SynGAP is a GTPase-activating protein (GAP) that is highly concentrated in postsynaptic densities (PSDs). Although SynGAP has a role in synaptic plasticity, the underlying mechanism is not clear. A study now finds that SynGAP exerts its effects on this process via a structural role in synapses.

During chemically induced long-term potentiation (cLTP), SynGAP is dispersed from the PSD and AMPA glutamate receptors (AMPARs) are recruited. Here, expression of a GAP domain-inactivated form of SynGAP had no effect on cLTP-mediated SynGAP dispersal or AMPAR recruitment. Moreover, mice expressing this form of SynGAP exhibited normal LTP. This suggests that SynGAP GAP activity is not required for synaptic plasticity.