MIT Finds 30% of Adult Brain Synapses Are Silent
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- MIT neuroscientists found that about 30% of synapses in the adult mouse cortex are electrically "silent" — containing NMDA receptors but no AMPA receptors, keeping them inactive until recruited for new memories.
- Dimitra Vardalaki (lead author) and Mark Harnett (senior author) published the findings in Nature, with the discovery emerging serendipitously when the team spotted "filopodia everywhere" during unrelated dendritic imaging work.
- The eMAP technique — epitope-preserving Magnified Analysis of the Proteome, developed with co-author Kwanghun Chung — physically expands brain tissue, allowing researchers to study filopodia too small for conventional tools.
- Silent synapses can be "unsilenced" by pairing glutamate release with an electrical signal, which causes AMPA receptors to accumulate — a process Harnett noted works on dormant filopodia but fails on already-mature synapses, which have a higher plasticity threshold.
- Prior theoretical work by Stefano Fusi and Larry Abbott predicted the brain needs a mix of flexible and stable synapses; the MIT team says this study is the first direct evidence in a mammalian brain that filopodia serve as the flexible substrate for new learning.
- The researchers are now investigating whether similar silent synapses exist in human brains and how they shift with age or in neurological conditions like Alzheimer's, with Harnett suggesting filopodia's molecular players could eventually be targeted to restore flexible memory.
- Clues from addiction research had long hinted that silent synapses might reappear or persist in adults, since addiction is considered a form of maladaptive learning — a thread that informed the MIT team's investigation of whether these dormant connections survive past early development.
Why it matters: The study provides the first direct mammalian evidence for how the adult brain juggles learning new things with preserving old memories — roughly 30% of cortical synapses stay dormant as a reserve pool. If follow-up work confirms similar mechanisms in humans, the molecular players that maintain these flexible filopodia-based synapses could become targets for treating age-related memory decline and Alzheimer's-related synaptic dysfunction.
