# Development of Retinal Ganglion Cell types

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA SANTA CRUZ · 2020 · $386,398

## Abstract

Project Summary
 The retina transforms the visual scene into ~30 different channels of information, each mediated
by a unique type of retinal ganglion cell (RGC). RGC types differ in their morphology, functional
response properties, brain targets, and the behaviors in which they participate. For reasons that are not yet
known, different RGC types have different susceptibilities to cell death after optic nerve injury. Several
fundamental aspects of each RGC type remain unknown: how each develops and maintains its unique
characteristics, how each contributes to the visual response properties of neurons in the brain, and
contributes to visually induced behaviors. Filling this gap in knowledge is not only a prerequisite to
understand how the visual system functions, it is also necessary if we are to either salvage or regenerate
RGCs that can integrate into the retinal circuitry and maintain their function after injury or disease.
 Satb1 and Satb2 are expressed in mouse DS RGCs and removing Satb1 and Satb2 during
development leads to the loss of direction selective retinal responses. Experiments in Aim 1 are designed
to elucidate the role of Satb1 and Satb2 in RGC development and to test the hypothesis that On-Off DS
RGCs contribute to the formation of direction selective cells in the brain and to motion visual behavior.
 In Aim 2 we will test the hypothesis that Tbr2 is necessary and sufficient for the development and
maintenance of non-image forming RGCs. Tbr2 is expressed in newly differentiated RGCs and
expression continues into adulthood. Mice lacking retinal Tbr2 during development fail to form non-
image forming circuits and lose light-dependent reflexes. We will test the hypothesis that Tbr2 is required
for maintaining a non-image forming RGC fate and by over expressing Tbr2 we will determine if Tbr2 is
sufficient to change developing or adult RGCs to a non-image forming fate.
 In Aim 3 we will examine if Tbr2 is necessary and sufficient for neuroprotection of RGCs after
injury. The optic nerve crush assay is used as a model to study the mechanisms counter to degeneration,
namely RGC survival and regeneration. We find that Tbr2 expressing RGCs are selectively spared after
nerve crush. Experiments in this aim will determine the role of Tbr2 in RGC survival.
 Upon completion of these aims we will significantly advance our understanding of how direction
selectivity is generated during development, discover mechanisms used to maintain RGC health and
function after its incorporation into circuits, and discover new mechanisms of neuroprotection.

## Key facts

- **NIH application ID:** 9933033
- **Project number:** 5R01EY022117-09
- **Recipient organization:** UNIVERSITY OF CALIFORNIA SANTA CRUZ
- **Principal Investigator:** DAVID A FELDHEIM
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $386,398
- **Award type:** 5
- **Project period:** 2012-07-01 → 2022-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9933033

## Citation

> US National Institutes of Health, RePORTER application 9933033, Development of Retinal Ganglion Cell types (5R01EY022117-09). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9933033. Licensed CC0.

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