GSG1L encodes an atypical auxiliary subunit that negatively regulates AMPA receptor (AMPAR) function, contrasting with the enhancing effects of typical TARP auxiliary subunits 1. As a component of the inner core of AMPAR complexes, GSG1L modifies receptor gating by suppressing AMPAR-mediated synaptic transmission and uniquely speeding up receptor deactivation and desensitization in hippocampal neurons 1. The protein reduces calcium-permeable AMPAR function by decreasing weighted mean single-channel conductance and calcium permeability while increasing polyamine-dependent rectification 2. Structurally, GSG1L favors the AMPAR desensitized state through profound rearrangements in the receptor's extracellular domain, with ligand-binding domain dimers losing their symmetry 3. Intracellular spermine is essential for GSG1L's negative regulatory effects on channel conductance and recovery from desensitization 4. Functionally, GSG1L knockout enhances AMPAR transmission and causes deficits in long-term potentiation and behavioral abnormalities in object recognition tests 1. The maximum stoichiometry is two GSG1L subunits per AMPAR tetramer, similar to type II TARPs 5. GSG1L represents a unique class of auxiliary subunit that extends the functional repertoire of AMPAR regulation by suppressing rather than enhancing receptor function 6.