Specific neurons that secrete oxytocin in the brain are disrupted in a mouse model of autism, neuroscientists have found. Stimulating these neurons restored social behaviors in these mice. These findings could help to develop new ways to treat autism.

[u/mvea]

https://www.riken.jp/en/news_pubs/research_news/rr/20250207_1/index.html

[u/mvea]

I’ve linked to the news release in the post above. In this comment, for those interested, here’s the link to the peer reviewed journal article:

https://www.nature.com/articles/s41467-024-53092-w

Abstract

Selective vulnerability offers a conceptual framework for understanding neurodegenerative disorders such as Parkinson’s disease, where specific neuronal types are selectively affected and adjacent ones are spared. However, the applicability of this framework to neurodevelopmental disorders, particularly those characterized by atypical social behaviors, such as autism spectrum disorder, remains uncertain. Here we show that an embryonic disturbance, known to induce social dysfunction in male mice, preferentially impaired the gene expression crucial for neural functions in parvocellular oxytocin (OT) neurons—a subtype linked to social rewards—while neighboring cell types experienced a lesser impact. Chemogenetic stimulation of OT neurons at the neonatal stage ameliorated social deficits in early adulthood, concurrent with cell-type-specific sustained recovery of pivotal gene expression within parvocellular OT neurons. Collectively, our data shed light on the transcriptomic selective vulnerability within the hypothalamic social behavioral center and provide a potential therapeutic target through specific neonatal neurostimulation.

From the linked article:

Specific neurons that secrete the neuropeptide oxytocin in the brain are disproportionately disrupted in a mouse model of autism, RIKEN neuroscientists have found1. Artificially stimulating neurons restored social behaviors in these mice. These findings could help to develop new ways to treat autism.

Neurodevelopmental disorders such as autism spectrum disorder have been widely studied, but the molecular mechanisms that underlie them remain largely unknown.

They used the valproic-acid mouse model of autism spectrum disorder; such mice exhibit reduced social behaviors as a result of being exposed to the anti-epileptic drug valproic acid in the womb.

Miyamichi and his team found that they also have lower oxytocin levels in the brain region housing parvocellular oxytocin neurons that mediate social reward processes. Single-cell RNA sequencing revealed that many genes crucial for neural function were expressed differently in these cells compared to control mice and that oxytocin gene expression is significantly reduced.

This came as a surprise to the team. “Given the systemic effects of valproic acid, impacting the entire body of embryos without spatial or cell type specificity, we didn’t expect that certain cell types would be disproportionately affected,” says Miyamichi.

Even more surprising was the finding that stimulating these cells shortly after birth led to a gradual but significant increase in oxytocin expression. It also enhanced social behaviors, with mice displaying more exploratory interactions with other mice. Remarkably, a single activation during the neonatal stage had a lasting effect, restoring gene expression and improving social behaviors into young adulthood.

Together, the findings suggest that the concept of selective neuronal vulnerability is applicable to neurodevelopmental disorders and that stimulating the affected cells could restore their function.

[u/a_dogs_mother → u/mvea]

Wow, I wonder if it's possible to do something similar for ADHD, which is highly heritable. I imagine being able to stimulate newborn brains as a prophylactic for various neurodevelopmental disorders.

[u/sprucenoose → u/mvea]

Well if it has to be administered neonatally it is less somewhat exciting for those humans who are already born and have autism, but promising nonetheless.

[u/alwaysboopthesnoot → u/mvea]

They’ve been studying oxytocin and its relationship to autism and other neurological disorders since the late 1990s. The first study I remember is from 1999-2000, from Emory Univ in Atlanta. Multiple studies since then have theorized that its depression or stimulation in pregnant women or neonates can be predictive or protective for autism. Too much oxytocin can be damaging to brain cells blood vessels and retinal cells, and cause hemorrhages in the placenta, some organs incl. the brain, eyes and heart— and too little can cause depression, anxiety, lack of affect/expression of emotion and depressed sexual arousal, an increased appetite for food, significantly disrupt sleep patterns, and interfere with mother-child bonding at and after birth.