As animals evolved to become increasingly social, their chances of coming into contact with pathogens and catching infections from their companions increased, leading to a greater need for a strong immune system.
Though this link may seem like a logical one, researchers from the University of Virginia have shown for the first time that the immune system of mice directly controls the parts of the brain that are responsible for social behavior, indicating that the evolution of sociability may have occurred as a result of this immunity.
Writing in the journal Nature, the researchers explain how mice that were bred to lack a particular pathogen-fighting immune molecule called interferon gamma (IFN-γ) displayed social deficits and autism-like behavior when interacting with other mice. To try and figure out what was causing this they used functional magnetic resonance imaging (fMRI) to observe the animals’ brain activity.
In doing so, they discovered that certain brain regions in the prefrontal cortex (PFC) that are known to control social behavior had become hyperactive, much like they are in humans with autism.
Following this, the study authors injected the mice with IFN-γ, noting that this instantly caused them to behave like healthy mice, with no social abnormalities. When monitoring the neural activity of these rodents, the team found that the introduction of IFN-γ led to an increase in levels of a neurotransmitter called GABA, which inhibits neurons in the PFC, alleviating their hyperactivity.
Commenting on this discovery, study co-author Jonathan Kipnis explained in a statement that “the brain and the adaptive immune system were thought to be isolated from each other, and any immune activity in the brain was perceived as a sign of a pathology. And now, not only are we showing that they are closely interacting, but some of our behavior traits might have evolved because of our immune response to pathogens.”
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