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PubMed1995

Muscimol induces retrograde amnesia for changes in reward magnitude.

These experiments examined the effect of the GABAA agonist, muscimol (MUS), on memory for changes in reward magnitude. In Experiment 1 rats were trained to run a straight alley for either a large or small food reward. After reaching asymptotic performance rats in the high reward group were shifted to the small food reward. Half the animals received 1.0 or 3.0 mg/kg (ip) of MUS or the equivalent volume of saline immediately after training. Shifted training continued for 3 more days and no further injections were given. Shifted saline animals displayed an increase in response latencies compared to unshifted controls with a sharp peak on the day after the shift. Shifted MUS receiving 1.0 mg/kg performed comparably to shifted saline animals. In contrast, Shifted MUS animals receiving 3.0 mg/kg displayed performance comparable to shifted saline animals on the day of the shift but displayed a sharp increase in response latencies on the second day after the shift. These findings indicate that post-training systemic MUS injections delay the peak increase in response latencies and suggest that MUS induces retrograde amnesia for reward reduction. Experiment 2 examined the effect of MUS on the memory of a reward increase. Rats were first trained as in Experiment 1 and rats under the high reward condition were then shifted to the small reward. On the next training session, the large food reward was reinstated.(ABSTRACT TRUNCATED AT 250 WORDS)

Amnesia, Retrograde↗

PubMed1985

Benzodiazepines reduce the tolerance to reward delay in rats.

This study investigated whether benzodiazepines reduce the capacity of animals to wait for food reward. Rats trained in a T-maze were allowed to choose between two magnitudes of reward: immediate, but small (two pellets) vs delayed, but large (eight pellets). The rats learned within ten sessions to select (80-100%) the arm leading to the largest reward. Separate groups of rats were then confined for 15, 30 or 60 s in the arm associated with the largest reward before gaining access to the spacially contiguous goal-box. The choice of the other arm was not followed by a period of waiting. Under these conditions, the frequency with which the small-reward arm was chosen increased linearly as a function of the duration of the waiting period. Diazepam (2-4 mg/kg IP) dose-dependently increased the number of times the small-reward arm was chosen during the sessions for which the waiting period was fixed at 15 or 30 s. Nitrazepam (2 mg/kg IP), chlordiazepoxide (16 mg/kg IP) and clobazam (16 mg/kg IP) had similar effects. The action of diazepam was counteracted by simultaneous administration of flumazepil (Ro 15-1788, 8 mg/kg PO). In the absence of confinement, these benzodiazepines, diazepam (4 mg/kg) excepted, did not modify selection of the large-reward arm. Conversely, the serotonin uptake blockers indalpine (2-4 mg/kg IP) and zimelidine (8-16 mg/kg IP) dose-dependently increased preference for the arm leading to the delayed (25 s) but large reward. These results suggest that benzodiazepines, perhaps by increasing impulsivity, render the animals less prone than controls to tolerate delayed access to reward.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Brain stimulation and morphine reward deficits in dopamine D2 receptor-deficient mice.

RATIONALE: The rewarding effects of lateral hypothalamic brain stimulation, various natural rewards, and several drugs of abuse are attenuated by D1 or D2 dopamine receptor (D1R or D2R) antagonists. Much of the evidence for dopaminergic involvement in rewards is based on pharmacological agents with limited or "relative" selectivity for dopamine receptor subtypes. Genetically engineered animal models provide a complementary approach to pharmacological investigations. OBJECTIVES: In the present study, we explored the contribution of dopamine D2Rs to (1) brain stimulation reward (BSR) and (2) the potentiation of this behavior by morphine and amphetamine using D2R-deficient mice. METHODS: Wild-type (D2Rwt), heterozygous (D2Rhet), and D2R knockout (D2Rko) mice were trained to turn a wheel for rewarding brain stimulation. Once equivalent rate-frequency curves were established, morphine-induced (0, 1.0, 3.0, and 5.6 mg/kg s.c.) and amphetamine-induced (0, 1.0, 2.0, and 4.0 mg/kg i.p.) potentiations of BSR were determined. RESULTS: The D2Rko mice required approximately 50% more stimulation than the D2Rwt mice did. With the equi-rewarding levels of stimulation current, amphetamine potentiated BSR equally across the three genotypes. In contrast, morphine potentiated rewarding stimulation in the D2Rwt, had no effect in the D2Rhet, and antagonized rewarding stimulation in the D2Rko mice. CONCLUSIONS: D2R elimination decreases, but does not eliminate, the rewarding effects of lateral hypothalamic stimulation. After compensation for this deficit, amphetamine continues to potentiate BSR, while morphine does not.

Amphetamine↗

PubMed2000

Chronic food restriction in rats augments the central rewarding effect of cocaine and the delta1 opioid agonist, DPDPE, but not the delta2 agonist, deltorphin-II.

RATIONALE: Chronic food restriction augments the self-administration and locomotor stimulating effects of opiates, psychostimulants and NMDA antagonists. The extent to which these effects can be attributed to changes in drug pharmacokinetics and bioavailability versus sensitivity of the neuronal circuits that mediate the affected behavioral functions, has not been established. Recent studies point to central adaptive changes insofar as rewarding, locomotor and c-fos-inducing effects of amphetamine and MK-801, injected directly into the lateral ventricle, are greater in food-restricted than ad libitum fed rats. The increased expression of c-fos in nucleus accumbens (NAC) shell, in particular, suggests that food restriction may augment drug reward by modulating dopamine (DA) synaptic function in this area. OBJECTIVES: The first purpose of this study was to investigate whether the rewarding effects of cocaine and the delta1 opioid agonist DPDPE, both of which increase DA synaptic transmission, are augmented by food restriction. The second purpose was to determine whether the delta2 opioid agonist, deltorphin-II, which has been reported to exert DA-independent rewarding effects, is subject to the potentiating effect of food restriction. METHODS: Rewarding effects of drugs were measured in terms of their ability to lower the threshold for lateral hypothalamic self-stimulation (LHSS) using a rate-frequency method. RESULTS: In separate experiments, cocaine (50, 100 and 150 microg, ICV) and DPDPE (10 and 25 microg, ICV) produced greater threshold-lowering effects in food-restricted than ad libitum fed rats. Deltorphin-II (5.0, 10 and 25 microg, ICV) had no effect on reward thresholds, regardless of feeding regimen. CONCLUSIONS: While the reported DA-independence of deltorphin-II rewarding effects seemed to offer a means of testing the hypothesis that DA transmission is the critical modulated variable in food-restricted subjects, rewarding effects of this compound could not be demonstrated in the LHSS paradigm. The present results do, however, confirm and extend prior findings indicating that the enhanced self-administration of abused drugs by food-restricted subjects is due to enhanced sensitivity of a final common pathway for drug reward.

Animals↗

PubMed1997

Differential effects of ondansetron and alpha-flupenthixol on responding for conditioned reward.

Previous experiments have suggested that 5-HT3 antagonists such as ondansetron may alter reward-related behaviour that is dependent in part upon raised mesolimbic dopamine activity. However, the evidence for this is far from conclusive. One major behavioural role of dopamine is in the control of behaviour elicited by conditioned rewarding stimuli. To date, the effects of 5-HT3 antagonists on this function of mesolimbic dopamine have not been examined. Two experimental procedures were employed to examine the effects of ondansetron (10 and 100 micrograms/kg) on the acquisition of responding for conditioned reward, and on the response potentiating effect of intra-accumbens d-amphetamine (10 micrograms). These effects were compared to those elicited by the dopamine antagonist alpha-flupenthixol (0.1 mg/kg). In the first procedure, rats were trained to associate food pellet delivery with a conditioned stimulus (CS). Rats subsequently allowed to respond on a lever delivering this CS, and on an inactive lever, showed a greater preference for the lever delivering the CS, indicating that this CS functioned as a conditioned reward (CR). Ondansetron administered during the conditioning phase did not alter subsequent responding for the CR, but alpha-flupenthixol induced a small but significant reduction in responding on the CR lever. These results suggest that blockade of dopamine receptors, but not 5-HT3 receptors interfere with the learning of stimulus reward relationships. In the second procedure, d-amphetamine injected into the nucleus accumbens markedly potentiated responding for CR. Ondansetron at 10 micrograms/kg induced a small attenuation of this effect, without altering responding in its own right. However, at a higher dose (100 micrograms/kg) ondansetron plus amphetamine treatment significantly enhanced responding on the inactive lever. At both doses, the net effect of ondansetron was to produce a subtle impairment in the allocation of responses such that the differential responding on the CR versus NCR lever was diminished. In contrast to these effects alpha-flupenthixol significantly attenuated d-amphetamine's selective enhancement of responding for conditioned reward, as well as impairing the ability of the conditioned reward to elicit and maintain behaviour. These results confirm the role of dopamine in responding for conditioned reward, and suggest a possible modulators role for 5-HT3 receptors in this process. However, the effects of ondansetron on the acquisition of, and responding for, conditioned reward are clearly different from those induced by blockade of dopamine receptors.

Animals↗

PubMed2006

Differential effects of reward and punishment on conscious and unconscious eye movements.

Very little is known about how human movements are influenced by abstract rewards and punishments relevant for human behaviour. The purpose of this study was to expand our knowledge of the behavioural effects of monetary reward and punishment. We introduced a high and low reward and punishment scheme into an antisaccade task where trials were either rewarded for a correct response (+1 or +25p) or punished for an incorrect response (-1 or -25p). The monetary value of the trial was indicated by the go signal, so subjects had to both program the location of the movement and determine the valence in the short interval before the eye movement was executed. We analysed both correct antisaccade responses and prosaccade errors. Importantly, the errors in this task can be either conscious (recognised) or unconscious (unrecognised). Saccades in both high-reward and high-punishment trials were slowed compared to saccades in low-reward and low-punishment trials, respectively. Therefore, unlike moderate rewards only (Blaukopf and DiGirolamo in Exp Brain Res 167:654-659, 2005), combining rewards and punishments and increasing motivation levels leads to a delay in movement execution during high valence trials where all actions are slowed, even errors. However, unconscious errors were differentially affected as they were speeded when punishment was high. We conclude that reward and punishment similarly influence the programming of conscious movements, but the strong saliency for punishment affords unconscious errors immunity from this delay.

Adult↗

PubMed1984

The effects of feeding and rewarding brain stimulation on lateral hypothalamic unit activity in freely moving rats.

In some medial forebrain bundle (MFB) sites, self-stimulation is often modulated by hunger or satiety. With electrodes in the nucleus accumbens (NAC) such modulation rarely occurs. The influence of food deprivation on MFB self-stimulation is the main basis for the hypothesis that electrical stimulation of the MFB can mimic the rewarding effect of food for hungry animals. To investigate this hypothesis, unit activity was recorded from the lateral hypothalamic area (LHA) of freely moving rats during rewarding stimulation at loci in both MFB and NAC, and during food ingestion. Of 63 neurons tested during MFB stimulation, 41 were inhibited, 19 were activated, and 3 were not influenced. NAC stimulation suppressed 8 of the 31 neurons tested, excited 16, and elicited no response in the remaining 7. During ingestion, 29 of the 63 neurons tested were inhibited and one was facilitated. Of 29 neurons suppressed by food, 20 were also inhibited by rewarding MFB stimulation, but 10 of 13 neurons inhibited by food were excited by rewarding NAC stimulation. Thus, most LHA neurons inhibited during feeding were also inhibited by rewarding MFB stimulation. Rewarding NAC stimulation, however, does not inhibit most LHA neurons that are inhibited by food. This result suggests that LHA neurons which are inhibited by food might be involved in mediation of the rewarding effect of electrical stimulation at some sites in the MFB. Nevertheless, self-stimulation may occur by activating reward processes other than those related to food, because rewarding NAC stimulation does not inhibit LHA neurons which are suppressed by food.

Action Potentials↗

PubMed1987

Quantitative determination of the effects of catecholaminergic agonists and antagonists on the rewarding efficacy of brain stimulation.

The effects of amphetamine, clonidine, molindone, pimozide and yohimbine on the rewarding efficacy of electrical stimulation of the medial forebrain bundle in the rat were determined from the effects of these drugs on the rate-frequency function, which is the plot of the rat's rate of pressing a lever against the frequency of the pulses in a rewarding train of fixed duration. These catecholaminergic agonists and antagonists produced dose-dependent alterations in the measurable rewarding efficacy, but only up to a factor of about 2, even though the method is capable of measuring 25-30-fold changes. At elevated doses, the effects on rewarding efficacy became unmeasurable, because the animals would not consistently self-stimulate at any parameters of stimulation. Amphetamine (0.5-3 mg/kg) enhanced rewarding efficacy. Clonidine (0.05-0.4 mg/kg), molindone (0.25-1 mg/kg) and pimozide (0.1-0.6 mg/kg) attenuated it. Pimozide and clonidine were equipotent despite their radically different receptor affinities. The effects of pimozide, clonidine and amphetamine were approximately additive (amphetamine cancelled the effects of pimozide and clonidine, while clonidine augmented the effect of pimozide). The alpha 2 antagonist yohimbine (0.05-10 mg/kg) had the same effect as the alpha 2 agonist clonidine (attenuation of rewarding efficacy), but these effects did not combine additively: yohimbine neither cancelled nor augmented the effect of clonidine. It is suggested that catecholaminergic agonists and antagonists do not alter the magnitude of the rewarding signal by acting on postsynaptic receptors in the reward pathway; rather, they may drive beyond functional limits a variable that is crucial to the proper recording of the magnitude of the rewarding signal.

Amphetamine↗

PubMed2006

Alterations in reward-related decision making in boys with recent and future depression.

BACKGROUND: Altered reward processing is postulated to be a feature of depression. Reward processing may be valuable to understanding early-onset depressive disorders, which tend to be chronic and recurrent. METHODS: Reward-related decision making was examined within a longitudinal study of 221 11-year-old boys, 25 of whom had a depressive disorder at age 10 or 11. Participants completed a behavioral decision-making task involving varying probability and magnitude of obtaining reward. RESULTS: Under conditions involving a high probability of winning, boys with depression failed to distinguish between options involving small or large possible reward. Boys with anxiety or externalizing disorders at age 10 or 11 did not differ from others in their reward-related decisions. Low frequency of choosing the high-probability, large reward option at age 11 predicted depressive disorders, anxiety disorders, and depressive symptoms 1 year later. Furthermore, reward-related decisions predicted later depressive or anxiety disorders even when adjusting for the continuity of such disorders and the presence of concurrent externalizing disorders. CONCLUSIONS: Findings are consistent with affective neuroscience models of altered reward processing and diminished positive affect in depression. This study represents a step toward elucidating the motivational and emotional aspects of early-onset depression.

Analysis of Variance↗

PubMed2004

Neural coding of basic reward terms of animal learning theory, game theory, microeconomics and behavioural ecology.

Neurons in a small number of brain structures detect rewards and reward-predicting stimuli and are active during the expectation of predictable food and liquid rewards. These neurons code the reward information according to basic terms of various behavioural theories that seek to explain reward-directed learning, approach behaviour and decision-making. The involved brain structures include groups of dopamine neurons, the striatum including the nucleus accumbens, the orbitofrontal cortex and the amygdala. The reward information is fed to brain structures involved in decision-making and organisation of behaviour, such as the dorsolateral prefrontal cortex and possibly the parietal cortex. The neural coding of basic reward terms derived from formal theories puts the neurophysiological investigation of reward mechanisms on firm conceptual grounds and provides neural correlates for the function of rewards in learning, approach behaviour and decision-making.

Animals↗

PubMed2006

Neural differentiation of expected reward and risk in human subcortical structures.

In decision-making under uncertainty, economic studies emphasize the importance of risk in addition to expected reward. Studies in neuroscience focus on expected reward and learning rather than risk. We combined functional imaging with a simple gambling task to vary expected reward and risk simultaneously and in an uncorrelated manner. Drawing on financial decision theory, we modeled expected reward as mathematical expectation of reward, and risk as reward variance. Activations in dopaminoceptive structures correlated with both mathematical parameters. These activations differentiated spatially and temporally. Temporally, the activation related to expected reward was immediate, while the activation related to risk was delayed. Analyses confirmed that our paradigm minimized confounds from learning, motivation, and salience. These results suggest that the primary task of the dopaminergic system is to convey signals of upcoming stochastic rewards, such as expected reward and risk, beyond its role in learning, motivation, and salience.

Adolescent↗

PubMed2006

Encoding of time-discounted rewards in orbitofrontal cortex is independent of value representation.

We monitored single-neuron activity in the orbitofrontal cortex of rats performing a time-discounting task in which the spatial location of the reward predicted whether the delay preceding reward delivery would be short or long. We found that rewards delivered after a short delay elicited a stronger neuronal response than those delivered after a long delay in most neurons. Activity in these neurons was not influenced by reward size when delays were held constant. This was also true for a minority of neurons that exhibited sustained increases in firing in anticipation of delayed reward. Thus, encoding of time-discounted rewards in orbitofrontal cortex is independent of the encoding of absolute reward value. These results are contrary to the proposal that orbitofrontal neurons signal the value of delayed rewards in a common currency and instead suggest alternative proposals for the role this region plays in guiding responses for delayed versus immediate rewards.

Action Potentials↗

PubMed2005

Neural bases of food-seeking: affect, arousal and reward in corticostriatolimbic circuits.

Recent studies suggest that there are multiple 'reward' or 'reward-like' systems that control food seeking; evidence points to two distinct learning processes and four modulatory processes that contribute to the performance of food-related instrumental actions. The learning processes subserve the acquisition of goal-directed and habitual actions and involve the dorsomedial and dorsolateral striatum, respectively. Access to food can function both to reinforce habits and as a reward or goal for actions. Encoding and retrieving the value of a goal appears to be mediated by distinct processes that, contrary to the somatic marker hypothesis, do not appear to depend on a common mechanism but on emotional and more abstract evaluative processes, respectively. The anticipation of reward on the basis of environmental events exerts a further modulatory influence on food seeking that can be dissociated from that of reward itself; earning a reward and anticipating a reward appear to be distinct processes and have been doubly dissociated at the level of the nucleus accumbens. Furthermore, the excitatory influence of reward-related cues can be both quite specific, based on the identity of the reward anticipated, or more general based on its motivational significance. The influence of these two processes on instrumental actions has also been doubly dissociated at the level of the amygdala. Although the complexity of food seeking provides a hurdle for the treatment of eating disorders, the suggestion that these apparently disparate determinants are functionally integrated within larger neural systems may provide novel approaches to these problems.

Affect↗

PubMed2000

Delta-opioid and 5-HT3 receptor antagonist effects on ethanol reward and discrimination in C57BL/6 mice.

The effects of the receptor antagonists MDL 72222 (MDL, 5-HT3) and naltrindole (delta-opioid) on ethanol reward and its discrimination were examined in ethanol-preferring C57BL/6 (C57) mice. MDL attenuated lever responding for 12% ethanol delivered on a fixed-ratio 8 reinforcement schedule at a dose that did not influence responding for water reward, thus confirming a previous report that ICS 205-930 reduced ethanol reward for Long-Evans rats. Our study in combination with the reduced ethanol consumption reported for C57 mice injected with odansetron indicates that 5-HT3 receptor systems are involved in mediating behavior directed toward obtaining ethanol as well as its consumption. By attenuating the rewarding effects of ethanol or of ethanol conditioned cues (e.g., the operant environment), 5-HT3 antagonists may be useful in the treatment of alcohol abuse. The 5-HT3 antagonist effects in this study are comparable with the effects of naltrexone on ethanol reward in C57 mice, although higher doses were required to reduce operant responding for ethanol reward. In contrast to the 5-HT3 antagonist and naltrexone effects, naltrindole, an antagonist with greater specificity for the delta-opioid receptor, was without effect on ethanol reward. This result and recent reports for rats and monkeys suggests that the general antagonists might be more efficacious in attenuating ethanol reward. Both MDL and naltrindole produced only slight reductions in the ethanol discriminative cue, suggesting that the rewarding and discriminative effects of ethanol are not likely mediated by identical neural mechanisms as previously suggested.

Animals↗

PubMed1998

Assessment of self-reward strategies for maintenance of breast self-examination.

This study examined the relative impact of different self-reward strategies on maintenance of breast self-examination (BSE) practice among 1649 women trained to do BSE. Training groups were randomized into four conditions: (a) self-reward instructions and materials delivered at the end of the BSE training session; (b) self-reward suggestions delivered through the mail each month, contingent upon the BSE performance; (c) external monetary rewards and self-reward suggestions delivered through the mail each month on an intermittent schedule, contingent upon BSE practice; and (d) a no-reward control condition. Follow-up assessments 12 months following training revealed a pattern of evidence in support of the benefits of external monetary rewards and self-reward prompts on BSE frequency and quality; however, it is likely that the value of that condition lies in the external reward component.

Adolescent↗

PubMed1985

Observing response acquisition: preference for unpredictable appetitive rewards obtained under conditions predicted by DMOD.

In five E-maze experiments, rats were given a choice between receiving reward and nonreward in a situation where stimuli were correlated with reward outcome (predictable situation) versus one where the stimuli were uncorrelated with reward outcome (unpredictable situation). Preference for the unpredictable situation occurred under the following conditions: (a) small (one 37-mg pellet), immediate rewards; (b) small, delayed (15 s) rewards, if the cues correlated with reward outcome were absent during the delay interval; (c) large (15 pellets), immediate rewards if a difficult discrimination was required; and (d) if the stimulus predicting nonreward was present at the choice point. Preference for the predictable situation was strongest if reinforcement was delayed and large or the stimulus predicting reward was present at the choice point. A weaker preference for the predictable situation occurred if reinforcement was immediate and large and a simple discrimination was required or if reinforcement was large and delayed and the cues that correlated with reward outcome were absent during the delay interval. The results support the predictions of DMOD (Daly modification of the Rescorla-Wagner model), a mathematical model of appetitive learning (Daly & Daly, 1982).

Animals↗

PubMed1984

Rewards and adolescent health behavior.

Research has indicated that contingent rewards can increase students' acceptance of novel preventive health activities. In the current research on adolescents' use of a fluoride rinse over two school years, however, the rinse habit tended to end when reward contingencies were withdrawn. Although participation in the rinse program was higher with a saturated schedule of reward contingencies in effect, the comparison partial schedule of rewards showed less immediate attrition when the reward contingencies were withdrawn. As a result, the long-term effects of the two schedules were largely equivalent. Other major findings included higher participation levels for girls compared to boys and for urban compared to suburban students. Self-management instruction, a strategy intended to compensate for the withdrawal of tangible rewards, worked temporarily among urban students but at the same time resulted in lower levels of post-reward rinsing among suburban students. This study confirmed the efficacy of contingent rewards for initiating new health habits among adolescents, but neither a partial schedule of reward nor instruction in self-management was sufficient to establish long-term continuation of the behavior. Implications of these findings for health psychologists and public health professionals are discussed briefly.

Adolescent↗

PubMed2006

Blockade of 5-HT2a receptors reduces haloperidol-induced attenuation of reward.

Previous studies have shown that effective antipsychotic medications attenuate reward, an effect that is generally attributed to their effectiveness at blocking the dopamine D2-like receptors. As blockade of the serotonin type 2a (5-HT2a) receptors is a common property of the newer antipsychotics, the present study compared the effect of haloperidol, clozapine, and M100907 (a selective 5-HT2a antagonist) and the combined effect of haloperidol and M100907 treatment on brain stimulation reward (BSR). Experiments were performed on male Sprague-Dawley rats trained to produce an operant response to obtain electrical stimulation in the lateral hypothalamus. Measures of reward threshold were determined in different groups of rats using the curve-shift method using fixed current intensity and variable frequency before and at different times after injection of haloperidol (0.01, 0.05, 0.1, and 0.25 mg/kg), clozapine (1, 7.5, 15, and 30 mg/kg), M100907 (0.033, 0.1, and 0.3 mg/kg), or their vehicle. The effect of M100907 (0.3 mg/kg) on the attenuation of BSR by a sub- and suprathreshold dose of haloperidol was studied in another group of rats. Clozapine produced a dose-orderly increase in reward threshold with a mean maximal increase of 50%; at high doses, clozapine induced cessation of responding in several animals at different time periods. Haloperidol induced a dose-dependent increase in reward threshold, with the mean maximal increase (75%) being observed at the highest dose; it also produced a dose-dependent reduction of maximum rates of responding. M100907 failed to alter reward at any of the doses tested and had no effect on the subthreshold dose (0.01 mg/kg) of haloperidol. But when combined with a suprathreshold dose of haloperidol, M100907 reduced the reward-attenuating effect of haloperidol. These results show that 5-HT2a receptors are unlikely to constitute a component of the reward-relevant pathway activated by lateral hypothalamic stimulation. However, blockade of 5-HT2a receptors may account for the relatively lower level of reward attenuation produced by clozapine, and predict that antipsychotic medications that have a high affinity for the 5-HT2a receptor may be less likely to induce dysphoria.

Analysis of Variance↗