Even partial loss of the autism-linked gene SYNGAP1 impairs the brain’s ability to respond to sensory experiences, according to a new study in mice. The finding may help to explain why people with SYNGAP1 mutations tend to have learning difficulties and a high tolerance for pain.
The SYNGAP1 protein abounds at excitator synapses and shapes plasticity there, helping neighboring neurons to strengthen or weaken their connections. But it was previously unclear how SYNGAP1 affects ‘ensembles,’ groups of neurons with coordinated activity that are considered the “direct neural correlate of behavior and thought,” says lead researcher Gavin Rumbaugh, professor of neuroscience at Scripps Research in Jupiter, Florida.
To encode new information about a sensory experience, a neuronal ensemble needs to redistribute its activity: Some neurons ramp up their chatter while others dial it down, keeping the group’s overall activity the same. “It’s learning, basically,” Rumbaugh says.
That redistribution is defunct in ...
