title: Target-Specific Glycinergic Transmission from VGluT3-Expressing Amacrine Cells Shapes Suppressive Contrast Responses in the Retina.
abstract: Neurons that release more than one transmitter exist throughout the CNS. Yet, how these neurons deploy multiple transmitters and shape the function of specific circuits is not well understood. VGluT3-expressing amacrine cells (VG3-ACs) provide glutamatergic input to ganglion cells activated by contrast and motion. Using optogenetics, we find that VG3-ACs provide selective glycinergic input to a retinal ganglion cell type suppressed by contrast and motion (SbC-RGCs). Firing of SbC-RGCs is suppressed at light ON and OFF over a broad range of stimulus sizes. Anatomical circuit reconstructions reveal that VG3-ACs form inhibitory synapses preferentially on processes that link ON and OFF arbors of SbC-RGC dendrites. Removal of VG3-ACs from mature circuits reduces inhibition and attenuates spike suppression of SbC-RGCs in a contrast- and size-selective manner, illustrating the modularity of retinal circuits. VG3-ACs thus use dual transmitters in a target-specific manner and shape suppressive contrast responses in the retina by glycinergic transmission.
authors.affiliation: Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, Saint Louis, MO 63110, USA; Graduate Program in Neuroscience, Washington University School of Medicine, Saint Louis, MO 63110, USA.
authors.forename: Nai-Wen
authors.initials: NW
authors.lastname: Tien
authors.affiliation: Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, Saint Louis, MO 63110, USA; Graduate Program in Neuroscience, Washington University School of Medicine, Saint Louis, MO 63110, USA.
authors.forename: Tahnbee
authors.initials: T
authors.lastname: Kim
authors.affiliation: Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, Saint Louis, MO 63110, USA; Department of Neuroscience, Washington University School of Medicine, Saint Louis, MO 63110, USA; Department of Biomedical Engineering, Washington University School of Medicine, Saint Louis, MO 63110, USA; Hope Center for Neurological Disorders, Washington University School of Medicine, Saint Louis, MO 63110, USA. Electronic address: dkerschensteiner@wustl.edu.
authors.forename: Daniel
authors.initials: D
authors.lastname: Kerschensteiner
mesh_terms: D000200:Action Potentials; D025042:Amacrine Cells / Q000378:metabolism*; D026922:Amino Acid Transport Systems, Acidic / Q000378:metabolism*; D000818:Animals; D015350:Contrast Sensitivity; D003712:Dendrites / Q000378:metabolism; D005998:Glycine / Q000378:metabolism*; D008822:Mice, Transgenic; D012165:Retinal Ganglion Cells / Q000378:metabolism; D013569:Synapses / Q000378:metabolism; D009435:Synaptic Transmission
chemical_list: D026922:Amino Acid Transport Systems, Acidic; D005998:Glycine; C504941:Slc17a8 protein, mouse