A minimal model for G protein-mediated synaptic facilitation and XXXX .

@entity141 @entity17535 @entity308
G protein-coupled receptors are ubiquitous in neurons, as well as other cell types. Activation of receptors by hormones or neurotransmitters splits the G protein heterotrimer into @entity17535 and Gbetagamma subunits. It is now clear that Gbetagamma directly inhibits @entity141 channels, putting them into a reluctant state. The effects of Gbetagamma depend on the specific beta and gamma subunits present, as well as the beta subunit isoform of the N-type @entity141 channel. We describe a minimal mathematical model for the effects of G protein action on the dynamics of synaptic transmission. The model is calibrated by data obtained by transfecting G protein and @entity141 channel subunits into tsA-201 cells. We demonstrate with numerical simulations that G protein action can provide a mechanism for either short-term synaptic facilitation or @entity308 , depending on the manner in which G protein-coupled receptors are activated. The G protein action performs high-pass filtering of the presynaptic signal, with a filter cutoff that depends on the combination of G protein and @entity141 channel subunits present. At stimulus frequencies above the cutoff, trains of single spikes are transmitted, while only doublets are transmitted at frequencies below the cutoff. Finally, we demonstrate that relief of G protein inhibition can contribute to paired-pulse facilitation.
