chloride. An analysis of data pooled across 6 experiments compares the nature of flavor-drug associations produced by various rewarding drugs (amphetamine, cocaine, methamphetamine, methylphenidate, morphine, nicotine and phencyclidine) with that produced by lithium. The data from the groups conditioned with the rewarding drugs and with lithium were combined into the two categories of low/moderate and high doses. When assessed by the CTA test, the rewarding drugs did not differ from lithium in the strength of the CTA at low/moderate or at high doses. However, when assessed by the TR test, lithium produced more prominent aversive taste reactions than did the rewarding drugs. These findings suggest that the flavor-drug association produced by lithium and rewarding drugs differs qualitatively. With the large pooled data set we also assessed the relationship among the various TR categories, resulting in two factors of "Ingestion" and "Aversion" accounting for 55% of the total variability within the data.

Animals↗