No abstract

The capacity of rodents to recognize and respond to emotional signs from a conspecific is a valuable adaptive behavior, which provides essential skills for species survival. However, repeated exposure to aversive situations may elicit maladaptive behavioral responses in subjects that experience noxious episodes and their colony members. Previous findings by our group demonstrated that living with a subject in neuropathic pain induces anxiogenic-like behaviors and hypernociception in mice. Whereas chronic pain may be considered a stressful stimulus, we extended our findings on stress-induced emotional transfer. For this purpose, we investigated whether cohabitation with a partner subjected to chronic restraint stress was able to promote alterations in anxiety-like behaviors, pain sensibility and defensive responses. Male Swiss mice were housed in pairs for 14days and then separated into control, stress, and cagemate groups. The stress group was subjected to 14days of restraint stress (1h/day) in the presence of the cagemates, while the pair-housed control group was left undisturbed. A day after last stress session control, stress, and cagemate groups were evaluated using elevated plus maze test, writhing test, and rat exposure test. Results demonstrated that chronic stress attenuated weight gain in the stress group. Moreover, cohabitation with mice subjected to chronic restraint stress induced anxiogenic-like behaviors, pain hypernociception, and alterations in defensive responses in both cagemate and stress groups. These preliminary findings suggest that chronic exposure to aversive stimulus may induce behavioral alterations even in observers.

resulted in increased itch, but decreased pain behaviors. When glutamatergic neurons in the PAG were selectively targeted we found that activation led to enhanced itch and decreased pain, while inhibition neurons produced decreased itch and increased pain. We conclude that the PAG bidirectionally modulates itch and pain signaling and is a neural control center for pruritus.

The affective component of pain may be shared among conspecifics through emotional contagion, a form of empathic expression. In this sense, reverberation of negative emotions could generate distress behavioral responses, such as pathological anxiety. Evidences reported that amygdala and its benzodiazepine receptors are involved in perception of pain in others. However, relatively little is known about the neural processes underlying emotional contagion induced by pain observation. In the present study, we investigated the effects of midazolam, an allosteric GABAergic receptor agonist, in anxiety-like behaviors induced by cohabitation with cagemate submitted to sciatic nerve constriction. For this purpose, we administrated systemic (0.5, 1.0 and 2.0 mg/kg) and intra-amygdala midazolam injections (3.0 and 30.0 nmol) in observer cagemates before elevated plus-maze (EPM) evaluation. We found that mice subjected to nerve constriction and their observer cagemates increased anxiety-like behavior in the EPM. Further, systemically (1.0 and 2.0 mg/kg) and intra-amygdala administration of midazolam (3.0 and 30 nmol) reverse this anxiogenic effect. Collectively, these results suggest that social interaction with a cagemate under chronic pain produces anxiety-like responses that could be blocked through midazolam application.