# Retinal inputs signal through astrocytes to recruit interneurons into visual thalamus

> **NIH NIH R21** · VIRGINIA POLYTECHNIC INST AND ST UNIV · 2020 · $195,634

## Abstract

Currently there are no effective treatments for patients with deficits in subcortical visual circuits. In response to
this unmet need, NEI has issued an Audacious Goals Initiative with the goal of gaining new knowledge that will
contribute to the development of regenerative therapies aimed at restoring subcortical visual circuits. To
accomplish this goal, we need a better understanding of the cell and molecular mechanisms that drive the
formation of these circuits during development. Although we have made progress in our understanding of how
retinal axons target and innervate subcortical brain regions (such as the dorsal and ventral lateral geniculate
nuclei [dLGN and vLGN, respectively]), we lack critical knowledge about how other inputs and cells target
these regions. Inputs from the cortex, thalamic nuclei, brainstem nuclei and local interneurons act as
modulatory or inhibitory inputs in visual thalamus and play essential roles in the processing of visual
information. These inputs far outnumber retinal inputs in visual thalamus. Interestingly, the recruitment and
incorporation of these non-retinal inputs (and cells) into thalamic circuits are regulated by retinal inputs. For
example, retinal inputs are necessary for the recruitment of GABAergic interneurons into visual thalamus and
the incorporation of their inputs into visual circuits. This is critical since these inhibitory synapses enhance
spatial and temporal selectivity of visual information as it is transmitted through the thalamus. At present we
lack a clear understanding of the mechanisms through which retinal inputs influence GABAergic neuron
recruitment and incorporation into visual thalamus. This proposal specifically addresses this question by testing
whether a novel axo-glial-neuron signaling pathway exists in visual thalamus. Specifically, we will test whether
retinal axons release SHH to induce astrocyte expression of FGF15, and whether astrocyte-derived FGF15 is
necessary for interneuron recruitment into visual thalamus. Identifying the novel axon-glia-neuron signaling
pathway proposed here will be a significant step forward in our understanding of the role of glia in
thalamic development and in the mechanisms underlying subcortical visual circuit assembly.

## Key facts

- **NIH application ID:** 9986815
- **Project number:** 5R21EY030568-02
- **Recipient organization:** VIRGINIA POLYTECHNIC INST AND ST UNIV
- **Principal Investigator:** MICHAEL A FOX
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $195,634
- **Award type:** 5
- **Project period:** 2019-08-01 → 2022-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9986815

## Citation

> US National Institutes of Health, RePORTER application 9986815, Retinal inputs signal through astrocytes to recruit interneurons into visual thalamus (5R21EY030568-02). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/9986815. Licensed CC0.

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