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Mount Sinai Researchers find social isolation during key developmental windows drives long term changes to activity patterns of neurons involved in initiating social approach in an animal model.

Corresponding Author: Hirofumi Morishita, MDPhD, together with Schahram Akbarian MDPhD Icahn School of Medicine at Mount Sinai, New York, and other coauthors (first author Lucy Bicks).

Bottom Line: 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.

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Results: Social behavior is composed of interactions where mice are actively exploring conspecifics 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.

Why the Research Is Interesting: 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.

Who: Mouse models deprived of social experience during the juvenile period.

When: Mice were deprived of social experience during a juvenile phase and their behavior and physiology were examined in adulthood.

What: The study measured activity of parvalbumin expressing inhibitory neurons during social interaction as well as input drive to these neurons.

How: We measured parvalbumin expressing inhibitory neuron activity during social behavior and manipulated activity of these neurons using advanced technologies.

Study Conclusions: Social experience early in life alters specific patterns of parvalbumin expressing inhibitory neurons in prefrontal cortex. This pattern of activity is essential for active social approach behavior in mice.

Paper Title: Prefrontal parvalbumin interneurons require juvenile social experience to establish adult social behavior.

Source:

The Mount Sinai Hospital / Mount Sinai School of Medicine

Journal reference:

Bicks, L.K., et al. (2020) Prefrontal parvalbumin interneurons require juvenile social experience to establish adult social behavior. Nature Communications. doi.org/10.1038/s41467-020-14740-z.

Two grants will fund interdisciplinary research at the Beckman Institute for Advanced Science and Technology, including a look at how neurons and muscle cells communicate with each other and also to develop a drug delivery system for treatment of Alzheimer's disease.

The grant from the National Science Foundation will facilitate the study of how neurons and muscle cells communicate with each other.

My group is interested in engineering functional muscle and using it to assemble autonomous bioactuator systems.

The muscle engineered in vitro is not the same as the muscles in our body because the system does not have any innervating motor neurons. This project is to understand how we can facilitate the innervation of the neurons into the muscle."

Hyunjoon Kong, a Robert W. Schafer professor of chemical and biomolecular engineering

Kong's lab will collaborate with Gabriel Popescu, a professor of electrical and computer engineering, and Martha Gillette, a professor of cell and developmental biology. All are affiliated with the Beckman Institute.

In addition to studying how the neurons and muscle cells communicate, the Kong group will also look at the interaction between neurons and glial cells, which influence neuronal activity. "Although glial cells are not well characterized, they are known to provide certain signals that make the neurons transmit their electrical signals," Kong said.

"I will be working with Martha Gillette's group, who are experts in neurobiology and can guide us in what type of neural cells to look at," Kong said. "Popescu group members are experts at imaging intracellular events and we want to use their imaging techniques to demonstrate the interaction between the neurons and the muscle cells."

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Members of the Kong group hope that the study will enable them to understand how neurons can be reactivated in injured muscle, which can help improve the treatment of various neuromuscular disorders and acute muscle injuries.

The second grant, from the Alzheimer's Foundation, will fund research by the Kong group in collaboration with Hee Jung Chung, an associate professor of molecular and integrative physiology and Beckman Institute faculty member.

The grant will study how a drug that has the potential to treat Alzheimer's disease can be delivered into the body. The drug was developed to target tau proteins that, along with β-amyloid proteins, cause the disease. "Historically, researchers have been focused on treatments that reduce the β-amyloid proteins. However, a large group of patients do not respond to those treatments because the tau proteins are also responsible," Kong said.

The Kong group hopes to join the research effort that is now focusing on synthesizing nano-sized drug carriers that can target the tau protein. "The drug that targets tau proteins cannot be currently used because it is hydrophobic and therefore cannot dissolve in water," Kong said. "As a result, you cannot deliver it orally or through injection." The group will try to solve the problem by encapsulating the drug in a nanoparticle system that can be used to target the diseased regions of the brain.

Source:

Beckman Institute for Advanced Science and Technology