The effect of emotion intensity on time perception: a study with transcranial random noise stimulation

Emotional facial expressions provide cues for social interactions and emotional events can distort our sense of time. The present study investigates the effect of facial emotional stimuli of anger and sadness on time perception. Moreover, to investigate the causal role of the orbitofrontal cortex (OFC) in emotional recognition, we employed transcranial random noise stimulation (tRNS) over OFC and tested the effect on participants' emotional recognition as well as on time processing. Participants performed a timing task in which they were asked to categorize as "short" or "long" temporal intervals marked by images of people expressing anger, sad or neutral emotional facial expressions. In addition, they were asked to judge if the image presented was of a person expressing anger or sadness. The visual stimuli were facial emotional stimuli indicating anger or sadness with different degrees of intensity at high (80%), medium (60%) and low (40%) intensity, along with neutral emotional face stimuli. In the emotional recognition task, results showed that participants were faster and more accurate when emotional intensity was higher. Moreover, tRNS over OFC interfered with emotion recognition, which is in line with its proposed role in emotion recognition. In the timing task, participants overestimated the duration of angry facial expressions, although neither emotional intensity not OFC stimulation significantly modulated this effect. Conversely, as the emotional intensity increased, participants exhibited a greater tendency to overestimate the duration of sad faces in the sham condition. However, this tendency disappeared with tRNS. Taken together, our results are partially consistent with previous findings showing an overestimation effect of emotionally arousing stimuli, revealing the involvement of OFC in emotional distortions of time, which needs further investigation

A global experiment on motivating social distancing during the COVID-19 pandemic

Finding communication strategies that effectively motivate social distancing continues to be a global public health priority during the COVID-19 pandemic. This cross-country, preregistered experiment (n = 25,718 from 89 countries) tested hypotheses concerning generalizable positive and negative outcomes of social distancing messages that promoted personal agency and reflective choices (i.e., an autonomy-supportive message) or were restrictive and shaming (i.e., a controlling message) compared with no message at all. Results partially supported experimental hypotheses in that the controlling message increased controlled motivation (a poorly internalized form of motivation relying on shame, guilt, and fear of social consequences) relative to no message. On the other hand, the autonomy-supportive message lowered feelings of defiance compared with the controlling message, but the controlling message did not differ from receiving no message at all. Unexpectedly, messages did not influence autonomous motivation (a highly internalized form of motivation relying on one’s core values) or behavioral intentions. Results supported hypothesized associations between people’s existing autonomous and controlled motivations and self-reported behavioral intentions to engage in social distancing. Controlled motivation was associated with more defiance and less long-term behavioral intention to engage in social distancing, whereas autonomous motivation was associated with less defiance and more short- and long-term intentions to social distance. Overall, this work highlights the potential harm of using shaming and pressuring language in public health communication, with implications for the current and future global health challenges

Cannabinoid CB1 receptor blockade enhances the protective effect of melanocortins in hemorrhagic shock in the rat

Activation of peripheral cannabinoid CB1 receptors contributes to hemorrhagic hypotension, and endocannabinoids produced by macrophages and platelets may be mediators of this effect. A number of studies have provided evidence that functional links exist in the mechanisms of action of cannabinoids and opioid peptides; and opioids too play an important role in the pathophysiology of hemorrhagic hypotension and shock. On the other hand, melanocortin peptides, which are the main endogenous functional antagonists of opioid peptides, have an antishock effect in animals and humans. Thus, we investigated whether an interaction exists between endocannabinoids and the endogenous opioid/antiopioid system also in a condition of hemorrhagic shock and, particularly, whether the blockade of cannabinoid CB1 receptors potentiates the antishock effect of melanocortins, Urethane-anesthetized rats were stepwise bled until mean arterial pressure decreased to, and stabilized at, 21-23 mm Hg. In this model of hemorrhagic shock, which caused the death of all control rats within 30 min after vehicle (tween 80, 5% in saline) injection, the intravenous (i.v.) bolus injection of the cannabinoid CB1 receptor antagonist N-pip -eridino-5-[4-chlorophenyl]-1-[2,4 dichlorophenyl]-4-methyl-3-pyrazolecarboxaniide (SR141716A) increased mean arterial pressure, pulse pressure, respiratory rate and survival rate in a dose-related manner (0.1-3 mg/kg), an almost complete recovery of mean arterial pressure, pulse pressure and respiratory rate, and 100% survival at the end of the observation period (2 h), occurring with the dose of 3 mg/kg. The melanocortin ACTH-(1-24) (adrenocorticotropin) also produced in a dose-related manner (0.02-0.16 mg/kg i.v.) a restoration of cardiovascular and respiratory functions, and increased survival rate, an almost complete recovery and 100% survival at the end of the observation period (2 h) occurring with the dose of 0.16 mg/kg. When a subactive dose of SR141716A (0.2 mg/kg; 30% survival) was associated with a subactive dose of ACTH-(1-24) (0.02 mg/kg; 12% survival), a complete reversal of the shock condition was obtained with 100% survival at the end of the 2-h observation period. The present results show that the concurrent inhibition of both endogenous opioid and cannabinoid systems produces a reversal of hemorrhagic shock more effective than that produced by the inhibition of either of them. These data suggest that functional interactions between endocannabinoids and opioid/antiopioid are at work also in the pathophysiology of hemorrhagic shock. (C) 2002 Elsevier Science B.V. All rights reserved

Dallo studio del meccanismo d'azione delle melanocortine nello shock all'individuazione di trattamenti farmacologici causali, inoovativi ed efficaci per questa condizione patologica

I neuropeptidi melanocortinic (ACTH-MSH) hanno un effetto salvavita in condizioni di shock emorragico nell'animale e nell'uomo. Tale effetto è indipendente dal surrene, è mediato da recettori melanocortinici MC4 localizzati nel sistema nervoso centrale ed è accompagnato dalla normalizzazione dei livelli ematici di vari mediatori dello shock

Central nervous system is involved in the effect of melanocortins in myocardial ischemia.

Central nervous system is involved in the effect of melanocortins in myocardial ischemia

Involvement of the central nervous system in the protective effect of melanocortins in myocardial ischaemia/reperfusion injury

AbstractMelanocortin peptides exert, in rats, a protective effect in myocardial ischaemia followed by reperfusion, or permanent occlusion of a coronary artery. Moreover, melanocortins have an anti-shock effect. Since the mechanism of the life-saving effect of these peptides in haemorrhagic shock includes an essential brain loop, we aimed to determine whether the central nervous system (CNS) is also involved in the protective effect against the outcome of short-term myocardial ischaemia followed by reperfusion. Ischaemia was produced in anaesthetized rats by ligature of the left anterior descending coronary artery for 5 min. Reperfusion-induced ventricular tachycardia (VT), ventricular fibrillation (VF) and lethality, and the time-course of arterial blood pressure over 5 min following reperfusion were evaluated. Groups of 8-14 rats were used. Intravenous (i.v.) injection of ACTH-(1-24) (0.16-0.48 mg/kg) during the ischaemic period dose dependently reduced the incidence of VT, VF and of lethality. In saline-treated rats, coronary reperfusion caused VT in 100% animals, VF in 86%, and death in 86%, The highest dose of ACTH-(1-24) (0.48 mg/kg) completely prevented the occurrence of VT, VF and death in all rats (P < 0.005). Moreover, the melanocortin peptide prevented the fall in mean arterial pressure (MAP) occurring during reperfusion. Treatment with ACTH-(1-24) by the intracerebroventricular (i.c.v.) route also reduced the incidence of VT, VF and lethality, and prevented the fall in MAP in a dose dependent manner. Complete (100%) protection occurred with an i.c.v. dose (0.048 mg/kg) 10 times less than that needed by the i.v. route. The present data show that in the protective effect of melanocortin peptides against the injury after myocardial ischaemia/reperfusion, the i.c.v. route of administration is more effective than the i.v. route. They suggest that a CNS mechanism, not yet identified, may be involved