Conditioned Disgust Research Articles

Neurocognitive mechanisms of mental imagery-based disgust learning

Disgust imagery represents a potential pathological mechanism for disgust-related disorders. However, it remains controversial as to whether disgust can be conditioned with disgust-evoking mental imagery serving as the unconditioned stimulus (US). Therefore, we examined this using a conditioned learning paradigm in combination with event-related potential (ERP) analysis in 35 healthy college students. The results indicated that the initial neutral face (conditioned stimulus, CS+) became more disgust-evoking, unpleasant, and arousing after pairing with disgust-evoking imagery (disgust CS+), compared to pairing with neutral (neutral CS+) and no (CS−) imagery. Moreover, we observed that mental imagery-based disgust conditioning was resistant to extinction. While the disgust CS + evoked larger P3 and late positive potential amplitudes than CS− during acquisition, no significant differences were found between disgust CS+ and neutral CS+, indicating a dissociation between self-reported and neurophysiological responses. Future studies may additionally acquire facial EMG as an implicit index of conditioned disgust. This study provides the first neurobiological evidence that associative disgust learning can occur without aversive physical stimuli, with implications for understanding how disgust-related disorders may manifest or deteriorate without external perceptual aversive experiences, such as in obsessive-compulsive disorder (OCD).

Conscious knowledge of CS-UCS contingency information affects extinction retrieval of conditioned disgust responses: Findings from an online de novo disgust conditioning task.

The present study aimed to establish and develop an online de novo conditioning paradigm for the measurement of conditioned disgust responses. We further explored the effects of explicit instructions about the CS-UCS contingency on extinction learning and retrieval of conditioned disgust responses. The study included a sample of 115 healthy participants. Geometric figures served as conditioned stimuli (CS) and disgust-evoking pictures as unconditioned stimuli (UCS). During disgust conditioning, the CS+ was paired with the UCS (66% reinforcement) and the CS- remained unpaired; during extinction and retrieval, no UCS was presented. Half of the participants (n=54) received instructions prior to the disgust extinction stating that the UCS will not be presented anymore. 1-2 days or 7-8 days later participants performed a retrieval test. CS-UCS contingency, disgust and valence ratings were used as dependent measures. Successful acquisition of conditioned disgust response was observed on the level of CS-UCS contingency, disgust and valence ratings. While some decline in valence and disgust ratings during the extinction stage was observed, contingency instructions did not significantly affect extinction performance. Retrieval one week later revealed that contingency instructions increased the discrimination of the CSs. Extinction of conditioned disgust responses is not affected by explicit knowledge of the CS-UCS contingencies. However, contingency instructions prior to extinction seem to have a detrimental effect on long-term extinction retrieval.

Immune activation attenuates memory acquisition and consolidation of conditioned disgust (anticipatory nausea) in rats

Anticipatory nausea is a classically conditioned response to cues (e.g. contexts) that have been previously paired with a nauseating stimulus, such as chemotherapy in humans. In rodents, anticipatory nausea can be modeled by pairing a novel context with lithium chloride (LiCl), which leads to conditioned disgust behaviours (such as gaping) when exposed to the context alone. Growing evidence suggests that selective immune activation attenuates various forms of learning and memory. The present study investigated the effects of the endotoxin lipopolysaccharide (LPS) on LiCl-induced anticipatory nausea across critical stages of associative memory including acquisition, consolidation, and extinction. Adult male Long Evans rats were subject to intraperitoneal (i.p.) LiCl (127 mg/kg) or vehicle control (NaCl) paired with a 30 min conditioning trial in a distinct context for a total of 4 trials. To study acquisition, rats were administered either LPS or NaCl (200 μg/kg, i.p.) 90 mins before the conditioning trials. To study consolidation, different rats were administered either LPS or NaCl (200 μg/kg, i.p.) immediately after the conditioning trials. These trials were followed by 4 drug-free extinction trials within the same context. LPS significantly reduced conditioned gaping behaviours by the 4th conditioning trial and on the 1st drug-free extinction trial when administered 90 mins before or immediately after the conditioning trials. LPS had no significant effect on extinction. The present study provides strong evidence for the attenuating effects of LPS exposure on the acquisition and consolidation of LiCl-induced anticipatory nausea.

Pavlovian Disgust Conditioning and Generalization: Specificity and Associations With Individual Differences

Although studies have identified differences between fear and disgust conditioning, much less is known about the generalization of conditioned disgust. This is an important gap in the literature given that overgeneralization of conditioned disgust to neutral stimuli may have clinical implications. To address this knowledge gap, female participants (n = 80) completed a Pavlovian conditioning procedure in which one neutral food item (conditioned stimulus; CS+) was followed by disgusting videos of individuals vomiting (unconditioned stimulus; US) and another neutral food item (CS–) was not reinforced with the disgusting video. Following this acquisition phase, there was an extinction phase in which both CSs were presented unreinforced. Importantly, participants also evaluated generalization stimuli (GS+, GS−) that resembled, but were distinct from, the CS after each conditioning phase. As predicted, the CS+ was rated as significantly more disgusting and fear inducing than the CS− after acquisition and this pattern persisted after extinction. However, disgust ratings of the CS+ after acquisition were significantly larger than fear ratings. Participants also rated the GS+ as significantly more disgusting, but not fear inducing, than the GS− after acquisition. However, this effect was not observed after extinction. Disgust proneness did predict a greater increase in disgust and fear ratings of the CS+ relative to the CS− after acquisition and extinction. In contrast, trait anxiety predicted only higher fear ratings to the CS+ relative to the CS− after acquisition and extinction. Disgust proneness nor trait anxiety predicted the greater increase in disgust to the GS+ relative to the GS− after acquisition. These findings suggest that while conditioned disgust can generalize, individual difference variables that predict generalization remain unclear. The implications of these findings for disorders of disgust are discussed.

Is Acquired Disgust More Difficult to Extinguish Than Acquired Fear? an Event-Related Potential Study.

This study used the classical conditioned acquisition and extinction paradigm to compare which of the two emotions, acquired disgust and acquired fear, was more difficult to extinguish, based on behavioral assessments and the event-related potential (ERP) technique. Behavioral assessments revealed that, following successful conditioned extinction, acquired disgust was more difficult to extinguish. The ERP results showed that, at the early stage of P1, the amplitude of conditioned fear was significantly smaller than that of conditioned disgust, and both were significantly different from the amplitude under neutral conditions; at the middle stage of N2, the difference between the amplitudes of conditioned disgust and conditioned fear disappeared, but they were still significantly different from the amplitudes of conditioned neutral stimuli; at the late stage of P3, the difference between conditioned disgust and conditioned neutral stimuli disappeared, but the difference between conditioned fear and neutral stimuli remained, suggesting that acquired fear was more difficult to extinguish than acquired disgust in terms of how the brain works.

Generalization of conditioned disgust and the attendant maladaptive avoidance: Validation of a novel paradigm and effects of trait disgust-proneness

Overgeneralization of conditioned fear to safe stimuli that resemble a previously-learned threat-cue is a well-studied correlate of clinical anxiety, yet whether conditioned disgust generalizes remains unknown, as does the extent to which such generalization is associated with disgust-related traits and maladaptive outcomes. The present study addresses this gap by adapting a validated fear-generalization paradigm to assess conditioned disgust and behavioral avoidance to a disgust-cue (CS+) paired with a disgusting video clip, and safe generalization stimuli parametrically varying in perceptual similarity to CS+. For comparison, levels of fear generalization were also assessed using the original fear-generalization paradigm. In both paradigms, costly and unnecessary avoidance to safe threat-cue approximations analogues maladaptive outcomes of generalization. In the disgust paradigm only, disgust-proneness was associated with elevated perceived risk to safe stimuli and increases in the extent to which such elevations were accompanied by maladaptive avoidance. Comparable levels of generalization, and positive associations between generalization and maladaptive avoidance, were found across disgust and fear paradigms. Results confirm that conditioned disgust is subject to generalization, implicate generalized disgust as a source of maladaptive avoidance particularly among those prone to disgust, and suggest a potential role for these processes in the etiology and maintenance of disgust-related disorders.

Acquisition and maintenance of disgust reactions in an OCD analogue sample: Efficiency of extinction strategies through a counter-conditioning procedure.

Obsessive-compulsive disorder (OCD) has long been considered as an anxiety disorder, disgust is the dominant emotion in contamination-based OCD. However, disgust seems resistant to exposure with response prevention partly due to the fact that disgust is acquired through evaluative conditioning. The present research investigates a counter-conditioning intervention in treating disgust-related emotional responses in two groups of individuals with high (High contamination concerns, HCC, n = 24) and low (Low contamination concerns LCC, n = 23) contamination concerns. The two groups completed a differential associative learning task in which neutral images were followed by disgusting images (conditioned stimulus; CS+), or not (CS-). Following this acquisition phase, there was a counter-conditioning procedure in which CS+ was followed by a very pleasant unconditional stimulus while CS- remained unreinforced. Following counter-conditioning, both groups reported significant reduction in their expectancy of US occurrence and reported less disgust with CS+. For both expectancy and disgust, reduction was lower in the HCC group than in the LCC group. Disgust sensitivity was highly correlated with both acquisition and maintenance of the response acquired, while US expectation was predicted by anxiety. Counter-conditioning procedure reduces both expectations and conditioned disgust.

Does an unconditioned stimulus memory devaluation procedure decrease disgust memories and conditioned disgust? Results of two laboratory studies

Research has demonstrated that disgust can be installed through classical conditioning by pairing neutral conditioned stimuli (CSs) with disgusting unconditioned stimuli (USs). Disgust has been argued to play an important role in maintaining fear-related disorders. This maintaining role may be explained by conditioned disgust being less sensitive to extinction (i.e., experiencing the CS in the absence of the US). Promising alternatives to extinction training are procedures that focus on the devaluation of US memory representations. In the current study, we investigated whether such devaluation procedures can be successful to counter conditioned disgust. We conducted two laboratory studies (N = 120 and N = 51) in which disgust was conditioned using audio-visual USs. Memory representations of the USs were devalued by having participants recall these USs while they performed a taxing eye-movement task or executed one of several control tasks. The results showed successful conditioned disgust acquisition. However, no strong evidence was obtained that an US memory devaluation procedure modulates disgust memory and diminishes conditioned disgust as indicated by subjective, behavioral, or psychophysiological measures. We discuss the relevance of our results for methodological improvements regarding US memory devaluation procedures and disgust conditioning.

Fast-forwarding disgust conditioning: US pre-exposure facilitates the acquisition of oculomotor avoidance

During human development, disgust is acquired to a broad range of stimuli, from rotting food to moral transgressions. Disgust’s expansion surely involves associative learning, yet little is known about Pavlovian disgust conditioning. The present study examined conditioned disgust responding as revealed by oculomotor avoidance, the tendency to look away from offensive stimuli. In two experiments, oculomotor avoidance was acquired to a neutral image associated with a disgusting image. However, to our surprise, participants initially dwelled on disgusting images, avoiding them only after multiple exposures. In Experiment 1, this “rubbernecking” response delayed oculomotor avoidance of the associated neutral image. In Experiment 2, we exhausted rubbernecking prior to conditioning by repeatedly exposing participants to the disgusting images. This procedure elicited earlier oculomotor avoidance of the associated neutral stimulus, essentially fast-forwarding conditioning. These findings reveal competing motivational tendencies elicited by disgust stimuli that complicate associative disgust learning.

Conditioned disgust in rats (anticipatory nausea) to a context paired with the effects of the toxin LiCl: Influence of sex and the estrous cycle

The role of sex and estrous phase in the conditioning of toxin-induced disgust reactions (anticipatory nausea) to a novel context were examined in adult rats. Conditioned oral gaping responses have been shown to be a reliable index of nausea in rats. In Experiment 1 male and female rats were injected with LiCl (0, 64, 96, or 128 mg/kg) on each of 4 conditioning trials (72 h apart) and then placed in a novel context for 30 min. 72 h following the last conditioning trial each animal was re-exposed to this context in a toxin-free state for 10 min and disgust responses (gapes, forelimb flails, chin rubs, and paw treads) were scored from video records. A significant toxin dose-related monotonic increase in conditioned gaping showed a significantly greater increase in females, relative to males. In Experiment 2 female rats were conditioned, using the same paradigm, on either diestrus or proestrus days (trials 96 h apart) with LiCl (96 mg/kg) or saline control injections. Disgust responses were recorded on each of the 4 conditioning trials and a toxin-free test trial. Significant increases in conditioned disgust were obtained on proestrus relative to diestrus days on the toxin-free test trial. However no significant estrous cycle differences in disgust responding were obtained on the acquisition trials. The sex difference in conditioned gaping and the increased conditioned disgust responses in proestrus suggest that increased levels of estradiol likely enhance the strength of the association of the toxin-induced nausea with the novel context in rats.

The effects of cognitive reappraisal on conditioned disgust in contamination-based OCD: An analogue study

Experimental research has shown that conditioned disgust is resistant to extinction, which may account for the slower habituation to disgust relative to fear in contamination-based obsessive-compulsive disorder (OCD). However, few studies have examined the efficacy of interventions that may attenuate conditioned disgust responses. Studies of cognitive reappraisal have demonstrated that reinterpreting a stimulus can alter emotional responding. This technique is based on cognitive theories which suggest that anxiety disorders arise from biased cognitions; therefore, changing a person’s thoughts will elicit durable changes in emotional responses. Given the demonstrated effectiveness of cognitive reappraisal, the present study examined whether cognitive reappraisal would attenuate conditioned disgust responses. We conditioned participants high in contamination fear (n=55) using images of neutral food items (conditioned stimuli; CS) paired with videos of individuals vomiting (unconditioned stimuli; US) while we obtained subjective disgust reports. After conditioning, half of the participants were randomly assigned to cognitive reappraisal training aimed at decreasing their emotional response to the US and CS, while the other half received no such training. The findings showed that cognitive reappraisal participants demonstrated a reduction in learned disgust across sessions and further benefited from extinction. These findings suggest that cognitive reappraisal may be an effective strategy for attenuating learned disgust.

Oxytocin, social factors, and the expression of conditioned disgust (anticipatory nausea) in male rats.

Disgust has been proposed to have evolved as a means to rid the body and mouth of noxious substances and toxins, as well as to motivate and facilitate avoidance of contact with disease-causing organisms and infectious materials. Nonemetic species, such as the rat, show distinctive facial expressions, including the gaping reaction, indicative of nausea-based disgust. These conditioned disgust responses can be used to model anticipatory nausea in humans, which is a learned response observed following chemotherapy treatment. As social factors play a role in the modulation and expression of conditioned disgust responses in rats, and the nonapeptide, oxytocin (OT), is involved in the modulation of social behavior, the present study examined the effects of an OT antagonist, L-368 899, on the development and expression of socially mediated conditioned disgust in male rats. When administered 10 min before testing in a distinct context (different from the original conditioning context), L-368 899 (5 mg/kg) significantly decreased gaping behavior in rats that were conditioned with a social partner. LiCl-treated rats administered L-368 899 before testing also showed decreased social initiations toward their social partner. These findings suggest that OT may play a role in the modulation and expression of socially mediated conditioned disgust in rats.

Rodent sex differences in disgust behaviors (anticipatory nausea) conditioned to a context associated with the effects of the toxin LiCl: Inhibition of conditioning following immune stimulation with lipopolysaccharide

This study examined sex differences in the establishment of lithium chloride (LiCl)-induced conditioned disgust behavior (anticipatory nausea) to a distinct context in adult male and female rats. Also examined were potential sex differences in response to treatment with the bacterial endotoxin, lipopolysaccharide (LPS), and its effect on learning and memory. Twenty-nine male and 31 female naïve Long-Evans rats were injected (intraperitoneally; i.p.) with either 200μg/kg LPS or 0.9% (NaCl), 90min prior to i.p. injections of either 128mg/kg LiCl or 0.9% NaCl, and immediately placed into a distinctive context for 30min (repeated over 4 conditioning days, spaced 72h apart). 72h following the final conditioning day, each subject was re-exposed to the context on a drug-free test day where orofacial and somatic behaviors were recorded. Results showed that LiCl-treated females conditioned stronger disgust reactions, relative to LiCl-treated males, as evidenced by significantly higher frequencies of conditioned “gaping” behavior (p<0.02) and forelimb flailing (p<0.01) in females. Pre-treatment with LPS during conditioning led to strong inhibition of conditioned disgust behavior, to levels that did not significantly differ from controls. Although there was no apparent sex difference in the degree of inhibition produced by LPS in this context-based rodent disgust model, males did exhibit significantly greater 24h body weight losses following LPS injections on the first two conditioning days, relative to females. The results of the current study provide strong evidence for a sex difference in the establishment of anticipatory nausea, as well as, evidence for a sex difference in the acute-phase response to endotoxin treatment.

Functional brain networks underlying latent inhibition of conditioned disgust in rats

The present experiment examined the neuronal networks involved in the latent inhibition of conditioned disgust by measuring brain oxidative metabolism. Rats were given nonreinforced intraoral (IO) exposure to saccharin (exposed groups) or water (non-exposed groups) followed by a conditioning trial in which the animals received an infusion of saccharin paired (or unpaired) with LiCl. On testing, taste reactivity responses displayed by the rats during the infusion of the saccharin were examined. Behavioral data showed that preexposure to saccharin attenuated the development of LiCl-induced conditioned disgust reactions, indicating that the effects of taste aversion on hedonic taste reactivity had been reduced. With respect to cumulative oxidative metabolic activity across the whole study period, the parabrachial nucleus was the only single region examined which showed differential activity between groups which received saccharin-LiCl pairings with and without prior non-reinforced saccharin exposure, suggesting a key role in the effects of latent inhibition of taste aversion learning. In addition, many functional connections between brain regions were revealed through correlational analysis of metabolic activity, in particular an accumbens-amygdala interaction that may be involved in both positive and negative hedonic responses.

Shaking That Icky Feeling: Effects of Extinction and Counterconditioning on Disgust-Related Evaluative Learning

Learned disgust appears to play an important role in certain anxiety disorders, and can be explained by the process of evaluative conditioning, in which an affective evaluative reaction evoked by an unconditional stimulus (US) is transferred to a conditional stimulus (CS). Much remains unknown about how disgust-related evaluative learning can be effectively eliminated. Study 1 of the present investigation examined the effects of extinction on reducing the negative evaluation of a CS that was acquired during disgust conditioning. Participants completed acquisition trials, with a disgusting picture as US and two neutral pictures as CS (CS+ was paired with the US; CS- was unpaired), followed by extinction trials ("CS only"; experimental condition) or a filler task (control condition). Extinction trials reduced acquired US expectancy to the CS+, but did not extinguish negative evaluations of the CS+. Study 2 examined the effects of counterconditioning on evaluative learned disgust. After disgust acquisition trials, counterconditioning trials followed in which the CS+ was paired with a pleasant US (experimental condition) or a filler task (control condition). Counterconditioning trials reduced acquired US expectancy to the CS+ and reduced evaluative conditioned disgust. Implications of the potential differential effects of extinction and counterconditioning on evaluative learning for exposure-based treatment of specific anxiety disorders are discussed.

Don’t look now! Oculomotor avoidance as a conditioned disgust response.

Pavlovian conditioning paradigms have revealed fear learning tendencies that may be implicated in the etiology and maintenance of anxiety disorders. Given the prominence of disgust in certain anxiety disorders, it may be fruitful to study disgust learning in addition to fear learning. The present study utilized eye tracking to examine the effects of disgust conditioning on attentional bias, a phenomenon that characterizes anxiety disorders. Participants completed either a disgust condition, in which a face (conditioned stimulus; CS+) was paired with videos of individuals vomiting (unconditioned stimulus; US), or a negative condition in which a face was paired with videos of individuals being harmed in motor-vehicle accidents. Eye movements were used to measure attentional biases related to the USs and the CSs. In line with prior research, attentional avoidance was observed for the disgust CS+. However, this effect did not reach significance until after extinction and was linked to self-reported disgust postacquisition, yet decoupled from self-reported disgust postextinction. Attentional avoidance of the CS+ was not found in the negative condition, and postextinction differences in attentional bias for the CS+ between conditions were found to be mediated by differences in attentional bias for the US, as only the disgust US elicited attentional avoidance. Also, individual differences in disgust sensitivity were found to be associated with attentional avoidance of the disgust US, and this effect was mediated by self-reported disgust in response to the US. Further, disgust sensitivity was associated with attentional avoidance of the disgust CS+, and this effect was mediated by attentional avoidance of the disgust US. These findings provide new insight into a complex pattern of relations between disgust, evaluative learning, and attention that may have implications for the etiology and maintenance of certain anxiety disorders.

Uncovering the neurochemistry of reward and aversiveness

In a recent issue of Science was published an interesting report regarding the role of dopaminergic neurons on reward and aversiveness (Fiorillo, 2013). In contrast to what is claimed by some physiological and computational models (e.g., Schultz et al., 1997), the author provides a number of arguments to support the suggestion that reward and punishment have to be considered as two distinct neural dimensions. In particular, the author focuses on the evidence that dopaminergic neurons are selectively activated by rewarding outcomes, while these same neurons are insensitive to aversiveness. Thus, the author concludes a selective role for dopamine in detecting reward, and suggests that other (not dopaminergic) neurons should be sensitive to aversiveness. Recent insights suggest that these neurons may be serotonergic. For example, Limebeer et al. (2004) have shown that depletion of forebrain serotonin (5-HT) by 5,7 dihydroxytryptamine (5,7-DHT) lesions prevents induced conditioned disgust reactions such as “gaping,” the predominant conditioned rejection reaction (Parker, 2003) to “taste-related” aversive stimulation. Wright et al. (2010) have shown that learning to avoid odors associated with the malaise caused by ingesting toxins is mediated by serotonin. Moreover, it was recently demonstrated that partial depletion of 5-HT, in the insular cortex, prevents induced conditioned disgust reactions (Tuerke et al., 2012; see also Vicario, 2013, in press for a recent discussion about this issue). Finally, there is evidence of altered serotoninergic activity in Anorexia Nervosa (AN) (e.g., Jean et al., 2012), a psychiatric disorder characterized by a marked aversive sensitivity for food (Vicario, 2013, in press). The works mentioned above support the “two dimensions” hypothesis (Fiorillo, 2013) for reward and aversiveness. In particular, it is suggested that serotoninergic neurons could be the principal candidate of aversiveness processing. The evidence provided by these studies, which are based on the behavioral effects of block (removal) of serotonin, are difficult to interpret given the relevant number of variables that remains out of control. Thus, the definitive evidence could come from experiments that monitor activity of serotonin neurons on a fast timescale and relate it to reward and aversiveness in carefully controlled experiments. Moreover, future works might wish to investigate the existence of “ON” or “OFF” operating mechanism also for serotonin. In fact, if serotonin is the key neurotransmitter underlying aversiveness, there may be some serotonin neurons that signal aversive-ON (punishment) and others that signal aversive-OFF (absence of punishment and “negative reinforcement”).

Double dissociation between regulation of conditioned disgust and taste avoidance by serotonin availability at the 5-HT(3) receptor in the posterior and anterior insular cortex.

A taste associated with emetic drugs produces conditioned disgust reactions in rats (predominantly gaping), unlike nonemetic drugs that can still produce conditioned taste avoidance but not conditioned disgust. That difference suggests nausea is a prerequisite for learning disgust reactions to tastes. Depletion of forebrain serotonin (5-HT) by 5,7-dihydroxytryptamine (5,7-DHT) lesions of the dorsal raphe nucleus and median raphe nucleus prevents LiCl-induced conditioned disgust reactions (Limebeer et al., 2004). Here we demonstrate that partial depletion of 5-HT in the insular cortex (IC) prevents LiCl-induced conditioned disgust reactions. Furthermore, a double dissociation occurred in the partial regulation of disgust and taste avoidance by selective 5-HT(3) receptor antagonism/agonism in the posterior (granular) region of the IC and the anterior (dorsal agranular) region of the IC, respectively. Intracranial administration of the 5-HT(3) receptor antagonist, ondansetron (OND), to the posterior IC impaired the establishment of LiCl-induced conditioned gaping reactions, but not LiCl-induced conditioned taste avoidance (CTA). Likewise, posterior IC administration of the 5-HT(3) receptor agonist m-chlorophenylbiguanide (mCPBG) enhanced the establishment of LiCl-induced conditioned gaping and produced conditioned gaping on its own (which was prevented by intracranially administered OND), with no effect on CTA. On the other hand, anterior IC administration of OND partially reduced the establishment of LiCl-induced CTA, and mCPBG produced a weak CTA, both without effect on gaping. These results suggest that activation of 5-HT(3) receptors in the posterior IC is important for the production of nausea-induced conditioned disgust reactions, while activation of 5-HT(3) receptors in the anterior IC are involved in the production of CTA.

Dissociation of conditioned taste avoidance from conditioned disgust reactions induced by wheel running in rats

It is well established that wheel running in rats produces conditioned taste avoidance; that is, rats that run in wheels after consuming a novel-tasting solution later consume less of that solution than rats that do not run. In experiment 1, we found that wheel running also produces conditioned disgust reactions, indicated by gapes elicited by both the taste and context that were experienced before running. Experiment 2 showed that the conditioned disgust reactions were likely not due to running itself but to a by-product of running, the rocking of the wheel that occurs when the running stops. When rocking was reduced, the disgust reactions were also reduced, but consumption of the taste solution was not changed, showing dissociation of conditioned taste avoidance and disgust. These findings indicate that the taste avoidance induced by wheel running itself is more like the taste avoidance produced by rewarding drugs than that produced by nausea-inducing drugs.

Neural correlates of disgust- and fear-conditioned responses

The understanding of individual differences in responses to disgusting stimuli is important to gain more insight into the development of certain psychiatric disorders. The aim of this study was to investigate conditioned disgust responses, its potential overlap with conditioned fear responses (CRs) and the influence of disgust sensitivity on blood oxygen level–dependent responses. Yet even though current studies report evidence that disgust sensitivity is a vulnerability factor, the knowledge about the underlying neural mechanisms remains very limited. Two groups were exposed either to a disgust- or a fear-conditioning paradigm. Using functional magnetic resonance imaging, we identified a conjoint activated network including the cingulate cortex, the nucleus accumbens, the orbitofrontal cortex, and the occipital cortex within the disgust- and the fear-conditioning group. Moreover, we report evidence of increased insula activation in the disgust-conditioning group. In addition, functional connectivity analysis revealed increased interconnections, most pronounced within the insula in the high disgust sensitivity group compared with the low disgust sensitivity group. The conjunction results suggest that the conditioned responses in disgust and fear conditioning recruit the same neural network, implicating that different conditioned responses of aversive learning depend on a common neural network. Increased insula activation within the disgust-conditioning group might be attributable to heightened interoceptive processes, which might be more pronounced in disgust. Finally, the findings regarding disgust sensitivity are discussed with respect to vulnerability factors for certain psychiatric disorders.