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PubMed2004

The rich get richer: students' discounting of hypothetical delayed rewards and real effortful extra credit.

The present research compared choices among students with higher or lower grades for rewards that were devalued by imposing a delay to their receipt (Study 1) or by requiring more work for a larger reward (Study 2). In Study 1, students chose between hypothetical and noncontingent smaller immediate or larger delayed monetary rewards. In Study 2, students chose from among different amounts of real, response-contingent academic rewards (extra credit) that required different amounts of work. The results of both studies were similar: The highest scoring students discounted the value of the delayed money less than did their lower scoring counterparts, and the highest scoring students also chose to do and actually did more extra-credit work than lower scoring students did. Differences in the discounting of devalued rewards might represent a fundamental difference between the highest and lower scoring students.

Choice Behavior↗
PubMed2006

Behavioral, but not reward, risk modulates activation of prefrontal, parietal, and insular cortices.

Risky decisions may involve uncertainty about possible outcomes (i.e., reward risk) or uncertainty about which action should be taken (i.e., behavioral risk). Determining whether different forms of risk have distinct neural correlates is a central goal of neuroeconomic research. In two functional magnetic resonance imaging experiments, subjects viewed shapes that had well-learned response-reward contingencies. Magnitude of a monetary reward was held constant within one experiment, whereas expected value was held constant within the other. Response selection, in the absence of behavioral risk, evoked activation within a broad set of brain regions, as had been found in prior studies. However, behavioral risk additionally modulated activation in prefrontal, parietal, and insular regions,within which no effect of reward risk was observed. Reward delivery, in comparison with omission, evoked increased activity in the ventromedial prefrontal cortex and the nucleus accumbens. We conclude that distinct brain systems are recruited for the resolution of different forms of risk.

Adolescent↗
PubMed1999

Naltrexone effects on ethanol reward and discrimination in C57BL/6 mice.

The effects of the opioid antagonist, naltrexone, on operant responding for oral ethanol reward delivered on a fixed-ratio schedule, and on the discriminative stimulus properties of intraperitoneally injected ethanol, was examined in two separate experiments. The ages, food/water motivational conditions, and naltrexone doses for the two experiments were similar to allow a direct comparison of naltrexone effects on the two measures. Male food-deprived C57BL/6 mice responded for ethanol during either preprandial (low thirst, high hunger motivation) or postprandial (high thirst, low hunger motivation tests). The reinforcing value of ethanol relative to water was greater during the preprandial tests; however, the amounts of ethanol consumed was greater during the postprandial tests, with some mice becoming unconscious during the 15-min test session. Naltrexone produced dose-responsive reductions in responding for ethanol under either testing condition. During postprandial tests, naltrexone reduced responding for ethanol reward at a dose (1.25 mg/kg) that had little effect on responding for water reward, suggesting some selectivity for ethanol reward. In addition, doses of naltrexone that reduced responding for ethanol rewards did not alter the discrimination of ethanol (g/kg) in an operant discrimination task, but did reduce the total number of responses made during these tests. Thus, under similar motivational and dosing conditions, the opiate antagonist attenuated the reinforcing, but not the discriminative properties of ethanol, suggesting that the latter is mediated by either different or additional neural mechanisms in C57BL/6 mice.

Animals↗
PubMed2001

Rewarding properties of methylphenidate: sensitization by prior exposure to the drug and effects of dopamine D1- and D2-receptor antagonists.

In drug addiction, a sensitization phenomenon has been postulated to play a critical role. The aim of our study was to evaluate whether sensitization occurs to the rewarding properties of methylphenidate, a psychostimulant drug known to possess abuse potential, as assessed with the biased conditioned place preference method in rats. In addition, since the brain dopaminergic system is considered to be important in drug-reward, the involvement of dopamine D1- and D2-receptors both in the rewarding properties of methylphenidate and in sensitization to these properties was assessed. Conditioning with methylphenidate at doses of 1.25 to 20 mg/kg increased preference for the paired environment, whereas a dose of 0.31 mg/kg was ineffective. However, following the 7-day sensitization treatment with methylphenidate (0.62-20 mg/kg), conditioning with a dose of 0.31 mg/kg resulted in an increased preference for the paired environment, i.e., the rewarding properties of methylphenidate appeared to be sensitized. Control experiments indicated that the enhancement of preference was not due to attenuation of sensitization treatment-induced withdrawal nor to tolerance to aversive properties of methylphenidate. When conditioned with methylphenidate, D1-antagonist SCH 23390 but not D2-antagonist raclopride prevented place preference. However, when coadministered with methylphenidate during the sensitization treatment, both SCH 23390 and raclopride prevented the development of sensitization. These data indicate that the rewarding properties of methylphenidate are sensitized by prior exposure to the drug and that both D1- and D2-receptors, the latter of which possibly more specifically, appear to be involved in the development of this sensitization.

Animals↗
PubMed2006

Implication of Src family kinase-dependent phosphorylation of NR2B subunit-containing NMDA receptor in the rewarding effect of morphine.

The present study was undertaken to further clarify the role of tyrosine phosphorylation of NR2B subunit-containing N-methyl-D-aspartate (NMDA) receptor in the development of the morphine-induced rewarding effect in mice. The morphine (5 mg/kg, sc)-induced rewarding effect was completely inhibited by pretreatment with a selective NR2B subunit-containing NMDA receptor antagonist ifenprodil (20 mg/kg, i.p.). The protein level of phospho-Tyr-1472, but not phospho-Ser-1303, NR2B subunit was significantly increased in the mouse limbic forebrain containing the nucleus accumbens (N.Acc.) of mice that had shown the morphine-induced rewarding effect. In addition, the level of phospho-Tyr-416 Src family kinase was also increased in the limbic forebrain of mice that had shown the morphine-induced rewarding effect. These findings suggest that Tyr-1472 phosphorylation of NR2B subunit-containing NMDA receptor associated with activation of Src family kinase in the limbic forebrain may be involved in the morphine-induced rewarding effect.

Animals↗
PubMed1985

Effects of material rewards on inkblot perception and organization.

To explore further the potential relationship between material rewards and developmental regression, this research examined the effects of material rewards on perceptual organization as measured by Holtzman inkblot responses. Forty introductory psychology students (20 males and 20 females) were assigned to either a reward or nonreward group initially matched on sex and IQ. Reward subjects had lower scores on form definiteness, form appropriateness, integration, human, movement, color, and shading; faster response time; and higher scores on location and on pathognomic verbalization. Although reward/nonreward differences reached significance only for form definiteness, form appropriateness, shading, and response time, the differences on all 10 Holtzman Inkblot Technique variables that are sensitive to developmental change were in the predicted direction of a lower level of functioning under reward.

Cognition↗
PubMedDate not supplied

Choice and social exchange theory and the rewards of African American caregivers.

Exploration of the perceived rewards of African American caregivers has received little attention, but is of acute importance because of their potential effects on symptoms of depression. In this non-experimental, cross-sectional study, the investigator used choice and social exchange theory as a framework for identifying potential rewards of African American caregivers of demented elders. Study findings indicated that African Americans perceived rewards which were internal or external in source and short-term or long-term in timing. With the exception of caregivers age and education, these rewards were little affected by sociodemographic characteristics of the caregiver or care recipient. Young, more educated caregivers tended to perceive fewer rewards than old, less educated caregivers. The implications of the findings for nursing practice care are discussed.

Adult↗
PubMed1998

Sensitization to the rewarding effects of the specific dopamine uptake inhibitor GBR12783.

The conditioned place preference (CPP) induced by increasing doses (1.25-40 mg/kg) of cocaine or the specific dopamine uptake inhibitor GBR12783 was investigated in rats previously treated with cocaine (10 or 20 mg/kg), GBR12783 (10 mg/kg) or morphine (10 mg/kg) for 15 days. In solvent-pretreated rats, cocaine- and GBR12783-induced CPPs were biphasic, with the highest scores observed at 20 mg/kg. Prior exposure to GBR12783 sensitized the rats to the rewarding effects of low doses of either GBR12783 or cocaine. Pretreatment with cocaine 20 mg/kg, but not 10 mg/kg, sensitized the rats to its own rewarding effects. Furthermore, it was less efficient than GBR12783 in sensitizing the animals to the rewarding effects of both drugs. These data confirm the major role of dopamine uptake inhibition in the sensitization process. On the other hand, the magnitude of CPP induced by a high dose of both drugs (20 mg/kg) was decreased after pretreatment with either GBR12783 or cocaine, reaching the lower scores observed at 40 mg/kg. This decrease was unrelated to altered anxiety level but was associated with sensitization to stereotypies. Morphine pretreatment modified neither the CPP induced by high doses of cocaine or GBR12783 nor cocaine- or GBR12783-induced stereotypies. However, prior exposure to morphine sensitized the rats to the rewarding effects of cocaine (2.5 mg/kg) but not to those of GBR12783, suggesting that other mechanisms working in concert with dopamine may facilitate the rewarding effect of cocaine without affecting that of GBR12783.

Animals↗
PubMed1998

Food restriction enhances the central rewarding effect of abused drugs.

Chronic food restriction increases the systemic self-administration and locomotor-stimulating effect of abused drugs. However, it is not clear whether these behavioral changes reflect enhanced rewarding potency or a CNS-based modulatory process. The purpose of this study was to determine whether food restriction specifically increases the rewarding potency of drugs, as indexed by their threshold-lowering effect on lateral hypothalamic self-stimulation, and whether any such effect can be attributed to an enhanced central response rather than changes in drug disposition. When drugs were administered systemically, food restriction potentiated the threshold-lowering effect of amphetamine (0.125, 0.25, and 0.5 mg/kg, i.p.), phencyclidine (1.0, 2.0, and 3.0 mg/kg, i.p.), and dizocilpine (MK-801) (0.0125, 0.05, and 0.1 mg/kg, i.p.) but not nicotine (0.15, 0.3, 0.45 mg/kg, s.c.). When amphetamine (25.0, 50.0, and 100.0 microgram) and MK-801 (5.0, 10.0, and 20.0 microgram) were administered via the intracerebroventricular route, food restriction again potentiated the threshold-lowering effects and increased the locomotor-stimulating effects of both drugs. These results indicate that food restriction increases the sensitivity of neural substrates for rewarding and stimulant effects of drugs. In light of work that attributes rewarding effects of MK-801 to blockade of NMDA receptors on medium spiny neurons in nucleus accumbens, the elements affected by food restriction may lie downstream from the mesoaccumbens dopamine neurons whose terminals are the site of amphetamine-rewarding action. Possible metabolic-endocrine triggers of this effect are discussed, as is the likelihood that mechanisms mediating the modulatory effect of food restriction differ from those mediating sensitization by intermittent drug exposure.

Amphetamine↗
PubMed1998

[Psychosocial factors at work and cardiovascular diseases: contribution of the Effort-Reward Imbalance model].

The effect of psychosocial factors at work on health, especially cardiovascular health, has given rise to growing concern in occupational epidemiology over the last few years. Two theoretical models, Karasek's model and the Effort-Reward Imbalance model, have been developed to evaluate psychosocial factors at work within specific conceptual frameworks in an attempt to take into account the serious methodological difficulties inherent in the evaluation of such factors. Karasek's model, the most widely used model, measures three factors: psychological demands, decision latitude and social support at work. Many studies have shown the predictive effects of these factors on cardiovascular diseases independently of well-known cardiovascular risk factors. More recently, the Effort-Reward Imbalance model takes into account the role of individual coping characteristics which was neglected in the Karasek model. The effort-reward imbalance model focuses on the reciprocity of exchange in occupational life where high-cost/low-gain conditions are considered particularly stressful. Three dimensions of rewards are distinguished: money, esteem and gratifications in terms of promotion prospects and job security. Some studies already support that high-effort/low reward-conditions are predictive of cardiovascular diseases.

Adaptation, Psychological↗
PubMed1986

Effects of propranolol on conditioned suppression, discriminated punishment and discriminated non-reward in the rat.

In Experiment I, two groups of rats were rewarded for lever-pressing under RI 64. During signalled 3-min intrusion periods shocks were delivered response-contingently (on RI 64) for the Punishment group and non-contingently (on RT 64) for the Conditioned Suppression group. d,l-Propranolol (2, 5 mg/kg) released intrusion responding to a similar extent in the two groups. Experiment II comprised two distinct experiments: two groups of rats were trained in parallel on signalled multiple schedules in which responding during the baseline component was rewarded on RI 20. For the second component responding was extinguished in Experiment IIa; it continued to be rewarded but was also punished by electric shock in Experiment IIb. Shock levels were adjusted individually so as to produce similar levels of response suppression in these two groups. d,l-Propranolol released non-rewarded responding (2-5 mg/kg; Expt IIa) but had no effect on punishment (2-10 mg/kg; Expt IIb). l-Propranolol (2.5 mg/kg) but not d-propranolol (2.5 mg/kg) also released non-rewarded responding in Expt IIa. In a further trial d,l-propranolol (5 mg/kg) released punished responding in Expt IIb in a group of animals in which response suppression had been partially relieved by reducing shock intensity. It is hypothesized that beta-adrenergic stimuli may influence response suppression to the extent that the unconditioned aversive event causing suppression is not salient.

Animals↗
PubMed1994

Effects of reward and nonreward on frustration and attention in attention deficit disorder.

The effects of reward schedule (100%, 50%, and 30%) and termination of rewards (extinction) on 30 attention deficit disorder with hyperactivity (ADD-H) and 30 normal children were studied using measures of frustration (speed/strength of lever pulling) and attention (reaction time to a light signal). ADD-Hs pulled harder on the lever than controls during extinction and on the lowest (30%) partial schedule, providing empirical evidence that they respond with greater frustration than normals when expected rewards fail to appear. The groups did not differ on the attentional measure on 100% reward. However, the partial schedules appeared to have an alerting or motivating effect on the controls, so that they responded more quickly and consistently than ADD-Hs on the partial schedules. Findings are discussed with reference to opposing theories regarding the nature of the abnormal response of ADD-Hs to reward.

Analysis of Variance↗
PubMed1995

Bromocriptine enhancement of responding for conditioned reward depends on intact D1 receptor function.

It has been suggested that reward-related learning may require intact functioning at the dopamine D1 receptor. The present experiment tested this hypothesis by challenging the reward-enhancing effects of the D2 agonist, bromocriptine, with a D1 antagonist, SCH 23390. For comparison, the effects of the D2 antagonist, pimozide, were also evaluated. Male rats (n = 240) were pre-exposed to a chamber with two levers, one producing a 3-s lights-off stimulus and the other a 3-s tone stimulus. Four conditioning sessions followed, during which levers were absent and presentations of the lights-off stimulus were paired with food. Testing consisted of comparing presses on each lever after conditioning to before conditioning for each rat. Control groups showed a significantly greater increase in responding for lights-off than tone, indicating that the lights-off stimulus had become a conditioned reward. Results showed that bromocriptine (0.25-10.0 mg/kg, IP, 60 min before test session) enhanced responding at doses of 2.5 and 5.0 mg/kg significantly more on the conditioned reward lever than on the other lever. The lowest dose of SCH 23390 (1.0 microgram/kg, SC, 2 h before testing) eliminated the bromocriptine-produced enhancement at 2.5 mg/kg and a significant enhancement was seen at 10.0 mg/kg. The higher doses of SCH 23390 (5.0 and 10.0 micrograms/kg) eliminated the bromocriptine effect and the conditioned reward effect itself, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1996

Devazepide, a CCKA receptor antagonist, impairs the acquisition of conditioned reward and conditioned activity.

Cholecystokinin (CCK) is co-localized with dopamine (DA) in portions of the mesolimbic system, where it may facilitate the function of DA through the CCKA receptor subtype. DA has been implicated in the acquisition of conditioned incentive learning, raising the possibility of a role for endogenous CCK in this learning process. This hypothesis was tested using two complementary behavioral paradigms. Experiment 1 examined the effects of systemic administration of the CCKA receptor selective antagonist, devazepide (0, 0.001, 0.01, 0.1 mg/kg), on the acquisition of conditioned reward. Two novel levers were presented to drug-free animals in a test session; depression of the conditioned reward (CR) lever produced a light-tone stimulus previously paired with food availability while depression of the non-CR lever produced no programmed consequence. Animals receiving vehicle pretreatment in the food-CS conditioning sessions responded more frequently on the CR lever during the test session. However, pre-treatment with devazepide (0.1 mg/kg but not 0.001 or 0.01 mg/kg) in the conditioning sessions blocked the acquisition of conditioned reward. In contrast, experiment 2 showed that the development of conditioned reward was not affected by similar administration of the CCKB selective antagonist, L-365,260 (0, 0.001, 0.01, or 0.1 mg/kg). The possibilities that devazepide (0.1 mg/kg) impaired the development of conditioned reward by decreasing the amount of food consumed or by inducing a conditioned taste aversion to the food were ruled out in experiments 3 and 4. The effects of devazepide on the acquisition of conditioned activity induced by amphetamine were assessed in experiment 5. During four conditioning sessions, rats received devazepide (0, 0.001, 0.01, 0.1 or 1.0 mg/kg) treatment prior to amphetamine-environment pairings. The conditioned activity effect was demonstrated if on the subsequent drug-free test day the environment alone elicited increased locomotion. Devazepide (0.1 or 1.0 mg/kg) attenuated the development of conditioned activity. Together, these results provide converging evidence that intact CCKA function may be necessary for the development of conditioned incentive learning.

Animals↗
PubMed1982

Lateral hypothalamic stimulation gates nucleus gigantocellularis-induced aversion via a reward-independent process.

A monophasic pulse-pair stimulation technique was used behaviorally to infer neurophysiological interaction between 'reward' sites in the lateral hypothalamus (LH) and pain-implicated nucleus reticularis gigantocellularis (NGC). Rats lever-pressed for 3 s escapes from an otherwise continuous train of 0.1 ms NGC pulses delivered every 40 ms. When pulses to the LH were interdigitated with those to NGC, inter-response latencies were significantly longer. This occurred whether LH pulses were also interrupted by each lever-press (experiment 1) or not (experiment 2). Further, the same intensities of LH stimulation which inhibited escape supported high rates of lever-pressing for 3 s LH trains during inescapable NGC stimulation even though these LH trains were not of sufficient intensity to support 'rewarding' lever-pressing in the absence of NGC stimulation. This finding indicates that escape-inhibition in the first two experiments was not due to interfering motor effects of LH stimulation but most probably due to LH amelioration of NGC-induced aversion. Indeed, when aversion was ameliorated by morphine, lever-pressing for sub-reward-threshold LH stimulation during inescapable NGC stimulation decreased although classical self-stimulation did not. In the escape experiments, inhibition was greatest when each NGC pulse was preceded by an LH pulse at an interval of 0.1 or 10 ms. During inescapable NGC stimulation, rates of lever-pressing for LH trains were greatest when LH pulses preceded NGC pulses again at intervals of 0.1 or 10 ms. This congruence of the temporal bimodal profiles in the response functions of these two different behavioral experiments strongly suggests that the same integrative mechanism underlies both LH inhibition of NGC escape and lever-pressing for LH trains during inescapable stimulation of NGC. Since gastric loading did not alter lever-pressing for sub-reward-threshold LH trains during inescapable NGC stimulation but did inhibit classical self-stimulation, it was concluded that the inferred common integrative mechanism mediates a supraspinal gating of aversion which is independent of the LH self-stimulation reward process.

Animals↗
PubMed1984

Brain stimulation reward and dopamine terminal fields. I. Caudate-putamen, nucleus accumbens and amygdala.

The boundaries and relative sensitivity of brain stimulation reward were mapped in relation to the dopamine (DA) terminal fields of the striatum and adjacent limbic structures. Brain stimulation was rewarding throughout the caudate and nucleus accumbens and in portions of the amygdala and olfactory tubercle. The best striatal sites were anterior, ventral and medial; this correlated with an anterior-posterior gradient but not with a dorsal-ventral or a medial-lateral gradient of DA terminal density. No close correspondence was seen between the boundaries of the reward system and those of the DA terminal fields as revealed by glyoxylic acid-induced DA fluorescence. Reward sites in the olfactory tubercle and amygdala were found in DA-free as well as DA-rich regions of these structures; stimulation in DA-rich regions did not always support self-stimulation. These data go against the view that direct activation of dopamine terminals or their efferent targets accounts for the rewarding quality of stimulation in these regions.

Amygdala↗
PubMed1995

Effects of granisetron, a 5-HT3 receptor antagonist, on morphine-induced potentiation of brain stimulation reward.

Using the curve-shift method, we studied the effects of four doses (0.003, 0.03, 0.3 and 3 mg/kg, s.c.) of granisetron (endo-N-(9-methyl-9-azabicyclo[3.3.1]non-3-yl)-1-methyl-1H-indazole-3- carboxamide hydrochloride), a selective 5-hydroxytryptamine3 (5-HT3) receptor antagonist, on the potentiation of brain stimulation reward by microinjection of 2.5 micrograms/0.25 microliters of morphine sulphate (7,8-didehydro-4,5-epoxy-17-methylmorphinan-3,6-diol sulphate) into the ventral tegmental area. As previously reported, morphine produced a significant reduction in reward threshold without altering maximal rates of responding. Granisetron attenuated the potentiating effect of morphine at the highest dose and failed to alter reward threshold or maximal rates of responding when given alone, except at the lowest dose where a small and statistically significant increase in threshold was found. These results provide additional evidence that 5-HT3 receptor antagonists may reduce the rewarding effect of opiates and do not impair the ability to produce operant responses. The weak attenuation observed with granisetron alone suggests that 5-HT3 receptors are unlikely to constitute an important influence on the directly stimulated reward-relevant pathway(s).

Analysis of Variance↗
PubMed1991

Controllability of stressors and rewarding brain stimulation: effect on the rate-intensity function.

Previous research in mice has shown that an uncontrollable stressor, but not a controllable stressor, depresses responding for rewarding electrical stimulation of the brain (ESB) (33). We reexamined this effect in rats by determining rate-intensity functions for rewarding brain stimulation 24 h and 48 h following stressor exposure. In each rat, two electrodes, one on each side of the brain, were aimed at the posterior, lateral hypothalamus. Self-stimulation rate-intensity functions were obtained for each electrode; stimulation of one electrode always caused stronger activity than equivalent stimulation of the other. If the rats had been stressed with uncontrollable shock the preceding day, their responding was significantly depressed to stimulation at the weaker electrode site but not the stronger electrode site. However, if the rat had control over the stressor, then rate-intensity functions were unchanged. Repeating the test for rate-intensity function 48 h after exposure to the stressor showed no effect of prior stress on self-stimulation. This work suggests that relatively brief exposure to an uncontrollable stressor can leave a residual, 24-h depressive influence on reward system substances. Some effects of exposure to uncontrollable stressors on acquisition and maintenance of responding for rewards may be due, therefore, to attenuation of reward strength.

Animals↗