Nitric oxide regulates synaptic transmission between spiny projection neurons.

Publication Type	Academic Article
Authors	Sagi Y, Heiman M, Peterson J, Musatov S, Scarduzio M, Logan S, Kaplitt M, Surmeier D, Heintz N, Greengard P
Journal	Proc Natl Acad Sci U S A
Volume	111
Issue	49
Pagination	17636-41
Date Published	11/20/2014
ISSN	1091-6490
Keywords	Basal Ganglia, Guanylate Cyclase, Neurons, Nitric Oxide, Synaptic Transmission, gamma-Aminobutyric Acid
Abstract	Recurrent axon collaterals are a major means of communication between spiny projection neurons (SPNs) in the striatum and profoundly affect the function of the basal ganglia. However, little is known about the molecular and cellular mechanisms that underlie this communication. We show that intrastriatal nitric oxide (NO) signaling elevates the expression of the vesicular GABA transporter (VGAT) within recurrent collaterals of SPNs. Down-regulation of striatal NO signaling resulted in an attenuation of GABAergic signaling in SPN local collaterals, down-regulation of VGAT expression in local processes of SPNs, and impaired motor behavior. PKG1 and cAMP response element-binding protein are involved in the signal transduction that transcriptionally regulates VGAT by NO. These data suggest that transcriptional control of the vesicular GABA transporter by NO regulates GABA transmission and action selection.
DOI	10.1073/pnas.1420162111
PubMed ID	25413364
PubMed Central ID	PMC4267338