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PubMed1999

Sensitivity to reward frequency in boys with attention deficit hyperactivity disorder.

Compared the sensitivity of boys with and without attention deficit hyperactivity disorder (ADHD) to differences in reward frequency. Fifteen boys with ADHD as diagnosed in the Diagnostic and Statistical Manual of Mental Disorders (3rd ed., rev.; American Psychiatric Association, 1987) and a matched control group completed a signal-detection task in which correct identification of 1 stimulus was rewarded 3 times as often as correct identification of the other. Boys in the ADHD group completed the task twice, on and off medication. Group differences emerged in response bias toward the more frequently rewarded alternative. Boys in the control group showed a stable pattern of response bias, irrespective of which alternative they were last rewarded on. Boys in the ADHD group showed different patterns of response bias following rewards on the 2 alternatives. These results suggest children with ADHD were more sensitive to individual instances of reward compared with controls, whose response bias is governed more by their reinforcement history. Methylphenidate improved discriminability and reduced sensitivity to individual instances of reward in the boys with ADHD.

Adolescent↗
PubMed2005

Dopamine cells respond to predicted events during classical conditioning: evidence for eligibility traces in the reward-learning network.

Behavioral conditioning of cue-reward pairing results in a shift of midbrain dopamine (DA) cell activity from responding to the reward to responding to the predictive cue. However, the precise time course and mechanism underlying this shift remain unclear. Here, we report a combined single-unit recording and temporal difference (TD) modeling approach to this question. The data from recordings in conscious rats showed that DA cells retain responses to predicted reward after responses to conditioned cues have developed, at least early in training. This contrasts with previous TD models that predict a gradual stepwise shift in latency with responses to rewards lost before responses develop to the conditioned cue. By exploring the TD parameter space, we demonstrate that the persistent reward responses of DA cells during conditioning are only accurately replicated by a TD model with long-lasting eligibility traces (nonzero values for the parameter lambda) and low learning rate (alpha). These physiological constraints for TD parameters suggest that eligibility traces and low per-trial rates of plastic modification may be essential features of neural circuits for reward learning in the brain. Such properties enable rapid but stable initiation of learning when the number of stimulus-reward pairings is limited, conferring significant adaptive advantages in real-world environments.

Action Potentials↗
PubMed2005

Neuronal signals in the monkey basolateral amygdala during reward schedules.

The amygdala is critical for connecting emotional reactions with environmental events. We recorded neurons from the basolateral complex of two monkeys while they performed visually cued schedules of sequential color discrimination trials, with both valid and random cues. When the cues were valid, the visual cue, which was present throughout each trial, indicated how many trials remained to be successfully completed before a reward. Seventy-six percent of recorded neurons showed response selectivity, with the selectivity depending on some aspects of the current schedule. After a reward, when the monkeys knew that the upcoming cue would be valid, 88 of 246 (36%) neurons responded between schedules, seemingly anticipating the receiving information about the upcoming schedule length. When the cue appeared, 102 of 246 (41%) neurons became selective, at this point encoding information about whether the current trial was the only trial required or how many more trials are needed to obtain a reward. These cue-related responses had a median latency of 120 ms (just between the latencies in inferior temporal visual area TE and perirhinal cortex). When the monkey was releasing a touch bar to complete the trial correctly, 71 of 246 (29%) neurons responded, with responses in the rewarded trials being similar no matter which schedule was ending, thus being sensitive to the reward contingency. Finally, 39 of 246 (16%) neurons responded around the reward. We suggest that basolateral amygdala, by anticipating and then delineating the schedule and representing reward contingency, provide contextual information that is important for adjusting motivational level as a function of immediate behavior goals.

Amygdala↗
PubMed1998

Neuropharmacological mechanisms of drug reward: beyond dopamine in the nucleus accumbens.

Multiple lines of research have implicated the mesolimbic dopamine system in drug reward measured by either the drug self-administration or conditioned place preference paradigm. The present review summarizes recent work that examines the neuropharmacological mechanisms by which drugs impinge on this dopaminergic neural circuitry, as well as other systems that provide input and output circuits to the mesolimbic dopamine system. Studies examining the effect of selective agonist and antagonist drugs administered systemically have indicated that multiple neurotransmitters are involved, including dopamine, serotonin, acetylcholine, glutamate, GABA, and various peptides. Direct microinjection studies have also provided crucial evidence indicating that, in addition to the mesolimbic dopamine system, other structures play a role in drug reward, including the ventral pallidum, amygdala, hippocampus, hypothalamus, and pedunculopontine tegmental nucleus. GABAergic circuitry descending from the nucleus accumbens to the pedunculopontine tegmental nucleus via the ventral pallidum appears to be especially important in directing the behavioral sequelae associated with reward produced by various drugs of abuse. However, activation of the reward circuitry is achieved differently for various drugs of abuse. With amphetamine and cocaine, initiation of reward is controlled within the nucleus accumbens and prefrontal cortex, respectively. With opiates, initiation of reward involves the ventral tegmental area, nucleus accumbens, hippocampus, and hypothalamus. It is not clear presently if these multiple anatomical structures mediate opiate reward by converging on a single output system or multiple output systems.

Animals↗
PubMed2003

Effects of anxiolytic drugs on rewarding and aversive behaviors induced by intracranial stimulation.

In considering the characteristics of the action of anxiolytic drugs and their mechanism in the brain, it may be necessary not only to study the behavioral pharmacology but also to perform brain site research. In the present study, the action of anxiolytic drugs was examined with respect to various behaviors that were induced by stimulating the brain areas related to emotions such as reward (pleasure) or aversion in rats. First, the low rate of response in lateral hypothalamic self-stimulation behavior was induced by schedules of low current brain stimulation, variable interval (VI) and differential reinforcement of low rate (DRL). Anxiolytic drugs such as benzodiazepines facilitated these low-rate responses. The drug susceptibility was highest in the low current stimulation, lower in the VI stimulation, and lowest in the DRL stimulation schedules. Furthermore, it was found by the auto-titration method in intracranial self-stimulation behavior that anxiolytic drugs decreased the threshold of stimulation reward. Second, it was recognized using the decremental lever pressing (DLP) paradigm that anxiolytic drugs increased the threshold of aversive stimulation of mesencephalic dorsal central gray (DCG), and this increasing effect of the drug was antagonized by GABA receptor blockers such as biccuculline. Finally, it was examined whether or not the conflict situation is established by combining brain stimulation reward and aversion, such as foot-shock or DCG stimulation. As a result, the conflict behavior was established by combining not only the brain stimulation reward and foot-shock aversion, but also the brain stimulation reward and DCG stimulation aversion. Further anxiolytic drugs exhibited anti-conflict action in both situations. The susceptibility of anxiolytic drugs was higher with respect to the conflict behavior induced by intracranial reward and aversion than to that induced by the conventional method based on milk reward and foot-shock aversion. These results suggest that behavioral methods using brain stimulation can examine the mechanisms of direct drug action at the brain stimulation site. Indeed, in the present brain stimulation behavioral study, anxiolytic drugs such as benzodiazepines increased the stimulation threshold in lateral hypothalamic self-stimulation and inhibited the DCG aversive stimulation, thus resulting in an anticonflict action of the drugs.

Animals↗
PubMed2001

Serotonergic manipulations both potentiate and reduce brain stimulation reward in rats: involvement of serotonin-1A receptors.

A discrete-trial current-threshold self-stimulation procedure was used to assess the effects of increased and decreased serotonergic neurotransmission, and 5-HT(1A) receptor activation on brain stimulation reward. Systemic administration of the 5-HT(1A) receptor agonist 8-OH-DPAT had a biphasic effect on brain reward thresholds, without affecting the latency to respond, a measure of performance. The low dose of 8-OH-DPAT (0.03 mg/kg) lowered reward thresholds, whereas higher doses (0.1 and 0.3 mg/kg) elevated thresholds. The 5-HT(1A) receptor antagonist p-MPPI had no effect on brain stimulation behavior, but reversed both the 8-OH-DPAT-induced lowering and elevation of thresholds, indicating that both of these effects of 8-OH-DPAT are mediated through the 5-HT(1A) receptor. Injections of 8-OH-DPAT into the median raphé nucleus also lowered brain reward thresholds, without affecting measures of performance, whereas injections of 8-OH-DPAT into the dorsal raphé nucleus had no effect. A high dose of the selective serotonin reuptake inhibitor fluoxetine (10 mg/kg) elevated reward thresholds and responses latencies, whereas lower doses (2.5 and 5.0 mg/kg) increased response latencies without affecting thresholds. Furthermore, the coadministration of a 5-HT(1A) antagonist, p-MPPI, and a previously ineffective dose of fluoxetine, a drug combination that increases serotonin levels, significantly elevated thresholds. Thus, it is suggested here that the reward-potentiating effects of systemically administered low doses of 8-OH-DPAT may be the result of reduced serotonergic neurotransmission, mediated by activation of 5-HT(1A) somatodendritic autoreceptors in the median, but not the dorsal, raphé nucleus. In conclusion, the present data support the hypothesis that serotonin exerts an inhibitory influence on reward processes.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2001

Incremental effects of reward on creativity.

The authors examined 2 ways reward might increase creativity. First, reward contingent on creativity might increase extrinsic motivation. Studies 1 and 2 found that repeatedly giving preadolescent students reward for creative performance in 1 task increased their creativity in subsequent tasks. Study 3 reported that reward promised for creativity increased college students' creative task performance. Second, expected reward for high performance might increase creativity by enhancing perceived self-determination and, therefore, intrinsic task interest. Study 4 found that employees' intrinsic job interest mediated a positive relationship between expected reward for high performance and creative suggestions offered at work. Study 5 found that employees' perceived self-determination mediated a positive relationship between expected reward for high performance and the creativity of anonymous suggestions for helping the organization.

Creativity↗
PubMed2004

[Effects of anxiolytic drugs on rewarding and aversive behaviors induced by intracranial stimulation].

In considering characteristics of action of anxiolytic drugs and the mechanism of drug action in the brain, it may be necessary to study not only the behavioral pharmacology but also the brain site. In the present study, anxiolytic drugs have been examined in various kinds of behaviors induced by stimulating the brain areas with regard to emotional expression such as reward (pleasure) or aversion in rats. First, the low rate responding on lateral hypothalamic self-stimulation behavior was induced by schedules of low current brain stimulation, variable interval (VI) and differential reinforcement of low rate (DRL). Anxiolytic drugs such as benzodiazepines facilitated these low rate responses. The drug susceptibility was high in the order of the low current stimulation > VI > DRL schedules. Furthermore, it was found by the auto-titration method on intracranial self-stimulation behavior that anxiolytic drugs decreased the threshold of stimulation reward. Second, it was recognized using the decremental lever pressing (DLP) paradigm that anxiolytic drugs increased the threshold of aversive stimulation of mesencephalic dorsal central gray (DCG), and this increasing effect of the drug was antagonized by GABA receptor blockers such as biccuculline. Third, it has been examined whether the conflict situation is established by combining with brain stimulation reward and aversion such as foot-shock or DCG stimulation. As a result, the conflict behavior was established by combining with not only the brain stimulation reward and foot shock aversion, but also the brain stimulation reward and DCG stimulation aversion. Further anxiolytic drugs exhibited the anti-conflict action to both situations. The susceptibility of anxiolytic drugs to the conflict behavior by intracranial reward and aversion was higher than the conventional method based on milk reward and foot shock aversion. Indeed, in the present brain stimulation behavioral study, anxiolytic drugs such as benzodiazepines increased the stimulation threshold in lateral hypothalamic self-stimulation and inhibited the DCG aversive stimulation, i.e. resulting in an anticonflict action of the drugs. Recently we have preliminarily established a new model for evaluating the drug which may facilitate the motivation contributing to result in various behaviors, using the priming stimulation paradigm in intracranial self-stimulation behavior. Diazepam, benzodiazepine, and nomifensine, an dopamine uptake inhibitor, exhibited a delay of the extinction process which included non-reinforcing stimulation and pretrial electric stimulation (priming stimulation) in the self-stimulation behavior. This action may be related to the brain-mechanism of motivation.

Animals↗
PubMed2004

The neurobiology of pleasure, reward processes, addiction and their health implications.

Modern science begins to understand pleasure as a potential component of salutogenesis. Thereby, pleasure is described as a state or feeling of happiness and satisfaction resulting from an experience that one enjoys. We examine the neurobiological factors underlying reward processes and pleasure phenomena. Further, health implications related to pleasurable activities are analyzed. With regard to possible negative effects of pleasure, we focus on addiction and motivational toxicity. Pleasure can serve cognition, productivity and health, but simultaneously promotes addiction and other negative behaviors, i.e., motivational toxicity. It is a complex neurobiological phenomenon, relying on reward circuitry or limbic activity. These processes involve dopaminergic signaling. Moreover, endorphin and endogenous morphinergic mechanisms may play a role. Natural rewarding activities are necessary for survival and appetitive motivation, usually governing beneficial biological behaviors like eating, sex and reproduction. Social contacts can further facilitate the positive effects exerted by pleasurable experiences. However, artificial stimulants can be detrimental, since flexibility and normal control of behavior are deteriorated. Additionally, addictive drugs are capable of directly acting on reward pathways. Thus, the concrete outcome of pleasant experiences may be a question of dose. Moderate pleasurable experiences are able to enhance biological flexibility and health. Hence, pleasure can be a resistance resource or may serve salutogenesis. Natural rewards are mediated by sensory organ stimulation, thereby exhibiting a potential association with complementary medical approaches. Trust and belief can be part of a self-healing potential connected with rewarding stimuli. Further, the placebo response physiologically resembles pleasure phenomena, since both involve brain's reward circuitry stimulation and subjective feelings of well-being. Pleasurable activities can stimulate personal growth and may help to induce healthy behavioral changes, including stress management. However, more research is needed to better understand the nature, neurobiology and maybe dangerous aspects of pleasure. Also, a possible involvement of endogenous morphinergic signaling has to be studied further.

Behavior, Addictive↗
PubMed1985

Brain mechanisms of drug reward and euphoria.

Drugs of abuse have in common the fact that they serve as biological rewards. They presumably do so because of their ability to activate endogenous brain circuitry. By determining the brain circuitry activated by rewarding drug injections, much can be learned about the degree to which there is a common basis for the abuse liability of seemingly different drugs. The brain circuitry activated by two classes of abused drugs, psychomotor stimulants and opiates, is now partially understood; the current evidence suggests a shared mechanism of stimulant reward and opiate reward. The identified portion of the circuitry involves dopamine-containing cells of the ventral tegmental area and their fiber projections to the cells of the nucleus accumbens. Morphine activates these cells in the region of the cell bodies; it may have direct actions on receptors imbedded in the dopaminergic cell membrane, or it may act on afferent terminals that synapse on the dopaminergic cell bodies or dendrites. Cocaine and amphetamine act at the terminals of the dopaminergic fibers to nucleus accumbens and perhaps other structures. The shared activation of the dopaminergic input to nucleus accumbens accounts for the behaviorally activating and the rewarding effects of both stimulants and opiates (the opiate stimulant action is not widely known because it is usually masked by depressant actions of opiates in other, antagonistic, brain circuits). The activation of dopaminergic systems also accounts for amphetamine euphoria; it almost certainly accounts for cocaine euphoria and it probably accounts for opiate euphoria as well. Opiates and psychomotor stimulants clearly have many other actions which are not shared; nonshared actions must account for the well-known differences in the subjective effects of opiates and stimulants. One of the major nonshared actions is physical dependence. Opiates gain access to a major component of the circuitry mediating opiate physical dependence through opiate receptors in the periaqueductal gray matter. This receptor population is anatomically distinct from the population mediating the rewarding effects of opiates in nondependent animals. While both opiates and stimulants can activate (though by quite different mechanisms and at quite different loci) the dopaminergic circuitry underlying reward phenomena, only opiates activate the separate circuitry underlying dependence phenomena.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Disconnection of the amygdala from visual association cortex impairs visual reward-association learning in monkeys.

Cynomolgus monkeys (Macaca fascicularis) were trained in a task that assessed their ability to associate visual stimuli with food reward. Acquisition of stimulus-reward associations was measured under 2 conditions, a 2-stimuli acquisition condition and a 1-stimulus acquisition condition. On each trial in the 2-stimuli condition, the positive (correct) and negative (incorrect) stimuli were presented side by side and the animal chose one by touching it; if the choice was correct, a food reward was dispensed. On each trial in the 1-stimulus condition, either the positive or the negative stimulus was presented alone; if the stimulus was the positive, it was followed by reward delivery, regardless of the animal's response to it, and if it was the negative, it was not followed by reward delivery. Thus, reward delivery was contingent upon the animal's response to the stimuli in the 2-stimuli condition but not in the 1-stimulus condition. The effect of acquisition trials under these 2 conditions was measured, in both conditions, by the animal's subsequent choice when presented with the 2 stimuli side by side. Following preoperative training in this task, the animals were first subjected to unilateral ablation of the inferotemporal cortex. This operation had little effect on the animals' learning ability. Then, the amygdala was ablated in the hemisphere contralateral to that in which the unilateral inferotemporal ablation had been carried out. This combination of crossed unilateral lesions of the amygdala and of the inferotemporal cortex, which disconnects the amygdala from the output of visual association cortex, produced a profound impairment in stimulus-reward-associative learning.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed1988

Effects of imipramine-like drugs and serotonin uptake blockers on delay of reward in rats. Possible implication in the behavioral mechanism of action of antidepressants.

This study investigated in rats the action of a variety of antidepressants in two behavioral models. In model 1, animals trained in a T-maze were allowed to choose between 2 magnitudes of reward: immediate but small reward (2 pellets) vs. a 25-sec delayed but large reward (10 pellets). Under this alternative, vehicle-injected rats selected the large-but-delayed reward in less than 40% of the trials. Desipramine 8 mg/kg, clomipramine 8 mg/kg, maprotiline 8 mg/kg, indalpine 2 to 4 mg/kg, zimelidine 8 to 16 mg/kg, nialamide 16 to 32 mg/kg and clenbuterol 0.03 to 0.06 mg/kg significantly increased the number of choices of the large-but-delayed reward. In model 2, rats were subjected to a fixed ratio 48 schedule of food reinforcement; after completion of a series of exactly 48 presses a food pellet was delivered, and if no further press occurred, a sequence of free pellets was initiated according to fixed, increasing intervals (from 5-80 sec). Pressing during the sequence stopped it and required the rat to complete again the fixed ratio 48 to be reinforced and to reintiate the sequence. Waiting for free reward was significantly lengthened by desipramine 8, clomipramine 16, indalpine 8, zimelidine 8 to 16, nialamide 32 and clenbuterol 0.007 to 0.06 mg/kg. These results suggest that, possibly through noradrenergic and serotonergic mechanisms, antidepressants markedly enhanced rats' ability to wait for food reward, an affect which might reflect the ability of these drugs to improve impulse control. The relevance of such a property in the therapeutic action of antidepressants remains to be delineated.

Animals↗
PubMed1984

Developmental analysis of the effects of reward on selected Wechsler subscales.

The authors recently proposed that adverse effects of material rewards on Wechsler subscale performance may be the result of a reward-produced developmental regression. The present study further explores that idea through an attempt to replicate earlier findings with adults and to extend the inquiry to children. Selected Wechsler subscales were administered to 32 subjects at each of three ages (5, 10, and 18 years) under either reward or nonreward conditions. Subscales were chosen to represent both algorithmic and heuristic types of tasks. Reward and nonreward groups (8 males and 8 females per group at each age) were matched initially on age and ability. For adults, consistent with earlier findings, reward had an adverse effect on performance on the heuristic subscales and tended to facilitate performance on the algorithmic subscales. However, rewards generally had no effect at the fourth-grade level and had a reverse effect at the nursery school level, i.e., rewards facilitated heuristic and hampered algorithmic performance. These findings appear to be more consistent with an explanation based on developmental regression than on any available alternative mechanism.

Adolescent↗
PubMed1984

Brain stimulation reward and dopamine terminal fields. II. Septal and cortical projections.

The boundaries and relative sensitivities of the substrates of septal and cortical brain stimulation reward were mapped in relation to the dopamine terminal fields in these regions using a dorsal-ventral moveable electrode. Brain stimulation was rewarding at all levels of the posterior lateral septum and not just in the region of dopamine terminal innervation. Reward thresholds, ease of training, maximum response rates and stability of responding were all unrelated to the proximity of the stimulating electrode to the band of dopamine terminals revealed by glyoxylic acid-induced dopamine fluorescence. Stimulation was also rewarding in the anterior lateral septum; the best sites were in the ventral portions of this region although dopamine terminal fluorescence was uniform throughout. Thus the anatomy of the brain stimulation reward substrate of the lateral septal nucleus does not bear a special relation to the anatomy of dopamine terminals within this region. Stimulation was also rewarding in each of the dopamine terminal fields of the cerebral cortex. The best self-stimulation was obtained with electrodes in the medial frontal cortex; sulcal frontal cortex was next best, entorhinal cortex was next, and pyriform cortex, though reliably positive, supported the weakest self-stimulation. Variations in self-stimulation threshold were seen as electrodes were moved through homogeneous regions of dopamine terminal density in some regions, while stable thresholds were associated with movements through areas of varying dopamine terminal density in others; thus, again, there was no special relation between goodness of self-stimulation and density of dopaminergic innervation. These data suggest that rewarding brain stimulation in these regions is not due to direct activation of either the dopaminergic terminals or the cells that they innervate.

Animals↗
PubMed2004

Food restriction and leptin impact brain reward circuitry in lean and obese Zucker rats.

The rewarding effect produced by electrically stimulating certain sites in the lateral hypothalamus (LH) can be potentiated by food restriction and body weight loss in lean rats. Central leptin and insulin administration can suppress the rewarding impact of the stimulation. To determine whether there are additional peripheral signals that mediate the effect of weight loss on brain reward circuitry, we assessed changes in LH-self-stimulation following food restriction in the obese Zucker rat which develops resistance to circulating leptin and insulin. In addition, we examined the impact of acute food deprivation and leptin administration on LH self-stimulation in lean and obese Zucker rats. The number of brain stimulation rewards earned was measured over a range of LH stimulation frequencies that drove reward rates from zero to asymptotic levels. Restriction reduced frequency thresholds in a subset of lean and obese rats, whereas BSR was unaltered by acute food deprivation. Despite impairment in leptin signaling, intraventricular leptin (4 microg) increased thresholds in most lean and obese rats in which the rewarding effect was sensitive to restriction. These results show that brain reward circuitry in the obese Zucker rat is sensitive to weight loss and leptin.

Analysis of Variance↗
PubMed2005

Early developmental exposure to methylphenidate reduces cocaine-induced potentiation of brain stimulation reward in rats.

BACKGROUND: Methylphenidate (MPH) is prescribed for the treatment of attention and hyperactivity disorders. We showed previously that early developmental exposure to MPH in rats causes behavioral alterations during adulthood, including reduced cocaine reward in place conditioning studies. Here we examined if early MPH exposure alters the ability of cocaine to potentiate the rewarding effects of electrical stimulation of the medial forebrain bundle (MFB) using intracranial self-stimulation (ICSS). METHODS: Rats received MPH or saline during pre-adolescence (P20-35) and were implanted with MFB stimulating electrodes at adulthood (P60). Rats then were tested with cocaine in the ICSS paradigm. RESULTS: Cocaine dose-dependently decreased ICSS thresholds in all rats, but the threshold-lowering effects of cocaine were smaller in rats exposed to MPH during pre-adolescence. There were no differences between groups in sensitivity to the rewarding effects of MFB stimulation itself. CONCLUSIONS: Early developmental exposure to MPH reduces the reward-related effects of cocaine in the ICSS paradigm. These results are consistent with previous studies in which early exposure to MPH reduced the ability of cocaine to establish conditioned place preferences, as well as the rewarding effects of sucrose and sexual behavior. Reduced sensitivity to these various types of reward may reflect general dysfunctions of brain reward systems.

Age Factors↗
PubMed2003

[Measuring psychosocial stress at work in Spanish hospital's personnel. Psychometric properties of the Spanish version of Effort-Reward Imbalance model].

BACKGROUND AND OBJECTIVE: Two main models are currently used to evaluate the psychosocial factors at work: the Demand-Control (or job strain) model developed by Karasek and the Effort-Reward Imbalance model, developed by Siegrist. A Spanish version of the first model has been validated, yet so far no validated Spanish version of the second model is available. The objective of this study was to explore the psychometric properties of the Spanish version of the Effort-Reward Imbalance model in terms of internal consistency, factorial validity, and discriminate validity. SUBJECTS AND METHODS: A cross-sectional study on a representative sample of 298 workers of the Spanish public hospital San Agustin in Asturias was performed. The Spanish version of Effort-Reward Imbalance Questionnaire (23 items) was obtained by a standard forward/backward translation procedure, and the information was gathered by a self-administered application. Exploratory factor analysis were performed to test the dimensional structure of the theoretical model. Cronbach's alpha coefficient was calculated to estimate the internal consistency reliability. Information on discriminate validity is given for sex, age and education. Differences were calculated with the t-test for two independent samples or ANOVA, respectively. RESULTS: Internal consistency was satisfactory for the two scales (reward and intrinsic effort) and Cronbach's Alpha coefficients higher than 0.80 were observed. The internal consistency for the scale of extrinsic effort was lower (alpha = 0.63). A three-factor solution was retained for the factor analysis of reward as expected, and these dimensions were interpreted as a) esteem, b) job promotion and salary and c) job instability. A one-factor solution was retained for the factor analysis of intrinsic effort. The factor analysis of the scale of extrinsic effort did not support the expected one-dimension structure. The analysis of discriminate validity displayed significant associations between measures of Effort-Reward Imbalance and the variables of sex, age and education level. CONCLUSIONS: This study is the first one supporting satisfactory psychometric properties of the Spanish version of the Effort-Reward Imbalance model. However, the factorial validity of the extrinsic effort could be questioned.

Adult↗
PubMed1996

Acquisition of conditioned reward blocked by intra-accumbens infusion of PD-140548, a CCKA receptor antagonist.

Cholecystokinin (CCK) is an endogenous peptide that is colocalized with dopamine (DA) in some mesolimbic neurons projecting to the nucleus accumbens (NAC). DA has been implicated in the acquisition of conditioned rewarding properties by neutral stimuli [conditioned stimuli (CS)] associated with a primary reward (such as food). A variety of experimental evidence suggests that exogenously applied CCK, acting at the CCKA receptor, potentiates the function of DA in the NAC. Thus, the present experiment examined the role of endogenous CCKA mechanisms in the NAC in the development of conditioned reward. The CCKA receptor-selective antagonist PD-140548 was microinjected into the NAC during the CS-food pairing phase of a conditioned reward experiment. In the test session, animals that previously received vehicle microinjections into the NAC or PD-140548 microinjections into areas surrounding the NAC pressed a lever that produced the CS more often than did a control lever. The CS had gained conditioned rewarding properties. However, animals that received PD-140548 microinjections into the NAC did not exhibit a preference for the CR lever. Results suggest that blockade of CCKA receptors in the NAC impairs the development of conditioned reward. These findings support a role for endogenous CCKA mechanisms in the NAC in the acquisition of stimulus-reward associations.

Animals↗