Target Personification Influences the Positive Emotional Link Between Generating and Implementing Malevolently Creative Ideas

Research on malevolent creativity has rarely linked the generation of harmful ideas with their implementation (i.e., malevolent innovation). To explain why people might act upon their malevolently creative ideas, we drew on affective events theory. Specifically, given evidence that aggressive and creative thought events can elicit positive emotions, we argued that generating new and harmful ideas can evoke positive emotional states that make malevolent innovation a more desirable course of action. We first tested our mediational pathway in two studies with different malevolent creativity tasks. Finding only partial support for our predictions in Study 1 (N = 126), but full support in Study 2 (N = 296), we reflected on our study tasks and suspected that our mixed results may have occurred because the target of ideas in Study 2 embodied more human qualities than in Study 1. Thus, we integrated theory on target personification to see if assigning personhood to a target moderated the malevolent creativity-innovation pathway. We tested our updated model in Study 3 (N = 214) and found that the indirect effect of malevolent creativity on the desire to implement ideas (through positive emotions) was indeed conditional upon individuals’ personification of a target. Plain Language Summary Little research has examined why and when people might act upon their malevolently creative (i.e., new and harmful) ideas. Given evidence that aggression and creativity can both arouse positive emotional states, it may be possible that forming malevolently creative ideas can make people feel more positively about implementing them later on. However, our research findings paint a more nuanced picture, suggesting that the emotional link between generating and implementing malevolently creative ideas only occurs when people see their targets as more human-like (i.e., they can assign personhood to their targets)

Induction of Long-Term Hyperexcitability by Memory-Related cAMP Signaling in Isolated Nociceptor Cell Bodies

Persistent hyperactivity of nociceptors is known to contribute significantly to long-lasting sensitization and ongoing pain in many clinical conditions. It is often assumed that nociceptor hyperactivity is mainly driven by continuing stimulation from inflammatory mediators. We have tested an additional possibility: that persistent increases in excitability promoting hyperactivity can be induced by a prototypical cellular signaling pathway long known to induce late-phase long-term potentiation (LTP) of synapses in brain regions involved in memory formation. This cAMP-PKA-CREB-gene transcription-protein synthesis pathway was tested using whole-cell current clamp methods on small dissociated sensory neurons (primarily nociceptors) from dorsal root ganglia (DRGs) excised from previously uninjured ( naïve ) male rats. Six-hour treatment with the specific Gαs-coupled 5-HT4 receptor agonist, prucalopride, or with the adenylyl cyclase activator forskolin induced long-term hyperexcitability (LTH) in DRG neurons that manifested 12-24 h later as action potential (AP) discharge (ongoing activity, OA) during artificial depolarization to -45 mV, a membrane potential that is normally subthreshold for AP generation. Prucalopride treatment also induced significant long-lasting depolarization of resting membrane potential (from -69 to -66 mV), enhanced depolarizing spontaneous fluctuations (DSFs) of membrane potential, and produced trends for reduced AP threshold and rheobase. LTH was prevented by co-treatment of prucalopride with inhibitors of PKA, CREB, gene transcription, or protein synthesis. As in the induction of synaptic memory, many other cellular signals are likely to be involved. However, the discovery that this prototypical memory induction pathway can induce nociceptor LTH, along with reports that cAMP signaling and CREB activity in DRGs can induce hyperalgesic priming, suggest that early, temporary, cAMP-induced transcriptional and translational mechanisms can induce nociceptor LTH that might last for long periods. The present results also raise the question of whether reactivation of primed signaling mechanisms by re-exposure to inflammatory mediators linked to cAMP synthesis during subsequent challenges to bodily integrity can reconsolidate nociceptor memory, extending the duration of persistent hyperexcitability