As a component of the outer core of AMPAR complex, may be involved in synaptic transmission in the central nervous system. In hippocampal neurons, in presynaptic terminals, plays an important role in the final steps of neurotransmitter release, possibly by regulating Ca(2+)-sensing (PubMed:27052163). In the cerebellum, may inhibit SNARE complex formation and down-regulate short-term facilitation (PubMed:29056747). Component of the outer core of AMPAR complex (PubMed:22632720, PubMed:25915028). AMPAR complex consists of an inner core made of 4 pore-forming GluA/GRIA proteins (GRIA1, GRIA2, GRIA3 and GRIA4) and 4 major auxiliary subunits arranged in a twofold symmetry. One of the two pairs of distinct binding sites is occupied either by CNIH2, CNIH3 or CACNG2, CACNG3. The other harbors CACNG2, CACNG3, CACNG4, CACNG8 or GSG1L. This inner core of AMPAR complex is complemented by outer core constituents binding directly to the GluA/GRIA proteins at sites distinct from the interaction sites of the inner core constituents. Outer core constituents include at least PRRT1, PRRT2, CKAMP44/SHISA9, FRRS1L and NRN1. The proteins of the inner and outer core serve as a platform for other, more peripherally associated AMPAR constituents. Alone or in combination, these auxiliary subunits control the gating and pharmacology of the AMPAR complex and profoundly impact their biogenesis and protein processing (PubMed:22632720). Interacts with intersectin 1/ITSN1 (PubMed:26797119). Interacts with SNARE complex components, including SNAP25, STX1A, SYT1 and SYT2; this interaction may inhibit SNARE complex formation (PubMed:22832103, PubMed:27052163, PubMed:29056747). Neuron-specific expression throughout the brain, with the highest levels in the cerebellum, basal ganglia, hippocampus, substantia nigra, and neocortex (at protein level) (PubMed:22101681, PubMed:22243967, PubMed:22832103, PubMed:22632720, PubMed:25915028, PubMed:27052163, PubMed:27172900, PubMed:28007585, PubMed:29056747). Highly expressed also in spinal cord (at protein level) (PubMed:22101681, PubMed:22832103). Detected at very low levels in the heart, lung, kidney and skin (PubMed:22101681). At the mRNA level, expressed at low levels in the developing brain before 16 dpc. Expression markedly increases during early postnatal stages with a peak at P14. At this stage, expressed throughout the brain, with high levels in the cerebral cortex (cortical layers), hippocampus and cerebellum (granule cells and Purkinje cell layers). Progressively declines to relatively low levels in adulthood. At the protein level, first detected at very low levels at 17.5 dpc. Expression increases at early postnatal stages in the cerebral cortex, hippocampus and cerebellum. Expression increases to reach a plateau around P14, a period of intense synapse formation and rearrangement, and starts to slightly decrease around P90 (at protein level) (PubMed:27052163, PubMed:29056747). Mutant mice are normal at birth, but display paroxysmal movements at the onset of locomotion that persist in the adulthood. Adult animals present abnormal motor behaviors characterized by wild running and jumping in response to audiogenic stimuli that are ineffective in wild-type mice and an increased sensitivity to the convulsive effects of pentylentetrazol. Although the overall brain structure is not affected by the knockout, the thickness of the neocortex in young adult is significantly reduced in medial and caudal regions compared to their wild-type littermates. No significant differences are observed in the thickness of the CA1, CA3 and DG regions of the hippocampus, as well as for the molecular and granule layers of the cerebellum (PubMed:28007585). Mice with a conditional knockout in the central nervous system develop normally, but showed poor performance in motor coordination functions (PubMed:29056747). Belongs to the CD225/Dispanin family.