# Glial Modulation of Electrical Synapses in the Retina

> **NIH NIH F31** · UNIVERSITY OF MINNESOTA · 2022 · $33,886

## Abstract

PROJECT SUMMARY
 Many neuronal cell types communicate with one another via electrical synapses, which allow the flow of
current and ions through channels called gap junctions. Electrical synapses play an integral role in fast
communication within sensorimotor processes, and in synchronous communication in many brain areas.
Though fast and synchronous communication is necessary for many central and peripheral brain functions, the
mechanisms behind gap junction modulation remain understudied. Studies in the retina have explored
neuromodulators and signaling cascades that lead to phosphorylation or dephosphorylation of gap junction
proteins, which alters the open probability of these channels. However, the role of glial cells in the modulation
of electrical synapse communication has not been previously addressed. Modulation of chemical synapse
communication by gliotransmission, or the release of molecules by glia, is well studied in the field of glial
biology. This project aims to determine if gliotransmission affects electrical synapse plasticity within the retina.
 Neurons of the light adaptation circuitry in the retina have mechanisms to facilitate the activation of
either the rod or cone pathways depending on ambient light levels. One such neuron, the AII amacrine cell,
facilitates this mechanism through the opening and closing of gap junctions at electrical synapses between
other AII cells and ON cone bipolar cells. The goal of this project is to determine if Müller glial cells play a role
in this transient plasticity. Müller glia are the principal astroglia of the retina which release gliotransmitters in
response to retinal activity. Aim 1 will determine if the gliotransmitter adenosine modulates gap junctions at AII
electrical synapses. Adenosine is a target of interest because adenosine levels increase in darkness. Aim 2 will
determine if stimulation or inhibition of Müller glia modulate gap junctions at AII electrical synapses. Müller cell
gliotransmission will be stimulated by CNO activation of Gq DREADDs, which will be targeted to Müller cells
with a viral vector under control of the GLAST promoter. The effect of Müller cell inhibition on AII electrical
synapses will be assessed using an IP3R2KO mouse model. Pharmacological antagonism of adenosine
receptors will reveal if adenosine mediates Müller glial modulation of these electrical synapses. The degree of
modulation will be determined using conductance measurements with dual whole-cell patch clamp
electrophysiology and neurobiotin tracing. The understanding of glial modulation of electrical synapses is
essential for clarifying electrical synapse function in the retina, as well as other systems, in health and
disease.

## Key facts

- **NIH application ID:** 10589506
- **Project number:** 3F31EY031578-02S1
- **Recipient organization:** UNIVERSITY OF MINNESOTA
- **Principal Investigator:** Chloe E Cable
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $33,886
- **Award type:** 3
- **Project period:** 2020-07-31 → 2023-07-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10589506

## Citation

> US National Institutes of Health, RePORTER application 10589506, Glial Modulation of Electrical Synapses in the Retina (3F31EY031578-02S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10589506. Licensed CC0.

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