Social isolation during adolescence drives long-term disruptions in social behavior
Social isolation during adolescence drives long-term disruptions in social behavior. Credit: CC0 Creative Commons
Mount Sinai Researchers find social isolation during key developmental windows drives long term changes to activity patterns of neurons involved in initiating social behavior in an animal model.
The research was led by Hirofumi Morishita, MD, PhD, together with Schahram Akbarian MD, PhD at the Icahn School of Medicine at Mount Sinai, New York, and other coauthors (first author Lucy Bicks).
Loneliness is increasingly being recognized as a serious threat to mental health and wellbeing in our society. Our study in an animal model shows that social isolation during adolescence leads to long-term disruptions in social behavior and disruptions to activity patterns of a type of inhibitory neuron in the brain, which are frequently disrupted in psychiatric disorders including Schizophrenia. Activity patterns of these inhibitory neurons are sufficient to rescue social deficits induced by juvenile social isolation.
Social behavior is composed of interactions where mice are actively exploring other mice or passively being explored. We find one population of neurons, parvalbumin-expressing inhibitory neurons, increases in activity prior to an active, but not a passive social interaction. Brief activity of these neurons is sufficient to promote increased active social behavior. Juvenile social isolation during adolescence disrupts the activity of these neurons, leading to a decoupling of their activity and subsequent active social behavior initiation. Increasing activity of these neurons in adult animals that were socially isolated during adolescence restores normal social behavior.
The findings help us to understand how social experience during key windows of development might shape long term behavioral outcomes through changes to specific circuits in the brain. Understanding how social experience shapes outcomes can help us to overcome social deficits in cases of early life trauma or in neurodevelopmental and psychiatric disorders with social deficits.
The study was carried out using mouse models deprived of social experience during the juvenile period and their behavior and physiology were examined in adulthood. The researchers measured the activity of parvalbumin-expressing inhibitory neurons during social interaction as well as input drive to these neurons. Neuronal activity was manipulated using advanced technologies.
The findings suggest that social experience early in life alters specific patterns of parvalbumin-expressing inhibitory neurons in the prefrontal cortex. This pattern of activity is essential for active social behavior in adult mice.
The study appears in Nature Communications.
Materials provided by The Mount Sinai Hospital / Mount Sinai School of Medicine. Content may be edited for clarity, style, and length.