Modulation of non-NMDA receptor gating by auxiliary subunits.

During the past decade, considerable evidence has accumulated that non-NMDA glutamate receptors (both AMPA and kainate subtypes) are modulated by the association of the core tetrameric receptor with auxiliary proteins that are integral components of native receptor assemblies. This short review focuses on the effect of two types of auxiliary subunits on the biophysical properties and kinetic behaviour of AMPA and kainate receptors at the level of single receptor molecules. Type I transmembrane AMPA receptor proteins increase the number of AMPA receptor openings that result from a single receptor activation as well as the proportion of openings to conductance levels above 30 pS, resulting in larger peak ensemble currents that decay more slowly and bi-exponentially. Co-expression of Neto1 and 2 with pore-forming kainate receptor subunits also increases the duration of bursts and destabilizes desensitized states, resulting in a rapid component of recovery and clusters of bursts that produce a slow component in desensitization decays. The distinct gating seen in the presence of auxiliary subunits reflects slow switching between gating modes with different single-channel kinetics and open probability. At any given time, the relative proportions of receptors in each gating mode determine both the shape and the amplitude of synaptic currents.