Presynaptic mechanisms underlying GABAB-receptor-mediated inhibition of spontaneous neurotransmitter release
Barış Alten, Natalie J. Guzikowski, Zack Zurawski, Heidi E. Hamm, Ege T. Kavalali
Abstract
signaling for both forms of release. In the case of spontaneous glutamate release, inhibition requires Gβγ interaction with the C terminus of the key fusion machinery component SNAP25, and it is modulated by synaptotagmin-1. Inhibition of spontaneous GABA release, on the other hand, is independent of these pathways and likely requires alternative Gβγ targets at the presynaptic terminal.
Topics & Concepts
GABAB receptorNeurotransmitterGlutamate receptorNeuroscienceMetabotropic glutamate receptorMetabotropic receptorNeuromodulationChemistryBiologyCell biologyReceptorBiochemistryAgonistCentral nervous systemNeuroscience and Neuropharmacology ResearchIon channel regulation and functionCellular transport and secretion