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  “Silent” NMDA synapses enhance motion sensitivity in a mature retinal circuit

Sethuramanujam, S., Yao, X., deRosenroll, G., Briggman, K. L., Field, G. D., & Awatramani, G. B. (2017). “Silent” NMDA synapses enhance motion sensitivity in a mature retinal circuit. Neuron, 96(5):.e3, pp. 1099-1111. doi:10.1016/j.neuron.2017.09.058.

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Sethuramunujam_Silent_2017.pdf (Publisher version), 13MB
 
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 Creators:
Sethuramanujam, S.1, Author
Yao, X.1, Author
deRosenroll, G.1, Author
Briggman, Kevin L.2, Author           
Field, G. D.1, Author
Awatramani, G. B.1, Author
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1External Organizations, ou_persistent22              
2Department of Computational Neuroethology, Center of Advanced European Studies and Research (caesar), Max Planck Society, ou_3034882              

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Free keywords: DSGC; E/I balance; NMDA; SBEM; arithmetic; contrast-invariant; retina; silent synapses; starburst
 Abstract: Retinal direction-selective ganglion cells (DSGCs) have the remarkable ability to encode motion over a wide range of contrasts, relying on well-coordinated excitation and inhibition (E/I). E/I is orchestrated by a diverse set of glutamatergic bipolar cells that drive DSGCs directly, as well as indirectly through feedforward GABAergic/cholinergic signals mediated by starburst amacrine cells. Determining how direction-selective responses are generated across varied stimulus conditions requires understanding how glutamate, acetylcholine, and GABA signals are precisely coordinated. Here, we use a combination of paired patch-clamp recordings, serial EM, and large-scale multi-electrode array recordings to show that a single high-sensitivity source of glutamate is processed differentially by starbursts via AMPA receptors and DSGCs via NMDA receptors. We further demonstrate how this novel synaptic arrangement enables DSGCs to encode direction robustly near threshold contrasts. Together, these results reveal a space-efficient synaptic circuit model for direction computations, in which "silent" NMDA receptors play critical roles.

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Language(s): eng - English
 Dates: 2017-11-052017-12-06
 Publication Status: Issued
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.1016/j.neuron.2017.09.058
PMID: 29107522
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Title: Neuron
  Abbreviation : Neuron
Source Genre: Journal
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Publ. Info: Cambridge, Mass. : Cell Press
Pages: - Volume / Issue: 96 (5) Sequence Number: .e3 Start / End Page: 1099 - 1111 Identifier: ISSN: 0896-6273
CoNE: https://pure.mpg.de/cone/journals/resource/954925560565