# Antisense oligonucleotide silencing rescues neurodevelopmental deficits in AMPA receptor gain-of-function mice

Source: [cell.com](https://www.cell.com/neuron/fulltext/S0896-6273(26)00809-3?rss=yes) · 2026-11-11 · Mind
Page: https://themorning.science/story/antisense-oligonucleotide-silencing-rescues-neurodevelopmental-deficits-in-ampa-5ef6768a4bb48cac
Kind: research · Impact: medium

## In brief

- Chen et al. report that the recurrent ASD/ID-associated GRIA1-A636T variant disrupts the postnatal restriction of AMPA receptor Ca2+ permeability.
- In knock-in mice, persistent Ca2+-permeable AMPAR activity leads to synaptic hyperexcitability and hippocampus-biased degeneration.
- Antisense oligonucleotide silencing rescued neurodevelopmental deficits in these mice.

## Why it matters

It shows that antisense silencing can rescue deficits in a mouse model of a GRIA1 variant linked to autism and intellectual disability, which bears on how such disorders might be studied and treated.

## Timeline

- 2026-11-11: Study by Chen et al. published in Neuron

## Coverage

- [Antisense oligonucleotide silencing rescues neurodevelopmental deficits in AMPA receptor gain-of-function mice](https://www.cell.com/neuron/fulltext/S0896-6273(26)00809-3?rss=yes) — cell.com, 2026-11-11

Tags: neuroscience, ampa receptors, autism, intellectual disability, antisense oligonucleotides, gria1

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Brief generated by AI (claude-haiku-5-5) from the reporting listed under Coverage. Headlines belong to their publishers. The Morning Science – https://themorning.science