Abstract:

Stress contagion refers to the phenomenon where people unconsciously absorb stress reactions from another individual in the stressed state, through observation or direct contact, and match their own physiological and psychological state to that individual. In experimental settings, individuals who experience stress are commonly referred to as demonstrators, while those who observe the demonstrator undergoing stress are referred to as observers. Sensory channels are important factors that influence the process of stress contagion, as different sensory channels transmit social information in varying ways. The experimental paradigm for stress contagion can be categorized into two types: vicarious stress and stress crossover. In the vicarious stress paradigm, the observer receives stress information transmitted by the demonstrator through one or multiple sensory channels, such as images, sounds, or pheromones that are emitted by the stressed demonstrator. In the stress crossover paradigm, the observer comes into direct contact with the demonstrator and receives stress information through multiple sensory channels after the demonstrator undergoes stress. Studies have found that different sensory information elicits similar behavioral responses during stress contagion, which are accompanied by decreased autonomic activity, increased anxiety-like behavior, and elevated cortisol levels. However, the underlying neural circuit and key regions differ depending on the type of sensory information. In stress contagion induced by visual information, the anterior cingulate cortex and insular cortex play crucial roles as key brain regions. On the other hand, in stress contagion induced by auditory information, the basolateral amygdala and periaqueductal gray are the key brain regions involved. The olfactory system’s primary receptors that receive stress pheromones are the grueneberg ganglion cell, while the basolateral amygdala and medial prefrontal cortex are the key areas responsible for stress transmission. Additionally, significant activation of the amygdala was observed in different types of stress contagion paradigms, suggesting that the amygdala may be a hotspot brain region for stress contagion. To date, no studies have investigated stress contagion induced by touch alone, and future research should explore the neural mechanisms underlying touch-induced stress contagion by developing new experimental paradigms. Additionally, future studies should aim to identify the specific brain regions that should be investigated based on the sensory channels that influence the neural mechanisms of stress contagion.

Key words: stress contagion, synchronization, sensory channel, stress response, amygdala