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At least 523 records · Page 29Linked to original sources
PubMed2006

Psychophysiological evidence for impaired reward anticipation in Parkinson's disease.

OBJECTIVE: According to a widely held view, mesencephalic dopamine neurons mediate feedback-based learning by broadcasting an error signal that indexes the difference between anticipated and actual response-contingent reward. The present experiment tested whether impaired learning of a probabilistic classification task by individuals with Parkinson's disease (PD) is associated with abnormal reward expectation. METHODS: The stimulus-preceding negativity (SPN), a brain potential known to reflect anticipation of motivationally significant events, was compared for blocks in which subjects anticipated high or low monetary rewards and punishments. RESULTS: The SPN was reduced in amplitude in patients relative to controls in the high monetary incentive condition. Furthermore, whereas the SPN varied in size as a function of cue complexity for control subjects, it did not for patients. CONCLUSIONS: These results suggest that anticipatory processes within cortical portions of the reward system are impaired by PD. SIGNIFICANCE: These data support previous claims that the SPN offers an electrophysiological index of activity within cortical portions of the reward pathway, and that reinforcement-based learning is impaired in PD.

Aged↗
PubMed2005

Beyond the reward hypothesis: alternative functions of nucleus accumbens dopamine.

According to the dopamine (DA) hypothesis of reward, DA systems in the brain, particularly in the nucleus accumbens, are thought to directly mediate the rewarding or primary motivational characteristics of natural stimuli such as food, water and sex, as well as various drugs of abuse. However, there are numerous problems associated with this hypothesis. Interference with accumbens DA transmission does not substantially blunt primary motivation for natural rewards such as food, but it does disrupt the propensity of animals to engage in effortful responding to obtain food. Electrophysiological and voltammetric studies indicate that novel stimuli, conditioned stimuli that predict reward, and instrumental behaviors that deliver natural rewards all act to stimulate DA activity. Accumbens DA acts as a modulator of several functions related to motivated behavior, and can influence normal and pathological cognitive function, activational aspects of motivation, anergia or psychomotor slowing in depression, the impact of conditioned stimuli, plasticity and a variety of sensorimotor functions.

Animals↗
PubMedDate not supplied

Long-term, low-level adolescent nicotine exposure produces dose-dependent changes in cocaine sensitivity and reward in adult mice.

Cigarette smoking by adolescents is a strong predictor of future drug use, abuse, and dependence. While this "gateway drug effect" is assumed to be related to psychosocial factors, data from our laboratory suggests that adolescent nicotine use may permanently disrupt reward systems through changes in dopamine receptor function. Behavioral pharmacological methods known to be indirectly (motor activity) and directly (conditioned-place-preference) related to drug reinforcement were used to examine changes in cocaine sensitivity. Testing was performed on adult mice that were exposed to nicotine (0.3, 1.0, and 3.0 mg/kg, SC, M-F, b.i.d.) or saline during adolescence (postnatal days 25-57). Prior to testing, subjects had a 28 day drug-free, time-off period. After acclimation to the testing apparatus, the locomotor effects (30 min, 30 cm traveled) of cocaine (5, 10, and 20 mg/kg, IP) were measured daily; cocaine tests were preceded and followed by saline control tests. Following the acute dose-response curve, mice received saline followed by 5 days of 20.0 mg/kg cocaine. Thereafter, mice underwent condition-place-preference testing. A pre-test was performed to determine compartment preference (i.e., no injection, 20 min test). Cocaine (10 mg/kg, IP) was paired with the subjects non-preferred side and saline with the other. Conditioning sessions were conducted for 8 days with the order of drug/saline injections counter-balanced across subjects. A drug-free, post-test occurred on the day following the final conditioning session. A dose-dependent relationship between adolescent nicotine exposure and cocaine reward was noted in the adult mice across both test conditions. Subjects exposed to nicotine showed an increased response to cocaine's motor activating effects and a decreased response to cocaine's rewarding effects. A follow-up study was undertaken to evaluate dopamine D1, D2, and D3 receptor function in adult mice exposed to the highest dose of nicotine from the first study. While both interesting and revealing, the results of motor activity tests with dopamine agonist only approached significance. Further research will be required to more fully examine the mechanism of action for the observed changes in cocaine reward. In summary, this is the first study to demonstrate a dose-response relationship between adolescent nicotine exposure and changes in cocaine reward and sensitivity during adulthood.

Adaptation, Physiological↗
PubMed2005

Novelty reward as a measure of anhedonia.

A decrease in sensitivity to pleasurable stimuli, anhedonia, is a major symptom of depression in humans. Several animal models have been developed to simulate this symptom (e.g. drug withdrawal, learned helplessness) using reward-sensitive procedures such as intracranial self-stimulation and progressive ratio responding as a measure of reward function. Recently, we introduced the use of another procedure, novel-object place conditioning in rats, to measure reward function in an associative learning situation. Withdrawal from chronic nicotine blocked a place preference conditioned by access to novel objects. This blockade was not due to impairment of object interaction, general activity, novelty detection, environmental familiarization, or expression of learning. Consequently, nicotine withdrawal directly reduced the rewarding properties of novelty. It is proposed that the novel-object place conditioning procedure could be usefully extended to other experimental situations and to genetically altered mice, so as to better understand the processes underlying changes in reward function.

Animals↗
PubMed2006

Effects of reward expectancy on sequential eye movements in monkeys.

Desirability of an action, often referred to as utility or value, is determined by various factors, such as the probability and timing of expected reward. We investigated how performance of monkeys in an oculomotor serial reaction time task is influenced by multiple motivational factors. The animals produced a series of visually-guided eye movements, while the sequence of target locations and the location of the rewarded target were systematically manipulated. The results show that error rates as well as saccade latencies were consistently influenced by the number of remaining movements necessary to obtain a reward. In addition, when the animal produced multiple saccades before fixating a given target, the first saccade tended to be directed towards the rewarded location, suggesting that saccades to rewarded location and visual target might be programmed concurrently. These results show that monkeys can utilize information about the required sequence of movements to update their subjective values.

Animals↗
PubMed2006

Neuronal activities in the reward phase in primary and higher-order gustatory cortices of monkeys.

We examined neuronal activities in the reward phase of a taste discrimination GO/NOGO task and the reversal from the primary (PGC; areas G, 3 and 1-2) and higher order gustatory cortices (HGC, PrCO and OFC) in the monkey. Sucrose was given as reward for both GO (lever pressing during LED) and NOGO responses when correct. Three ON responses, synchronous with sucrose onset at correct or LED offset at incorrect trials were found: C- and I- types increased discharges only at correct or incorrect trials, while C-I type changed discharges at both. Of the latter two classes were noted; Class I increased discharges at correct and decreased them at incorrect trials, and Class II increased discharges at both. C-type and Class I were most numerous in both PGC and HGC except for the OFC in which Class II responses predominated. I-type was rare. Onset latencies at correct and incorrect trials were significantly correlated in the HGC but not in the PGC. It was suggested that C-type responses represented the gustatory nature of reward, I-type neurons error signals, and that Class I of C-I type indicated the arrival or omission of the reward, and Class II anticipation of reward delivery.

Action Potentials↗
PubMed2004

Genetic and genomic approaches to reward and addiction.

Drug addiction is recognized as a mental disease affecting the brain's natural reward system. Drugs of abuse strongly activate reward structures in the brain and induce lasting changes in behavior that reflect changes in neuron physiology and biochemistry. With the ultimate goal of developing therapeutic interventions, it is of interest to determine the molecular and cellular components of motivation and reward, and identify those gene products that contribute to the process of drug addiction. Our laboratory has chosen three general genetic approaches to examine reward and addiction: reverse genetics to assess the role of candidate genes in drug responsiveness, forward genetics to discover novel regulators of dopamine transmission, and gene expression profiling to define gene sets in different brain structures that contribute to the molecular and neurobiological basis of reward.

Animals↗
PubMed2006

Mid- to late gestational morphine exposure does not alter the rewarding properties of morphine in adult male rats.

Prenatal exposure to drugs of abuse often leads to physiological and neurobiological abnormalities including decreased brain and body weight, cognitive deficits and behavioral alterations. A handful of studies showed increased vulnerability to drug abuse in prenatally drug-exposed offspring. Our work also demonstrated that prenatal exposure to analgesic doses of morphine during gestation days 11-18 increases mu-opioid receptor density in the nucleus accumbens and central amygdala of adult male rats. Both the nucleus accumbens and central amygdala play important roles in modulating drug-induced reward via the mesolimbic dopaminergic system. Therefore, two types of behavioral paradigms were used to test the hypothesis that the same prenatal morphine exposure would enhance the rewarding effects of morphine, making drug-exposed offspring more vulnerable to abuse this drug in adulthood. All experiments were performed with adult male offspring of saline-injected, morphine-injected or non-injected (control) dams. (1) The unbiased conditioned place preference (CPP) paradigm was used to investigate whether prenatal morphine exposure sensitizes adult male rats to non-contingent morphine reward. These adult animals were conditioned with 0.1, 0.3, 1, 3 or 5 mg/kg morphine. All control, prenatally saline- and morphine-exposed male rats preferred the morphine-paired compartment relative to the saline-paired compartment. However, the magnitude of morphine CPP in adult male rats was not dependent on the conditioning dose of morphine or prenatal morphine exposure. (2) Intravenous morphine self-administration was used to assess the behavioral response to contingent morphine reward. Each rat self-administered one of four doses of morphine (0.3, 1, 2 or 3 mg/kg/infusion). Morphine self-administration was not altered in prenatally morphine-exposed adult male offspring. Control males self-administered significantly less morphine at the lowest dose of morphine than both prenatally saline- and morphine-exposed males. Although our data show that prenatal exposure to an analgesic dose of morphine during the time of opioid receptor appearance does not enhance morphine CPP or self-administration, they do not exclude the possibility that this prenatal morphine exposure enhances the rewarding properties of other drugs of abuse.

Analgesics, Opioid↗
PubMed2005

Feeding, body weight, and sensitivity to non-ingestive reward stimuli during and after 12-day continuous central infusions of melanocortin receptor ligands.

The brain melanocortin system mediates downstream effects of hypothalamic leptin and insulin signaling. Yet, there have been few studies of chronic intracerebroventricular (i.c.v.) melanocortin receptor (MCR) agonist or antagonist infusion. Although there is evidence of interaction between melanocortin and dopamine (DA) systems, effects of chronic MCR ligand infusion on behavioral sensitivity to non-ingestive reward stimuli have not been investigated. The objective of this study was to investigate effects of chronic i.c.v. infusion of the MCR agonist, MTII, and the MCR antagonist, SHU9119, on food intake, body weight, and sensitivity to rewarding lateral hypothalamic electrical stimulation (LHSS) and the reward-potentiating (i.e., threshold-lowering) effect of D-amphetamine. The MCR antagonist, SHU9119 (0.02 microg/h) produced sustained hyperphagia and weight gain during the 12-day infusion period, followed by compensatory hypophagia and an arrest of body weight gain during the 24-day post-infusion period. At no point during the experiment was sensitivity to LHSS or D-amphetamine (0.25mg/kg, i.p.) altered. The MCR agonist, MTII (0.02 microg/h) produced a brief hypophagia (3 days) followed by a return to control levels of daily intake, but with body weight remaining at a reduced level throughout the 12-day infusion period. This was followed by compensatory hyperphagia and weight gain during the 24-day post-infusion period. There was no change in sensitivity to non-ingestive reward stimuli during the infusion of MTII. However, sensitivity to D-amphetamine was increased during the 24-day post-infusion period. It therefore seems that changes in ingestive behavior that occur during chronic MCR ligand infusion may not affect the response to non-ingestive reward stimuli. However, it is possible that the drive to re-feed and restore body weight following MCR agonist treatment includes neuroadaptations that enhance the incentive effects of drug stimuli.

Animals↗
PubMed2006

Chronic food restriction: enhancing effects on drug reward and striatal cell signaling.

Chronic food restriction (FR) increases behavioral sensitivity to drugs of abuse in animal models and is associated with binge eating, which shares comorbidity with drug abuse, in clinical populations. Behavioral, biochemical and molecular studies conducted in this laboratory to elucidate the functional and mechanistic bases of these phenomena are briefly reviewed. Results obtained to date indicate that FR increases the reward magnitude and locomotor-activating effects of abused drugs, and direct dopamine (DA) receptor agonists, as a result of neuroadaptations rather than changes in drug disposition. Changes in striatal DA dynamics, and postsynaptic cell signaling and gene expression in response to D-1 DA receptor stimulation have been observed. Of particular interest is an upregulation of NMDA receptor-dependent MAP kinase and CaM Kinase II signaling, CREB phosphorylation, and immediate-early and neuropeptide gene expression in nucleus accumbens (NAc) which may facilitate reward-related learning, but also play a role in the genesis of maladaptive goal-directed behaviors. Covariation of altered drug reward sensitivity with body weight loss and recovery suggests a triggering role for one of the endocrine adiposity hormones. However, neither acute nor chronic central infusions of leptin or the melanocortin 3/4 receptor agonist, MTII, have attenuated d-amphetamine reward or locomotor activation in FR rats. Interestingly, chronic intracerebroventricular leptin infusion in ad libitum fed (AL) rats produced a sustained decrease in food intake and body weight that was accompanied by a reversible potentiation of rewarding and locomotor-activating effects of d-amphetamine. This raises the interesting possibility that rapid progressive weight loss is sufficient to increase behavioral sensitivity to drugs of abuse. Whether weight loss produced by leptin infusion produces the same neuroadaptations as experimenter-imposed FR, and whether any of the observed neuroadaptations are necessary for expression of increased behavioral responsiveness to acute drug challenge remain to be investigated.

Animals↗
PubMed2026

Post-weaning social isolation increases reward-seeking behavior in mice.

Social isolation is a growing public health concern. Although isolation at any age is harmful, previous studies have shown that isolation during adolescence, correlating with critical periods of brain development, can impair cognitive function and increase the risk for psychiatric illness later in life. In this study, we utilized a mouse model of social isolation (SI) during adolescence (postnatal day 21-35) and compared performance of isolated and group-housed mice on a touchscreen-based continuous performance test (rCPT) and fixed ratio/progressive ratio (FR/PR) tasks in adulthood. SI improved performance in the rCPT and the improvement in performance was consistent across time bins within the 45-minute testing session. There were no effects of SI on reaction times or reward retrieval latencies. A possible confound for performance in the rCPT would be SI-induced changes in reward-seeking or motivation for the strawberry milk reward. We next compared the SI mice to their group-housed littermate controls on both PR and FR schedules of reinforcement and found that SI mice had higher breakpoints on a PR4 schedule and earned significantly more reinforcers on an FR1 schedule of reinforcement compared to their group-housed littermates, suggesting that high performance in the CPT may be due to increased motivation for food rewards. These data indicate that SI during adolescence has significant effects on reward-seeking behavior in adult mice and may provide a useful behavioral model for studying the link between SI and risk for neuropsychiatric disorders.

Animals↗
PubMed1998

The real and imagined harmful effects of rewards: implications for clinical practice.

In recent years, a number of researchers and social critics have cautioned against the widespread application of behavioral interventions on the grounds that the philosophy of behaviorism is fundamentally manipulative and damaging to creative and intrinsically motivated behavior. Most central to their arguments are concerns about the harmful effects of "extrinsic" rewards. Though concerns about the allegedly harmful effects of "rewards" on intrinsically motivated actions may have been partially allayed by a recent meta-analysis, proponents of the view that intrinsic interest is eroded by the delivery of contingent rewards will likely continue to attest to the dangers of operant conditioning and its application to human behavior. The present manuscript addresses the content of claims about the harmful effects of extrinsic rewards. While consideration is given to the existing behavior therapy literature and its treatment of "natural" versus "arbitrary" rewards, some surprising convergences between the views of self-determination theorists and behavioral practitioners are noted.

Behavior Therapy↗
PubMed1998

Differential effects of interleukin (IL)-1beta, IL-2 and IL-6 on responding for rewarding lateral hypothalamic stimulation.

Bacterial endotoxin and interleukin-1 (IL-1) challenge induce a constellation of symptoms associated with illness. While such treatment may result in anhedonia, it is often difficult to dissociate this effect from the anorexia induced by these agents, particularly in paradigms that involve appetitive motivation. The present investigation assessed the effects of several systemically administered cytokines (IL-1beta, IL-2 and IL-6) on reward processes by evaluating responding for rewarding intracranial self-stimulation (ICSS) from the lateral hypothalamus. Systemic administration of interleukin-2 (IL-2) disrupted responding from the medial forebrain bundle, and this disturbance persisted as long as 1 week following initial cytokine treatment. In contrast to reinforced responding, following IL-2 treatment, non-reinforced behavior was unaffected, indicating that the cytokine did not provoke reward-unrelated performance deficits. It was suggested that the effects of IL-2 on ICSS likely do not involve motoric, soporific, attentional or cognitive changes, but instead involve specific actions on motivational arousal. Although IL-6 was previously found to produce mesolimbic dopamine (DA) changes as marked as those induced by IL-2, systemic IL-6 treatment did not influence responding for rewarding brain stimulation. Likewise, although IL-1 at the dosage used reliably induces sickness behavior, responding for rewarding brain stimulation was unaffected. Thus it seems that anhedonia is not necessarily a component of the sickness response associated with IL-1 treatment.

Animals↗
PubMed1996

Involvement of delta- and mu-opioid receptors in the potentiation of brain-stimulation reward.

A rate-free method of determining brain-stimulation reward thresholds was used to identify the rewarding effects of the delta-opioid receptor and mu-opioid receptor agonist peptides, [D-Pen2, D-Pen5]enkephalin (DPDPE) and [D-Ala2-MePhe4-Gly(o1)5]enkephalin (DAMGO). The nucleus accumbens-delivered opioid receptor agonists produced marked lowering of the threshold for ventral tegmental area brain-stimulation reward. No change in baseline thresholds was seen after peripheral administration of the nonpeptide delta-opioid receptor antagonist, naltrindole. However, an unexpected finding was that naltrindole blocked the threshold-lowering effects of both DPDPE and DAMGO. These data demonstrate nucleus accumbens activation of delta- and mu-opioid receptors and ventral tegmental area brain-stimulation reward share common brain substrates. In addition, the interference of both delta- and mu-opioid receptor mediated reward by naltrindole may have implications for therapeutic use.

Analgesics↗
PubMed2001

Both GABA(B) receptor agonist and antagonists decreased brain stimulation reward in the rat.

The present experiments were designed to determine the role of GABA(B) receptor function on brain stimulation reward. Using a discrete-trial current-intensity threshold procedure, dose-effect functions were generated for the GABA(B) receptor agonist CGP 44532 (0-1.0 mg/kg, s.c.) and the GABA(B) receptor antagonists CGP 56433A (0-10.0 mg/kg, s.c.) and CGP 51176 (0-300.0 mg/kg, s.c.) on brain reward thresholds in rats. The GABA(B) receptor antagonists CGP 56433A and CGP 51176 were used also to examine interaction effects with the GABA(B) receptor agonist CGP 44532 on reward thresholds. Administration of the highest doses of both the GABA(B) receptor agonist and antagonists elevated reward thresholds. Thus, both the agonist and antagonists used induced a reward decrement when administered separately. In addition, the co-administration of either of the two receptor antagonists with the agonist induced an additive effect on thresholds, rather than blocking the agonist-induced threshold elevations. These results suggest that activation of GABA(B) receptors modulates intracranial self-stimulation behavior in a complex fashion, possibly through differential effects of GABA(B) agonists and antagonists on pre- and post-synaptic GABA(B) receptors.

Animals↗
PubMed1998

Acute and chronic fluoxetine treatment decreases the sensitivity of rats to rewarding brain stimulation.

The effects of fluoxetine on rewarding brain stimulation were determined in eight Wistar rats using a rate-independent discrete-trial threshold measure. Rats were implanted with bipolar, stainless steel electrodes either into the ventral tegmental area (VTA) or medial forebrain bundle (MFB). Acute administration of fluoxetine significantly raised the reward threshold (decreased sensitivity) at doses of 2.5, 5.0, 10.0, and 20.0 mg/kg, i.p., without altering latency of response. There were no significant differences between VTA and MFB groups. To determine the effects of chronic treatment, daily injections of 5.0 mg/kg fluoxetine were administered to rats for 21 days. Chronic treatment of fluoxetine continued to significantly elevate reward thresholds with no evidence of tolerance. The results of these experiments suggest that fluoxetine does not possess abuse potential and that serotonin produces an inhibitory effect on the mesolimbic dopaminergic reward system. Furthermore, these results suggest that the antidepressant effects of fluoxetine are not the direct result of excitation of brain reward systems, at least in the same manner as abused substances, for example, cocaine.

Animals↗
PubMedDate not supplied

Multiple reward systems and the prefrontal cortex.

Electrical stimulation of the major divisions of the prefrontal cortex, the mediodorsal and sulcal areas, can serve as a reinforcing stimulus. Studies of self-stimulation of the prefrontal cortex have produced behavioral, anatomical and pharmacological evidence that the substrate of these rewarding effects can be dissociated from that subserving self-stimulation of ventral diencephalic sites such as the lateral hypothalamus. Other studies indicate that within the prefrontal cortex itself, self-stimulation of the medial and sulcal divisions can be attributed to dissociable processes. These observations suggest the existence of multiple, largely autonomous prefrontal subsystems involved in reinforcement. This raises the question of the functional significance of such systems, and of their organization. An approach to this problem is to consider the relationship between the behavioral functions of the prefrontal divisions and the characteristics of stimulation-induced reward obtained at each site. Studies of the effects of restricted prefrontal lesions indicate that the medial and sulcal divisions can be dissociated according to their involvement in the control of distinct types of sensory and motor events. Further experiments indicate that damage to each division causes selective deficits in the learning of stimulus-reinforcer and response-reinforcer relations, depending in part on the nature of the reinforcing event. Conditioning experiments further show that the rewarding effects produced by stimulation of these areas are preferentially associated to sensory events which correspond to the functional specialization of each division. These data are interpreted to suggest that different rewarding events and/or different attributes of rewarding stimuli are processed by distinct systems which are reflected by the organization of dissociable self-stimulation pathways.

Animals↗
PubMed2003

Standard housed rats are more sensitive to rewards than enriched housed rats as reflected by their anticipatory behaviour.

The present study was designed to investigate the effects of potentially stressful standard housing conditions for laboratory rats on the sensitivity to rewards as reflected by their anticipatory behaviour for sucrose. This anticipatory response is evoked in a conditioning paradigm in which a sucrose reward is repeatedly announced by a stimulus. The underlying neurocircuitry of this anticipatory response in expectation of a reward involves mesolimbic dopaminergic systems of which it is known that they can be sensitised by stressors. The results show that the anticipatory response for the sucrose reward is stronger in the standard housed animals which indicates that these animals are more sensitive to the reward than the enriched animals. From this, it is concluded that standard housed rats are stressed which is likely to be caused by deprivation of the ability to satisfy behavioural needs in these impoverished housing conditions.

Analysis of Variance↗