
Affect sharing, or emotional contagion, is the ability to vicariously feel the emotions of others, and is the basis of empathy. Researchers have discovered that the brain has specific neurons in the anterior cingulate cortex (ACC) that fire both when we feel pain and when we see someone suffering. In mice, these neurons help trigger fear responses when observing another person in distress. This discovery shows that empathy may be an innate biological process, not dependent solely on past experiences, and may help us better understand conditions such as autism and other disorders linked to empathy.
Affect sharing, also called emotional contagion, is the ability to feel and reflect the emotions of others, and is the basis of empathy. This process occurs because our brain has neural networks that are activated both when we experience an emotion and when we observe it in another person.
For example, when we see someone in fear or pain, our brains may react as if we were going through the same situation, triggering similar emotional and behavioral responses.

In rodents, this phenomenon can be measured by “vicarious freezing,” a behavior in which the animal freezes when witnessing another being subjected to painful stimuli.
The anterior cingulate cortex (ACC), a region of the brain associated with pain, negative affect, and social interactions, plays a central role in this process, being activated both when an individual feels pain and when observing another in distress.
To better understand how the brain processes this empathy for pain, researchers at the Institute for Basic Science in South Korea studied the activity of neurons in the anterior cingulate cortex in mice that observed others undergoing painful experiences.
Using an advanced imaging technique called calcium fluorescence, they analyzed the activation of these neurons in different situations: when the animals saw another in pain, when they directly felt pain, and when they witnessed an inanimate threat.

Different subregions within the prefrontal cortex. In the book: In Consciousness we Trust. License CC BY-NC-ND 4.0
The results showed that a specific group of neurons in the anterior cingulate cortex maintains a stable pattern of activity over time, encoding negative emotions linked to pain and contributing to vicarious freezing behavior.
In addition, the researchers found that certain neurons in the anterior cingulate cortex connect to the periaqueductal gray (PAG), an area of the brain involved in controlling reactions to fear and pain.
These neurons, and not those connected to the basolateral amygdala (BLA), appear to be responsible for transmitting the emotional information of pain, regulating the observational fear response.
This suggests that empathy for the pain of others may be more influenced by the affective experience than by a simple sensory perception of pain.

An experiment to study how mice react to fear observed in others. (a) In the experiment, an “observer” (OB) mouse and a “demonstrator” (DM) mouse are placed in separate but transparent cages. First, they explore the environment for 5 minutes. Then, the observer mouse watches the demonstrator receive small electric shocks to the feet for 4 minutes. This allows us to see whether the observer learns to associate the situation with fear, even without directly feeling the pain. (b) The study uses a technique called calcium imaging to record the activity of neurons in the anterior cingulate cortex (ACC), a region of the brain linked to pain and empathy. (c) The image shows the expression of a fluorescent protein (GCaMP6f), which is used to visualize the activity of brain cells in the ACC, with the help of a special lens implanted in the mouse brain. (d) A representative image shows the fluorescent signals that indicate the activity of neurons during the experiment. (e) The diagram illustrates three behaviors analyzed: the observer mouse freezing (when it becomes immobile out of fear), the demonstrator’s reaction to shock, and the demonstrator’s freezing after shock. (f) Graphs show the neuronal activity associated with each of these behaviors, highlighting how different brain cells respond to perceived and observed fear.
Empathy plays a crucial role in how we learn and respond to the environment. Previous studies have shown that the dorsomedial prefrontal cortex helps associate perceived threats with environmental stimuli and that the ventromedial prefrontal cortex regulates avoidance behaviors based on the observation of others’ distress.
However, the role of the anterior cingulate cortex in encoding the distress of others has not been fully understood. While some studies have analyzed anterior cingulate cortex activity in animals previously exposed to aversive experiences, little is known about its role in emotional contagion in individuals without prior experience with fear or pain.

This study revealed that the anterior cingulate cortex contains specific populations of neurons that encode the experience of pain in others, even if the observer has not experienced the same situation before.
This discovery reinforces the idea that sharing emotions does not depend solely on previous experiences, but rather on specialized neural circuits that enable innate empathy.
Furthermore, by identifying which areas of the brain are responsible for this transmission of emotions, scientists may in the future be able to better understand disorders linked to empathy, such as autism spectrum disorders or certain psychiatric conditions.
READ MORE:
Cortical representations of affective pain shape empathic fear in male mice
Jiye Choi, Young-Beom Lee, Dahm So, Jee Yeon Kim, Sungjoon Choi, Sowon Kim, and Sehoon Keum
Nature Communications, volume 16, Article number: 1937 (2025)
Abstract:
Affect sharing, the ability to vicariously feel others’ emotions, constitutes the primary component of empathy. However, the neural basis for encoding others’ distress and representing shared affective experiences remains poorly understood. Here, using miniature endoscopic calcium imaging, we identify distinct and dynamic neural ensembles in the anterior cingulate cortex (ACC) that encode observational fear across both excitatory and inhibitory neurons in male mice. Notably, we discover that the population dynamics encoding vicarious freezing information are conserved in ACC pyramidal neurons and are specifically represented by affective, rather than sensory, responses to direct pain experience. Furthermore, using circuit-specific imaging and optogenetic manipulations, we demonstrate that distinct populations of ACC neurons projecting to the periaqueductal gray (PAG), but not to the basolateral amygdala (BLA), selectively convey affective pain information and regulate observational fear. Taken together, our findings highlight the critical role of ACC neural representations in shaping empathic freezing through the encoding of affective pain.
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