Research
Antisense oligonucleotide silencing rescues neurodevelopmental deficits in AMPA receptor gain-of-function mice
Neuron · By Chih-Ming Chen, Yu-Min Huang, Chih-Ching Chung, Richard C. Johnson, Cheng-Ya Tsai, Yu-Han Chen, Han L. Tan, Fu-Yun Hsiao, Richard L. Huganir & Shu-Ling Chiu ·
The 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.
Who’s affected
- neuroscientists studying synaptic physiology
- researchers on autism and intellectual disability
- #neuroscience
- #ampa receptors
- #autism
- #intellectual disability
- #antisense oligonucleotides
- #gria1
Chen et al. show that a recurrent ASD/ID-associated GRIA1-A636T variant disrupts the postnatal restriction of AMPAR Ca2+ permeability. In knock-in mice, persistent Ca2+-permeable AMPAR activity leads to synaptic hyperexcitability, hippocampus-biased degeneration, and behavioral…
Timeline
Study by Chen et al. published in Neuron
cell.com
Antisense oligonucleotide silencing rescues neurodevelopmental deficits in AMPA receptor gain-of-function mice