Ligand gated cation channels of the AMPA subtype are composed of different GluA subunits and interact with a family of proteins termed transmembrane AMPA-receptor regulatory proteins (TARPs) also known as voltage gated calcium channel gamma subunits or CNAGs (1). These proteins regulate the surface expression and biophysical properties like the gating time of AMPA glutamate receptors (1). Six transmembrane AMPA receptor regulatory protein (TARP) isoforms, classified as Type I (γ-2, -3, -4, and -8) and Type II (γ-5 and -7), are discretely expressed in specific neuronal and glial populations and differentially regulate synaptic transmission throughout the brain (2). One key feature of TARP-gamma2 and TARP-gamma8 is the differential regulation of synaptic strength in the hippocampus that is determined by the number and density of AMPA glutamate receptors (3).
Especially, TARP-gamma8 shows high expression levels in the hippocampus and is only sparsely expressed in other brain areas (4).
The TARP-gamma3 gene locus shows a linkage to childhood absence epilepsy (CAE) (5).