Disabling Gβγ-SNAP-25 interaction in gene targeted mice results in enhancement of LTP at Schaffer collateral-CA1 synapses in hippocampus
In: Neuroreport, 2019
academicJournal
Zugriff:
Three SNARE proteins, SNAP-25, syntaxin 1A, and VAMP2 or synaptobrevin 2, constitutes the minimal functional machinery needed for the regulated secretion of neurotransmitters. Dynamic changes in the regulated release of neurotransmitters are associated with the induction of long-term plasticity at central synapses. In vitro studies have validated the C-terminus of SNAP-25 as a target for inhibitory G(i/o)-coupled GPCRs at a number of synapses. The physiological consequences of the interaction between G(i/o) proteins and SNAP-25 in the context of activity-dependent long-term synaptic plasticity are not well understood. Here, we report direct ex vivo evidence of the involvement of the C-terminus of SNAP-25 in inducing long-term potentiation (LTP) of synaptic strength at Schaffer collateral-CA1 synapses using a gene targeted mouse model with truncated C-terminus (carboxyl terminus) of SNAP-25. It has been shown previously that truncation of the three extreme C-terminal residues in SNAP-25Δ3 homozygote mice reduces its interaction with the inhibitory Gβγ subunits two fold. In in vitro hippocampal slices, we show that these SNAP-25Δ3 mice express significantly larger magnitude of LTP at hippocampal Schaffer collateral-CA1 synapses.
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Disabling Gβγ-SNAP-25 interaction in gene targeted mice results in enhancement of LTP at Schaffer collateral-CA1 synapses in hippocampus
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Autor/in / Beteiligte Person: | Irfan, Muhammad ; Zurawski, Zack ; Hamm, Heidi ; Bark, Christina ; Stanton, Patric K. |
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Zeitschrift: | Neuroreport, 2019 |
Veröffentlichung: | 2019 |
Medientyp: | academicJournal |
DOI: | 10.1097/WNR.0000000000001258 |
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