التفاصيل البيبلوغرافية
| العنوان: |
SNAP25 differentially contributes to Gi/o-coupled receptor function at glutamatergic synapses in the nucleus accumbens. |
| المؤلفون: |
Manz, Kevin M., Zepeda, José C., Zurawski, Zack, Hamm, Heidi E., Grueter, Brad A. |
| المصدر: |
Frontiers in Cellular Neuroscience; 2023, p1-10, 10p |
| مصطلحات موضوعية: |
NUCLEUS accumbens, GLUTAMATE receptors, SYNAPSES, HISTAMINE receptors, OPIOID receptors, TRANSGENIC mice, NEUROPLASTICITY |
| مستخلص: |
The nucleus accumbens (NAc) guides reward-related motivated behavior implicated in pathological behavioral states, including addiction and depression. These behaviors depend on the precise neuromodulatory actions of Gi=o-coupled G-protein-coupled receptors (GPCRs) at glutamatergic synapses onto medium spiny projection neurons (MSNs). Previous work has shown that discrete classes of Gi=o-coupled GPCR mobilize Gbg to inhibit vesicular neurotransmitter release via t-SNARE protein, SNAP25. However, it remains unknown which Gai/o systems in the NAc utilize Gbg-SNARE signaling to dampen glutamatergic transmission. Utilizing patch-clamp electrophysiology and pharmacology in a transgenic mouse line with a C-terminal three-residue deletion of SNAP25 (SNAP2513) weaking the Gbg-SNARE interaction, we surveyed a broad cohort of Gi=o-coupled GPCRs with robust inhibitory actions at glutamatergic synapses in the NAc. We find that basal presynaptic glutamate release probability is reduced in SNAP2513 mice. While k opioid, CB1, adenosine A1, group II metabotropic glutamate receptors, and histamine H3 receptors inhibit glutamatergic transmission onto MSNs independent of SNAP25, we report that SNAP25 contributes significantly to the actions of GABAB, 5-HT1B=D, and m opioid receptors. These findings demonstrate that presynaptic Gi=o-coupled GPCRs recruit heterogenous effector mechanisms at glutamatergic synapses in the NAc, with a subset requiring SNA25-dependent Gbg signaling. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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