Physiological roles for neuromodulation via Gi/o GPCRs working through Gβγ–SNARE interaction
Author:
Publisher
Springer Science and Business Media LLC
Subject
Psychiatry and Mental health,Pharmacology
Link
http://www.nature.com/articles/s41386-019-0497-2.pdf
Reference6 articles.
1. Blackmer T, Larsen EC, Takahashi M, Martin TF, Alford S, Hamm HE. G protein βγ subunit-mediated presynaptic inhibition: regulation of exocytotic fusion downstream of Ca2+ entry. Science. 2001;292:293–297.
2. Photowala H, Blackmer T, Schwartz E, Hamm HE, Alford S. G protein βγsubunits activated by serotonin mediate presynaptic inhibition by regulating vesicle fusion properties. Proc Natl Acad Sci USA. 2006;103:4281–4286.
3. Hamid E, Church E, Wells CA, Zurawski Z, Hamm HE, Alford S. Modulation of neurotransmission by GPCRs is dependent upon the microarchitecture of the primed vesicle complex. J Neurosci. 2014;34:260–274.
4. Yim YY, Betke KM, McDonald WH, Gilsbach R, Chen Y, Hyde K, Wang Q, Hein L, Hamm HE. The in vivo specificity of synaptic G β and G γ subunits to the alpha2a adrenergic receptor at CNS synapses. Sci Rep. 2019;9:1718.
5. Gerachshenko T, Blackmer T, Yoon E-J, Bartleson C, Hamm HE, Alford S. G βγ acts at the C terminus of SNAP-25 to mediate presynaptic inhibition. Nat Neurosci. 2005;8:597–605.
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