# The role of astrocytes in visual critical period plasticity

> **NIH NIH F32** · SALK INSTITUTE FOR BIOLOGICAL STUDIES · 2022 · $69,802

## Abstract

Project Summary/ Abstract
 Astrocytes play a crucial role in regulating the structure, physiology, and plasticity of neural circuits. The
visual critical period provides an experimentally tractable paradigm in which to better understand how astrocytic
factors can precisely modulate plasticity in cortical circuits. The critical period is a stereotyped developmental
period during which proper visual experience is essential for the normal establishment of cortical circuits. As
manipulations of visual input during the critical period lead to well-described cortical remodeling and lasting
changes, these paradigms can be used to study the role of astrocytic factors in this form of plasticity. Cyr61 is a
potential key astrocytic plasticity-regulating factor, as its mRNA expression increases throughout development
and decreases after plasticity manipulations, suggesting it may be an “anti-plasticity” factor acting to restrict
plasticity in adulthood. In Aim 1, the role of Cyr61 during the critical period will be examined by overexpressing
it selectively in astrocytes in the mouse visual cortex. Mice will undergo monocular deprivation which typically
results in cortical remodeling. Electrophysiology and in vivo imaging will be performed to assess remodeling
differences between Cyr61 overexpressing and control mice. If Cyr61 is inhibiting plasticity, then overexpressing
Cyr61 during the critical period is expected to reduce plasticity in response to monocular deprivation. Aim 2 asks
if reducing the expression of Cyr61 in adulthood is sufficient to re-open the critical period for plasticity. To address
this adult transgenic mice with Cyr61 knockout selectively in astrocytes will undergo monocular deprivation, and
plasticity assessed in the same way as Aim 1. If Cyr61 is inhibiting adult plasticity, then removing it from adult
astrocytes is predicted to increase the remodeling response to monocular deprivation. To determine how CYR61
regulates plasticity, Aim 3 uses mass spectrometry to identify binding partners of CYR61 protein. This will
contribute to understanding the mechanism of action and will provide future avenues of investigation. The goal
of these experiments is to examine whether specific astrocytic factors are necessary and sufficient to modulate
critical period plasticity. This research proposal has important implications for understanding how to promote
synaptic repair and circuit rewiring after neurological disease, damage, or developmental disruptions.
 The research and training plan will take place at the Salk Institute for Biological Studies, where there are
multiple opportunities for postdoctoral researchers to enhance their training experience. The Salk Institute hosts
a series of research seminars in which postdoctoral scholars both have the opportunity to interact with outside
faculty and to present their own research. Moreover, the proposed training plan will include weekly meetings with
the Sponsor to maintain progress, writing review...

## Key facts

- **NIH application ID:** 10536694
- **Project number:** 1F32EY033629-01A1
- **Recipient organization:** SALK INSTITUTE FOR BIOLOGICAL STUDIES
- **Principal Investigator:** Laura Sancho Fernandez
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $69,802
- **Award type:** 1
- **Project period:** 2022-09-01 → 2025-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10536694

## Citation

> US National Institutes of Health, RePORTER application 10536694, The role of astrocytes in visual critical period plasticity (1F32EY033629-01A1). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10536694. Licensed CC0.

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