Nitric oxide regulates synaptic transmission between spiny projection neurons
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Sagi-2014-Nitric oxide regulat.pdf
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1.32 MB
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Author(s)
Sagi, Yotam
Heiman, Myriam
Peterson, Jayms D.
Musatov, Sergei
Scarduzio, Mariangela
Logan, Stephen M.
Kaplitt, Michael G.
Surmeier, Dalton J.
Heintz, Nathaniel
Greengard, Paul
Date Issued
December 2014
Journal
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences (U.S.)
Citation
Sagi, Yotam, Myriam Heiman, Jayms D. Peterson, Sergei Musatov, Mariangela Scarduzio, Stephen M. Logan, Michael G. Kaplitt, Dalton J. Surmeier, Nathaniel Heintz, and Paul Greengard. “Nitric Oxide Regulates Synaptic Transmission Between Spiny Projection Neurons.” Proceedings of the National Academy of Sciences 111, no. 49 (November 20, 2014): 17636–17641.
Version
Final published version
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.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Picower Institute for Learning and Memory
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DOI of Published Version
https://doi.org/10.1073/pnas.1420162111
