Embodied Cognition and Humor: The Impact of Weight Sensations on Humor Experience and the Moderating Role of Gender

Research in the field of embodied cognition has shown that incidental weight sensations influence people’s evaluation of different issues. The present study expands the scope of weight-related embodiment research and investigates whether experienced funniness of cartoons is affected by haptic sensorimotor experiences. We found an interaction between gender and weight sensations (light versus heavy clipboard) on the experienced funniness of nonsense cartoons. The experienced funniness in male recipients was enhanced by heaviness, but this effect was reversed in the group of females. The effect was also present when inferring the funniness experience of other recipients. Moreover, the participants’ general mood was worsened by heaviness. Weight did not affect the extent to which serious social issues are considered with humor, but men showed a stronger tendency to do so. Overall, the results expand the current scope in embodiment research, highlight the necessity to consider inter-individual differences in this field and introduce new aspects to humor research.     

Differential roles for hippocampal areas CA1 and CA3 in the contextual encoding and retrieval of extinguished fear

Recent studies demonstrate that context-specific memory retrieval after extinction requires the hippocampus. However, the contribution of hippocampal subfields to the context-dependent expression of extinction is not known. In the present experiments, we examined the roles of areas CA1 and CA3 of the dorsal hippocampus in the context specificity of extinction. After pairing an auditory conditional stimulus (CS) with an aversive footshock (unconditional stimulus or US), rats received extinction sessions in which the CS was presented without the US. In Experiment 1, pretraining neurotoxic lesions in either CA1 or CA3 eliminated the context dependence of extinguished fear. In Experiment 2, lesions of CA1 or CA3 were made after extinction training. In this case, only CA1 lesions impaired the context dependence of extinction. Collectively, these results reveal that both hippocampal areas CA1 and CA3 contribute to the acquisition of context-dependent extinction, but that only area CA1 is required for contextual memory retrieval.     

Contextual and auditory fear conditioning are mediated by the lateral, basal, and central amygdaloid nuclei in rats

A large body of literature implicates the amygdala in Pavlovian fear conditioning. In this study, we examined the contribution of individual amygdaloid nuclei to contextual and auditory fear conditioning in rats. Prior to fear conditioning, rats received a large electrolytic lesion of the amygdala in one hemisphere, and a nucleus-specific neurotoxic lesion in the contralateral hemisphere. Neurotoxic lesions targeted either the lateral nucleus (LA), basolateral and basomedial nuclei (basal nuclei), or central nucleus (CE) of the amygdala. LA and CE lesions attenuated freezing to both contextual and auditory conditional stimuli (CSs). Lesions of the basal nuclei produced deficits in contextual and auditory fear conditioning only when the damage extended into the anterior divisions of the basal nuclei; damage limited to the posterior divisions of the basal nuclei did not significantly impair conditioning to either auditory or contextual CS. These effects were typically not lateralized, although neurotoxic lesions of the posterior divisions of the basal nuclei had greater effects on contextual fear conditioning when the contralateral electrolytic lesion was placed in the right hemisphere. These results indicate that there is significant overlap within the amygdala in the neural pathways mediating fear conditioning to contextual and acoustic CS, and that these forms of learning are not anatomically dissociable at the level of amygdaloid nuclei.     

Enhancement of auditory fear conditioning after housing in a complex environment is attenuated by prior treatment with amphetamine

Prior exposure to drugs of abuse has been shown to occlude the structural plasticity associated with living in a complex environment. Amphetamine treatment may also occlude some cognitive advantages normally associated with living in a complex environment. To test this hypothesis we examined the influence of prior exposure to amphetamine on fear conditioning in rats housed in either a standard or complex environment. Housing in a complex environment facilitated fear learning to an auditory conditioned stimulus (CS), but not to the training context, relative to animals housed singly or in a social group. Prior treatment with amphetamine eliminated this effect. These results indicate that living in a complex environment facilitates conditional freezing to an auditory CS, and that this effect is abolished by pretreatment with amphetamine.     

The central nucleus of the amygdala is essential for acquiring and expressing conditional fear after overtraining

The basolateral complex of the amygdala (BLA) is critical for the acquisition and expression of Pavlovian fear conditioning in rats. Nonetheless, rats with neurotoxic BLA lesions can acquire conditional fear after overtraining (75 trials). The capacity of rats with BLA lesions to acquire fear memory may be mediated by the central nucleus of the amygdala (CEA). To examine this issue, we examined the influence of neurotoxic CEA lesions or reversible inactivation of the CEA on the acquisition and expression of conditional freezing after overtraining in rats. Rats with pretraining CEA lesions (whether alone or in combination with BLA lesions) did not acquire conditional freezing to either the conditioning context or an auditory conditional stimulus after extensive overtraining. Similarly, post-training lesions of the CEA or BLA prevented the expression of overtrained fear. Lastly, muscimol infusions into the CEA prevented both the acquisition and the expression of overtrained fear, demonstrating that the effects of CEA lesions are not likely due to the destruction of en passant axons. These results suggest that the CEA is essential for conditional freezing after Pavlovian fear conditioning. Moreover, overtraining may engage a compensatory fear conditioning circuit involving the CEA in animals with damage to the BLA.