Researchers Discover a Specific Brain Circuit Damaged by Social Isolation During Childhood

brain-circuit-damage
The Brain Cell

Researchers have discovered specific sub-populations of brain circuit (cells) in the prefrontal cortex, a key part of the brain that regulates social behavior, that are required for normal sociability in adulthood and are profoundly vulnerable to juvenile social isolation in mice.

Loneliness is recognized as a negative impact to mental health. As we find our self in a computer age with numerous internet platforms, there is growing sense of isolation among our your people in the society. The COVID-19 pandemic, which forced many countries to implement social distancing and school closures, magnifies the need for understanding the mental health consequences of social isolation and loneliness. While research has shown that social isolation during childhood, in particular, is detrimental to adult brain function and behavior across mammalian species, the underlying neural circuit mechanisms have remained poorly understood.

Brain Circuit Damaged Finding

A research team from the Icahn School of Medicine at Mount Sinai has now identified specific sub-populations of brain cells in the prefrontal cortex, a key part of the brain that regulates social behavior, that are required for normal sociability in adulthood and are profoundly vulnerable to juvenile social isolation in mice. The study findings, which appear in the August 31 issue of Nature Neuroscience, shed light on a previously unrecognized role of these cells, known as medial prefrontal cortex neurons projecting to the paraventricular thalamus, the brain area that relays signals to various components of the brain’s reward circuitry. If the finding is replicated in humans, it could lead to treatments for psychiatric disorders connected to isolation.

brain-circuit-damage-image
The Engine Room of The Human Body

“In addition to identifying this specific circuit in the prefrontal cortex that is particularly vulnerable to social isolation during childhood, we also demonstrated that the vulnerable circuit we identified is a promising target for treatments of social behavior deficits,” says Hirofumi Morishita, MD, PhD, Associate Professor of Psychiatry, Neuroscience, and Ophthalmology at the Icahn School of Medicine at Mount Sinai, a faculty member of The Friedman Brain Institute and the Mindich Child Health and Development Institute, and senior author of the paper. “Through stimulation of the specific prefrontal circuit projecting to the thalamic area in adulthood, we were able to rescue the sociability deficits caused by juvenile social isolation.”

Specifically, the team found that, in male mice, two weeks of social isolation immediately following weaning leads to a failure to activate medial prefrontal cortex neurons projecting to the paraventricular thalamus during social exposure in adulthood. Researchers found that juvenile isolation led to both reduced excitability of the prefrontal neurons projecting to the paraventricular thalamus and increased inhibitory input from other related neurons, suggesting a circuit mechanism underlying sociability deficits caused by juvenile social isolation. To determine whether acute restoration of the activity of prefrontal projections to the paraventricular thalamus is sufficient to ameliorate sociability deficits in adult mice that underwent juvenile social isolation, the team employed a technique known as optogenetics to selectively stimulate the prefrontal projections to paraventricular thalamus. The researchers also used chemogenetics in their study. While optogenetics enables researchers to stimulate particular neurons in freely moving animals with pulses of light, chemogenetics allows non-invasive chemical control over cell populations. By employing both of these techniques, the researchers were able to quickly increase social interaction in these mice once light pulses or drugs were administered to them.

“We checked the presence of social behavior deficits just prior to stimulation and when we checked the behavior while the stimulation was ongoing, we found that the social behavior deficits were reversed,” said Dr. Morishita.

Given that social behavior deficits are a common dimension of many neurodevelopmental and psychiatric disorders, such as autism and schizophrenia, identification of these specific prefrontal neurons will point toward therapeutic targets for the improvement of social behavior deficits shared across a range of psychiatric disorders. The circuits identified in this study could potentially be modulated using techniques like transcranial magnetic stimulation and/or transcranial direct current stimulation.

This work was supported by grants from the National Institutes of Health and the National Institute of Mental Health and The Simons Foundation.

Source: The Mount Sinai Hospital / Mount Sinai School of Medicine

11 Comments

  1. I am truly pleased to glance at this weblog posts which carries lots of valuable information, thanks for providing these kinds of information. Karry Langsdon Ellissa

  2. Hello! I could have sworn I’ve been to this blog before but after browsing through some of the post I realized it’s new to me. Anyways, I’m definitely happy I found it and I’ll be book-marking and checking back frequently!

  3. I intended to write you a bit of word to finally give many thanks the moment again just for the great opinions you have shown here. It is simply pretty generous of you to deliver publicly exactly what a few individuals could possibly have offered for sale as an e-book to get some dough for their own end, principally given that you might have done it if you ever considered necessary. Those advice likewise served to become fantastic way to realize that most people have similar passion just as my very own to grasp a little more in terms of this problem. I am sure there are numerous more fun times ahead for people who take a look at your blog post. Ismael Mengwasser

Leave a Reply

Your email address will not be published.


*