# Elucidating the Role of Dorsal Lateral Geniculate Nucleus Burst-Mode Firing in Retinal Inactivation Induced Recovery from Monocular Deprivation

> **NIH NIH F31** · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · 2022 · $46,752

## Abstract

Amblyopia is a common disorder of visual system development, resulting in poor visual acuity in one eye.
Though there has been much research to understand the pathophysiology of the disorder, treating older
children and adults with amblyopia remains a challenge. Interestingly, there have been clinical reports
suggesting gains in the visual acuity of the amblyopic eye may be possible in adults following removal of the
normal eye due to injury or disease. Motivated by these clinical reports, our lab recently discovered that
temporarily silencing the retina of the normal eye via intravitreal injection of the sodium channel blocker
tetrodotoxin (TTX) is effective at promoting a recovery in visual acuity in both cat and mouse models of
amblyopia. Amazingly, this treatment is effective in older, more treatment resistant animals and does not cause
any penalty to the injected eye. By elucidating the mechanism by which retinal inactivation is promoting
recovery from a period of amblyopic rearing in animal models, we have the potential to determine how to best
exploit this mechanism for the treatment of human amblyopia. It was initially hypothesized that silencing the
retina via TTX injection would result in reduced activity in the dorsal lateral geniculate nucleus (dLGN),
because the dLGN relays activity from retina to cortex. Surprisingly, this turned out to be incorrect; in actuality,
neurons in the dLGN exhibit more spontaneous bursting activity following retinal inactivation. The proposed
project will focus on investigating the hypothesis that this increase in dLGN burst mode firing is the mechanism
by which retinal inactivation drives recovery from amblyopic rearing. To investigate this hypothesis, we will first
describe dLGN activity following retinal inactivation via TTX with the use of chronic unit recordings. dLGN
bursting will then be pharmacologically blocked to determine whether dLGN bursting is necessary for TTX
mediated recovery from amblyopic rearing. Finally, dLGN burst-like activity will be imposed via optogenetic
manipulation in order to determine whether bursting is sufficient to drive recovery from a period of amblyopic
rearing. By enhancing our understanding of the role of dLGN activity in retinal inactivation induced recovery
from amblyopic rearing, this project has the potential to inform our future research and suggest novel clinical
approaches for treating amblyopia. This project will be carried out in the lab of Dr. Mark Bear in the Brain and
Cognitive Sciences Department (BCS) at the Massachusetts Institute of Technology (MIT). The Bear lab
contains all required equipment for the proposed project. All necessary training regarding required laboratory
techniques will be provided by senior lab members or through collaboration with other labs in BCS. The Bear
lab, BCS, and MIT will offer quality scientific and professional development resources to facilitate a successful
transition into the next stage of the applicant’s research car...

## Key facts

- **NIH application ID:** 10464250
- **Project number:** 1F31EY033996-01
- **Recipient organization:** MASSACHUSETTS INSTITUTE OF TECHNOLOGY
- **Principal Investigator:** Madison Leet
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $46,752
- **Award type:** 1
- **Project period:** 2022-04-01 → 2025-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10464250

## Citation

> US National Institutes of Health, RePORTER application 10464250, Elucidating the Role of Dorsal Lateral Geniculate Nucleus Burst-Mode Firing in Retinal Inactivation Induced Recovery from Monocular Deprivation (1F31EY033996-01). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10464250. Licensed CC0.

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