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A Minimal Model for G Protein–Mediated Synaptic Facilitation and Depression

¹ Department of Mathematics, Florida State University, Tallahassee, Florida 32306; ² Kasha Institute of Biophysics, Florida State University, Tallahassee, Florida 32306; ³ Departments of Physiology and Biophysics and of Pharmacology and Therapeutics, Cellular and Molecular Neurobiology Research Group, University of Calgary, Calgary T2N 4N1, Canada

Submitted 27 February 2003; accepted in final form 23 April 2003

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 G and G subunits. It is now clear that G directly inhibits Ca²⁺ channels, putting them into a reluctant state. The effects of G depend on the specific and subunits present, as well as the subunit isoform of the N-type Ca²⁺ 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 Ca²⁺ 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 depression, 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 Ca²⁺ 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.

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