Our cognitive abilities come down to how well the connections, or synapses, between our brain cells transmit signals. Now a new study by researchers at MIT’s Picower Institute for Learning and Memory has dug deeply into the molecular mechanisms that enable synaptic transmission to show the distinct role of a protein that, when mutated, has been linked to causing intellectual disability.
The key protein, called SAP102, is one of four members of a family of proteins, called PSD-MAGUKs, that regulate the transport and placement of key receptors called AMPARs on the receiving end of a synapse. But how each member of the family works — for instance, as the brain progresses through development to maturity — is not well understood. The new study, published in the Journal of Neurophysiology, shows that SAP102 and other family members like PSD-95, work in different ways, a feature whose evolution may have contributed to the greater cognitive capacity of mammals and other vertebrates.
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