NYMC Faculty Publications
Disabling Gbetagamma-SNAP-25 Interaction in Gene-Targeted Mice Results in Enhancement of Long-Term Potentiation at Schaffer Collateral-CA1 Synapses in the Hippocampus
DOI
10.1097/WNR.0000000000001258
Journal Title
Neuroreport
First Page
695
Last Page
699
Document Type
Article
Publication Date
July 2019
Department
Cell Biology and Anatomy
Abstract
Three SNARE proteins, SNAP-25, syntaxin 1A, and VAMP2 or synaptobrevin 2, constitute 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 Gi/o-coupled G-protein coupled receptors at a number of synapses. The physiological consequences of the interaction between Gi/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 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-25[INCREMENT]3 homozygote mice reduces its interaction with the inhibitory Gbetagamma subunits two-fold. In in-vitro hippocampal slices, we show that these SNAP-25[INCREMENT]3 mice express significantly larger magnitude of long-term potentiation at hippocampal Schaffer collateral-CA1 synapses.
Recommended Citation
Irfan, M., Zurawski, Z., Hamm, H., Bark, C., & Stanton, P. (2019). Disabling Gbetagamma-SNAP-25 Interaction in Gene-Targeted Mice Results in Enhancement of Long-Term Potentiation at Schaffer Collateral-CA1 Synapses in the Hippocampus. Neuroreport, 30 (10), 695-699. https://doi.org/10.1097/WNR.0000000000001258