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PubMed1988

Are pheromones their own reward?

Hamster vaginal discharge (HVD) contains a variety of intersexual pheromones which are powerful promoters of male reproductive behavior. Males avidly investigate and then consume HVD from females or from artificial sources. We measured the reward strength of HVD and other sapid substances with operant techniques. The highest fixed ratio at which males would bar press, the break point, varied with the level of water deprivation and the volume of water reward. Break points for sucrose rewards, in undeprived animals, were higher than for water and varied with concentration. Water, vanillin and HVD solutions were comparable reinforcers irrespective of deprivation level. Sexual experience did not increase bar pressing for HVD rewards. Moreover, naive animals could not be trained to bar press for HVD. These results contrast with other evidence that HVD is highly palatable and challenge the notion that the pheromones present in it are innately rewarding. However, this conclusion may be mitigated by constraints on learning which limit the utility of operant techniques to evaluate the reinforcing properties of HVD.

Animals↗
PubMed1996

Rewarding electrical brain stimulation: similar thresholds for Flinders Sensitive Line Hypercholinergic and Flinders Resistant Line Hypocholinergic rats.

Flinders Sensitive Line hypercholinergic rats, which exhibit augmented hypothermic responses to the cholinesterase inhibitor physostigmine and to the muscarinic agonist oxotremorine, have been proposed to represent a useful animal model for some aspects of human depression. With disturbance of reward processes considered to be a core feature of depression, the present studies were designed to investigate the neuropharmacology of brain stimulation-reward (BSR) in Flinders Sensitive Line (FSL) rats, Flinders Resistant Line (FRL) rats, and outbred control Sprague-Dawley rats. All animals were tested in a rate-free, current-threshold brain stimulation-reward paradigm, following acute challenges with the monoamine reuptake inhibitor cocaine, the dopamine D1 receptor antagonist SCH-23390, the cholinergic muscarinic antagonist scopolamine, and the serotonin reuptake inhibitor fluoxetine. Baseline BSR thresholds did not differ across the three groups. For all groups, cocaine lowered thresholds, SCH-23390 and scopolamine-elevated thresholds, while fluoxetine had no significant effect. Thresholds for the three groups were not differentially affected by pharmacological locomotor activity relative to outbred Sprague-Dawley controls. These results suggest that both Flinders lines exhibit behavioral differences from outbred control rats, but not with regard to reward processes as assessed by rewarding electrical stimulation of the lateral hypothalamus.

Animals↗
PubMed1986

Haloperidol induces a partial reinforcement extinction effect in rats: implications for a dopamine involvement in food reward.

The hypothesis that dopamine antagonist drugs attenuate the reinforcing properties of food was investigated in hungry rats trained to traverse a straight runway for food reward. Testing consisted of a single trial per day during which latencies to leave the start box and to traverse the alley were recorded. In each experiment, a reinforcement phase lasting 30 consecutive days was immediately followed by a 21 day extinction phase. The runway responses of animals that experienced intermittent food reward during the reinforcement phase of the experiments, was later found to be more resistant to extinction than those of continuously reinforced animals. This "partial reinforcement extinction effect" (PREE) was also observed in animals that experienced periodic reductions in the quantity, but not quality, of food reward. Intermittent pretreatment with 0.15 mg/kg of haloperidol during the reinforcement phase produced a PREE that was indistinguishable from that produced by reward omission on those same trials. Control groups for motor debilitation and for non-associative drug effects did not demonstrate a PREE. These results are consistent with the view that central dopamine substrates play a role in the neural basis of food reward.

Animals↗
PubMed1987

The combined effects of morphine and d-amphetamine on the threshold for brain stimulation reward.

The effect of morphine and d-amphetamine co-administration on the threshold for rewarding intracranial electrical stimulation was studied in rats with electrodes stereotaxically implanted in the medial forebrain bundle-lateral hypothalamic or ventral tegmental area of the brain. Thresholds were determined by means of a rate-independent psychophysical method. Individually, morphine and d-amphetamine both caused a dose-related lowering of the reward threshold. Low doses of morphine or d-amphetamine which were ineffective or minimally effective in lowering the reward threshold were then tested with various doses of either d-amphetamine or morphine, respectively. In both cases, the combined administration of morphine and d-amphetamine resulted in a lowering of the reward threshold that was greater than for the corresponding doses of morphine and d-amphetamine when given alone. Given that increased sensitivity for rewarding brain stimulation has been suggested to be an animal model of drug-induced euphoria, this effect is congruent with the reported increase in the degree of euphoria produced when amphetamine is used in conjunction with opiate drugs.

Animals↗
PubMed1987

Some effects of pimozide on nondeprived rats' lever pressing maintained by a sucrose reward in an anhedonia paradigm.

The present work examined the generalizability of the anhedonia phenomenon (extinction-like responding with repeated neuroleptic treatment) by examining the effects of pimozide (PIM) on nondeprived rats lever pressing for a sucrose solution reward (32%) in an eight day dosing regime. The procedures used replicated the essential features of a previous study (Gramling et al. [10]) wherein the effects of PIM on rats licking directly a sucrose solution were assessed. Thirty nondeprived rats were trained to lever press on a CRF schedule for a 32% sucrose solution reward and then assigned to one of five treatment groups (N = 6). The treatment conditions included a no-reward group (EXT; vehicle injections), two pimozide (PIM) with reward conditions (either PIM 0.25 mg/kg + RWD or PIM 0.5 mg/kg + RWD), and a vehicle control group (RWD; vehicle injections). These four groups each received their respective injections and operant exposure for eight consecutive days. The fifth group was a home cage (HC) control condition wherein the rats were injected with 0.5 mg/kg PIM each test day but did not receive operant exposure until the fourth test day. The PIM treated rats exhibited a significant curvilinear pattern of responding on the rate measure across eight days of testing, whereas rats in the no-reward condition exhibited a significant downward linear trend across eight days of testing. Within-session analysis revealed that rats in the EXT group responded at significantly higher rates during the first five minutes of testing on the first test day compared to rats in the PIM 0.5 + RWD condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

The effects of amfonelic acid alone and in combination with naloxone on brain-stimulation reward.

Thresholds for rewarding brain stimulation delivered to the medial forebrain bundle-lateral hypothalamus were determined by means of a rate-free psychophysical method. Amfonelic acid (AFA), an indirect dopamine agonist, alone caused a significant dose-dependent lowering of the rewarding threshold. Although naloxone treatment by itself did not significantly alter the reward threshold, it blocked AFA's threshold lowering effect in every animal at one or more of the dose combinations of the two drugs tested. Naloxone was found to be more effective in blocking the threshold lowering actions of a higher (1 mg/kg) dose as opposed to a lower (0.25 mg/kg) dose of AFA. Since a lowering of threshold for rewarding intracranial stimulation is a model for drug-induced euphoria, the findings presented here indicate that AFA may have abuse potential. Furthermore, these results suggest that endogenous opioid systems may begin to modulate the effects of AFA on the reward system only when a certain level of activation of dopaminergic systems is reached.

Animals↗
PubMed1989

The effect of amfonelic acid or nisoxetine in combination with morphine on brain-stimulation reward.

Many drugs of abuse, including stimulants such as cocaine and amphetamine, and opioids like morphine and heroin, will lower threshold at which rats will work to receive electrical stimulation to the medial forebrain bundle-lateral hypothalamic region (MFB-LH). This effect is even greater when the two classes of drugs are coadministered. The underlying mechanisms by which this occurs are not completely understood, however there is considerable evidence suggesting that the catecholamines play a major role in mediating the reinforcing effects of these drugs. The present study was conducted to investigate the effects of amfonelic acid, an indirect dopamine agonist, and nisoxetine, a highly selective norepinephrine uptake blocker, alone and in combination with morphine, on the reward threshold for rewarding electrical intracranial stimulation. As in previous studies, morphine, as well as amfonelic acid, lowered the reward threshold with the amfonelic acid causing greater threshold lowerings than that of morphine. When a low (ineffective) dose of amfonelic acid was administered concomitantly with morphine, the threshold lowerings observed were larger than those seen with either drug alone and were often more than additive. Nisoxetine alone had no effect on the reward threshold and produced inconsistent results when combined with morphine. These findings support the thesis that amfonelic acid has abuse potential, and that its reinforcing effects may, in fact, be even greater than that of the opioids. Further, these results support the hypothesis that dopamine plays a more critical role in mediating brain-stimulation reward than dose norepinephrine.

Animals↗
PubMed1990

Postcocaine depression and sensitization of brain-stimulation reward: analysis of reinforcement and performance effects.

The effects of acute and chronic cocaine administration on intracranial self-stimulation (ICSS) were evaluated in a two-hole nose-poke discrimination paradigm. Analysis of ICSS rates as a function of current intensity revealed that cocaine increased rates of responding in a dose-dependent manner (5.0-20.0 mg/kg), resulted in a shift to the left of the rate-intensity function, and decreased thresholds for half-maximal responding. Brain-stimulation reward was modified by chronic exposure to cocaine, however, the direction of change was dependent on the schedule of drug administration. Repeated daily administration of cocaine (40.0 mg/kg) and ICSS testing 24 hr postinjection decreased rates and increased reward thresholds. A response depression was also observed when time-dependent variations in ICSS performance were evaluated after repeated cocaine administration. Using a different chronic cocaine/test schedule (30.0 mg/kg, twice daily), a sensitization of ICSS and decreased reward thresholds developed when rate-intensity functions were determined after 5-day drug intervals. These findings were discussed in terms of the role of dopamine in modulating central reward processes. It was suggested that depressed reward-system functioning might reflect reduced dopamine synthesis following cocaine withdrawal, and the ICSS sensitization was related to long-term compensatory changes in dopamine neurotransmission possibly involving presynpatic mechanisms.

Animals↗
PubMed1992

Long-term influence of d-amphetamine on mesolimbic brain-stimulation reward: comparison to chronic haloperidol and naloxone effects.

Rate-intensity functions for brain-stimulation reward from the dopamine (DA) A10 cell region of the ventral tegmental area (VTA) were assessed following chronic exposure to d-amphetamine (10.0 mg/kg), haloperidol (1.0 mg/kg), and naloxone (20.0 mg/kg). A reward depression developed when animals were tested daily 24 h following injection of amphetamine and haloperidol. In the case of amphetamine, this effect was transitory and a full recovery of intracranial self-stimulation (ICSS) was evident 5 days after drug abstinence. Low-dose (0.5 mg/kg) amphetamine challenge administered 50 days postdrug treatment decreased current thresholds indicating a long-lasting sensitization of mesolimbic reward processes. The reward depression induced by chronic haloperidol exposure showed no signs of recovery during the abstinence period and ICSS rates remained significantly reduced after amphetamine challenge 50 days later. These behavioral observations suggest that under conditions of continued demand the functional aspects of neuroleptic-induced depolarization inactivation of VTA neurons are enduring. Chronic exposure to naloxone did not modify reward thresholds indicating that opioid hypoactivity may not be a factor in the ICSS depression induced by long-term amphetamine and haloperidol treatment. These data were related to the possibility that stimulant-induced sensitization of motivational processes may evolve as a compensatory response to the transitory development of withdrawal depression.

Animals↗
PubMed1992

Drugs of abuse: anatomy, pharmacology and function of reward pathways.

Drugs of abuse are very powerful reinforcers, and even in conditions of limited access (where the organism is not dependent) these drugs will motivate high rates of operant responding. This presumed hedonic property and the drugs' neuropharmacological specificity provide a means of studying the neuropharmacology and neuroanatomy of brain reward. Three major brain systems appear to be involved in drug reward--dopamine, opioid and GABA. Evidence suggests a midbrain-forebrain-extrapyramidal circuit with its focus in the nucleus accumbens. Data implicating dopamine and opioid systems in indirect sympathomimetic and opiate reward include critical elements in both the nucleus accumbens and ventral tegmental areas. Ethanol reward appears to depend on an interaction with the GABAA receptor complex but may also involve common elements such as dopamine and opioid peptides in this midbrain-forebrain-extrapyramidal circuit. These results suggest that brain reward systems have a multidetermined neuropharmacological basis that may involve some common neuroanatomical elements.

Animals↗
PubMed1981

Evidence for the sequential participation of inferior temporal cortex and amygdala in the acquisition of stimulus-reward associations.

On a test of one-trial learning of object-reward associations, monkeys showed marked impairment after lesions of either the anterior part of inferior temporal cortex (area TE) or the amygdala (A). By contrast, little or no loss followed lesions of either the posterior part of inferior temporal cortex (area TEO) or the fusiform-hippocampal gyrus and hippocampus (FHH). The finding of impairment after either the area TE or A lesions fits the view [11] that stimulus-reward learning in vision is mediated by a functional chain connecting the visual system to the limbic system through relays in the inferior temporal cortex and the amygdala. Area TE is considered to be the last purely visual link in this pathway. A previous study [19] showed that damage to area TE, but not to other temporal lobe structures (TEO, A or FHH), severely impairs performance on a one-trial-learning test of object recognition as distinguished from object-reward association. Presumably, the impairment after TE lesions in the present study was due to this same basic recognition disorder. The impairment after amygdalectomy, however, not being attributable to a recognition disorder, appears to reflect instead a disorder in object-reward association learning. Together, these results provide evidence that the formation of object-reward associations in vision involves the sequential participation of a recognition mechanism dependent on the inferior temporal cortex and an associative process dependent on the amygdala.

Amygdala↗
PubMedDate not supplied

Cholecystokinin and bombesin effects on rewarded and nonrewarded operants.

Rats were food-rationed (15 g/day) and trained to bar-press for food. In Experiment 1, the animals were injected with cholecystokinin octapeptide (CCK, 2 micrograms/day), bombesin (BBS, 12 micrograms/kg), normal saline, or prefed with 20 Noyes 45 mg pellets. The animals were then tested for one hour for bar-pressing responses with food reward. In Experiment 2, the animals were similarly trained, treated, and tested for bar-pressing responses without food reward. The results showed that BBS and prefeeding decreased bar-pressing, rewarded or non-rewarded, but the CCK effect was greatly decreased when food was withheld. It appeared that the CCK effect was more dependent upon the presence of food than the BBS or prefeeding effects. The results were discussed in terms of involvement of the food and reward-related oropharyngeal stimuli for the CCK effect and the drive-related stimuli for the BBS and prefeeding effects.

Animals↗
PubMed1991

Sensitization of mesolimbic brain stimulation reward after electrical kindling of the amygdala.

The effects of partial kindling of the central amygdaloid nucleus on brain stimulation reward were evaluated. Intracranial self-stimulation (ICSS) rate intensity functions were determined using a two-hole nose-poke discrimination paradigm in rats implanted with electrodes in the A10 dopamine (DA) neuronal region of the ventral tegmental area (VTA), and in the medial forebrain bundle (MFB) at the level of the lateral hypothalamus. The kindling process did not influence ICSS baseline rates from either site. However, following stage 4 kindling, a low dose amphetamine challenge increased ICSS, resulted in a significant shift to the left of the rate intensity functions, and decreased reward thresholds. Analysis of the error scores which consisted of nonreinforced responses made during ICSS testing revealed that the interaction between kindling and amphetamine on ICSS was specific to changes in central reward processes, and could not be attributed to the influence of rate-enhancing performance variables. The kindling-elicited sensitization of mesolimbic DA reward functioning seen after amphetamine challenge was discussed in relation to the role of the central amygdala in the integration of stimulus-reward associations, and in the conditioning of affective emotional states.

Amphetamine↗
PubMed2004

Sensitivity to punishment and sensitivity to reward and traffic violations.

The aim of our study consists of contributing information on the relationship between the personality variables derived from Gray's model and the conduct that accompanies the infringement of the road traffic rules. Seven hundred and ninety-two adults of both sexes took part in the study (389 men and 403 women), all of whom had driving licences and drove frequently. The subjects answered "The Sensitivity to Punishment and Sensitivity to Reward Questionnaire", a scale of monotony avoidance, and two Likert scales of attitude and behaviour in connection with traffic violations. We found a high positive relationship between attitude and behaviour, with the men infringing the rules more than the women. Hypotheses regarding a relationship between traffic offences and sensibility to reward and monotony avoidance were confirmed. Those people with high scores in sensitivity to punishment and low ones in sensitivity to reward were those who drove within the law, while those with low sensitivity to punishment and high sensitivity to reward were those who broke it more. Sensitivity to reward was a stronger determinant in encouraging infringement of the rules than was sensitivity to punishment in discouraging the subjects to do so.

Accidents, Traffic↗
PubMed2006

Effects of genetic background and environmental novelty on wheel running as a rewarding behaviour in mice.

Recent studies suggest running wheel activity to be naturally rewarding and reinforcing; considering the shared neuro-behavioural characteristics with drug-induced reward situations, wheel running behaviour gains interest as a tool to study mechanisms underlying reward-sensitivity. Previously, we showed that wheel running has the potential to disrupt the daily organization of home cage behaviour in female C57BL/6 [de Visser L, van den Bos R, Spruijt BM. Automated home cage observations as a tool to measure the effects of wheel running on cage floor locomotion. Behav Brain Res 2005;160:382-8]. In the present study, we investigated the effects of novelty-induced stress on wheel running and its impact on home cage behaviour in male C57BL/6 and DBA/2 mice. Our aim was to determine whether wheel running may be used as a tool to study both genetic and environmentally induced differences in sensitivity to rewarding behaviour in mice. One group of male mice was placed in an automated home cage observation system for 2 weeks with a wheel integrated in the cage. A second group of mice was allowed to habituate to this cage for 1 week before a running wheel was introduced. Results showed a pronounced sensitising effect of novelty on the level of wheel running in C57Bl/6 mice but not in DBA mice. Overall levels of wheel running were higher in DBA/2 mice. Furthermore, wheel running affected circadian rhythmicity in DBA/2 mice but not in C57BL/6 mice. From these findings we tentatively suggest that wheel running behaviour could serve as a tool to study the interaction between genetic and environmental factors in sensitivity to rewarding behaviour in mice. As it is displayed spontaneously and easy to monitor, wheel running may be well suitable to be included in high-throughput phenotyping assays.

Analysis of Variance↗
PubMed2005

Severe deficit in brain reward function associated with fentanyl withdrawal in rats.

BACKGROUND: During the last decade, there has been a strong increase in the use of the mu-opioid receptor agonist fentanyl. The aim of these studies was to investigate the effects of fentanyl withdrawal on brain reward function and somatic withdrawal signs. METHODS: Fentanyl and saline were chronically administered via minipumps. An intracranial self-stimulation procedure was used to provide a measure of brain reward function. Somatic signs were recorded from a checklist of opioid abstinence signs. RESULTS: The opioid receptor antagonist naloxone induced a dose-dependent elevation in brain reward thresholds and somatic withdrawal signs in fentanyl-treated rats. Discontinuation of fentanyl administration resulted in a time-dependent elevation of brain reward thresholds and somatic withdrawal signs. CONCLUSIONS: These findings indicate that fentanyl withdrawal is associated with affective and somatic withdrawal signs. The severity of the deficit in brain reward function in this animal model suggests that affective fentanyl withdrawal symptoms may be a strong deterrent to abstinence.

Affect↗
PubMed2006

Acute stress reduces reward responsiveness: implications for depression.

BACKGROUND: Stress, one of the strongest risk factors for depression, has been linked to "anhedonic" behavior and dysfunctional reward-related neural circuitry in preclinical models. METHODS: To test if acute stress reduces reward responsiveness (i.e., the ability to modulate behavior as a function of past reward), a signal-detection task coupled with a differential reinforcement schedule was utilized. Eighty female participants completed the task under both a stress condition, either threat-of-shock (n = 38) or negative performance feedback (n = 42), and a no-stress condition. RESULTS: Stress increased negative affect and anxiety. As hypothesized based on preclinical findings, stress, particularly the threat-of-shock condition, impaired reward responsiveness. Regression analyses indicate that self-report measures of anhedonia predicted stress-induced hedonic deficits even after controlling for anxiety symptoms. CONCLUSIONS: These findings indicate that acute stress reduces reward responsiveness, particularly in individuals with anhedonic symptoms. Stress-induced hedonic deficit is a promising candidate mechanism linking stressful experiences to depression.

Adolescent↗
PubMed2004

Interhemispheric involvement of the anterior cortical nuclei of the amygdala in rewarding brain stimulation.

The amygdaloid complex is one of the structures thought to modulate brain stimulation reward (BSR) elicited from the median forebrain bundle (MFB). Previous metabolic and behavioral data from our laboratory point to the amygdaloid cortical nuclei as key to this process. In this study, thresholds for rewarding stimulation of the MFB were determined for 42 days, 21 days following an electrolytic lesion to amygdaloid nuclei ipsilateral to the stimulation electrode, and 21 days following one applied to the contralateral amygdala. A subset of animals showed post-lesion changes in MFB frequency thresholds that were maintained if not augmented after the second lesion. These ranged from 26% to 150% compared to baseline values, among the largest ever reported to our knowledge. Interestingly, damage to anterior sites within the cortical nuclei was the most effective in producing modifications to the rewarding value of the stimulation. Equally singular was the finding that contralateral lesions tended to alter thresholds more than ipsilateral ones, confirming our earlier finding of interhemispheric connectivity in amygdaloid modulation of MFB reward signals. This interpretation was substantiated by tracking long-term metabolic activity in the amygdala using cytochrome oxidase histochemistry. The density of reaction product at damaged amygdala sites was negatively correlated (r=-0.90) with the increases in thresholds obtained at contralateral MFB loci. Together with the fact that such large lesion effects are seldom obtained, our metabolic results point to the existence of a relationship between these nuclei and reward signals generated at the MFB. Moreover, our data suggest that this communication takes place interhemispherically.

Amygdala↗