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• W3100731978 abstract "Abstract In presynaptic terminals membrane-delimited G i/o -mediated presynaptic inhibition is ubiquitous and acts through Gβγ to inhibit Ca 2+ entry, or directly at SNARE complexes to inhibit Ca 2+ -dependent synaptotagmin-SNARE complex interactions. At CA1-subicular presynaptic terminals 5-HT 1B and GABA B receptors colocalize. GABA B receptors inhibit Ca 2+ entry, whereas 5-HT 1B receptors target SNARE complexes. We demonstrate in male and female rats that GABA B receptors receptors alter P r , whereas 5-HT 1B receptors reduce evoked cleft glutamate concentrations allowing differential inhibition of AMPA and NMDA receptor EPSCs. This reduction in cleft glutamate concentration was confirmed by imaging glutamate release using a genetic sensor (iGluSnFR).Simulations of glutamate release and postsynaptic glutamate receptor currents were made. We tested effects of changes in vesicle numbers undergoing fusion at single synapses, relative placement of fusing vesicles and postsynaptic receptors, and the rate of release of glutamate from a fusion pore. Experimental effects of P r changes, consistent with GABA B receptor effects, were straightforwardly represented by changes in numbers of synapses. The effects of 5-HT 1B receptor-mediated inhibition are well-fit by simulated modulation of the release rate of glutamate into the cleft. Colocalization of different actions of GPCRs provide synaptic integration within presynaptic terminals. Train-dependent presynaptic Ca 2+ accumulation forces frequency-dependent recovery of neurotransmission during 5-HT 1B receptor activation. This is consistent with competition between Ca 2+ -synaptotagmin and Gβγ at SNARE complexes. Thus, stimulus trains in 5-HT 1B receptor agonist unveil dynamic synaptic modulation and a sophisticated hippocampal output filter that itself is modulated by colocalized GABA B receptors which alter presynaptic Ca 2+ . In combination these pathways allow complex presynaptic integration. Significance Statement Two G protein coupled receptors colocalize at presynaptic sites, to mediate presynaptic modulation by Gβγ, but one – a GABA B receptor inhibits Ca 2+ entry while another – a 5-HT 1B receptor competes with Ca 2+ -synaptotagmin binding to the synaptic vesicle machinery. We have investigated downstream effects of signaling and integrative properties of these receptors. Their effects are profoundly different. GABA B receptors alter P r leaving synaptic properties unchanged, while 5-HT 1B receptors fundamentally change properties of synaptic transmission, modifying AMPA receptor but sparing NMDA receptor responses. Co-activation of these receptors allows synaptic integration because of convergence of GABA B receptor alteration on Ca 2+ and the effect of this altered Ca 2+ signal on 5-HT 1B receptor signaling. This presynaptic convergence provides a novel form of synaptic integration." @default.
• W3100731978 created "2020-11-23" @default.
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• W3100731978 date "2020-11-12" @default.
• W3100731978 modified "2023-10-17" @default.
• W3100731978 title "Synaptic integration of subquantal neurotransmission by co-localized G protein coupled receptors in presynaptic terminals" @default.
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• W3100731978 doi "https://doi.org/10.1101/2020.11.12.362491" @default.
• W3100731978 hasPublicationYear "2020" @default.
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