Formation of retinal direction-selective circuitry initiated by starburst amacrine cell homotypic contact.
Abstract
A common strategy by which developing neurons locate their synaptic partners is through
projections to circuit-specific neuropil sublayers. Once established, sublayers serve
as a substrate for selective synapse formation, but how sublayers arise during neurodevelopment
remains unknown. Here we identify the earliest events that initiate formation of the
direction-selective circuit in the inner plexiform layer of mouse retina. We demonstrate
that radially-migrating newborn starburst amacrine cells establish homotypic contacts
on arrival at the inner retina. These contacts, mediated by the cell-surface protein
MEGF10, trigger neuropil innervation resulting in generation of two sublayers comprising
starburst-cell dendrites. This dendritic scaffold then recruits projections from circuit
partners. Abolishing MEGF10-mediated contacts profoundly delays and ultimately disrupts
sublayer formation, leading to broader direction tuning and weaker direction-selectivity
in retinal ganglion cells. Our findings reveal a mechanism by which differentiating
neurons transition from migratory to mature morphology, and highlight this mechanism's
importance in forming circuit-specific sublayers.
Type
Journal articlePermalink
https://hdl.handle.net/10161/16624Published Version (Please cite this version)
10.7554/elife.34241Publication Info
Ray, Thomas A; Roy, Suva; Kozlowski, Christopher; Wang, Jingjing; Cafaro, Jon; Hulbert,
Samuel W; ... Kay, Jeremy N (2018). Formation of retinal direction-selective circuitry initiated by starburst amacrine
cell homotypic contact. eLife, 7. 10.7554/elife.34241. Retrieved from https://hdl.handle.net/10161/16624.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Greg D. Field
Adjunct Associate Professor of Neurobiology
My laboratory studies how the retina processes visual scenes and transmits this information
to the brain. We use multi-electrode arrays to record the activity of hundreds of
retina neurons simultaneously in conjunction with transgenic mouse lines and chemogenetics
to manipulate neural circuit function. We are interested in three major areas. First,
we work to understand how neurons in the retina are functionally connected. Second
we are studying how light-adaptation and circadian rhythms a
Samuel Hulbert
Student
Jeremy N. Kay
Associate Professor of Neurobiology
We study how neural circuits devoted to specific visual processing tasks arise during
development of the retina, and the consequences for circuit function when development
goes wrong. The tools of mouse genetics are central to our approach, and we draw on
a wide range of molecular, genetic, and imaging methods.
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