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Updated: Jul 24, 2025
Monocular Visual Deprivation and Ocular Dominance Plasticity Measurement in the Mouse Primary Visual Cortex
Published on: February 8, 2020
Regulatory role of the p38 MAPK/ATF2 signaling pathway in visual function and visual cortical plasticity in mice with
Guiqu Wang1, Yanqiong Tu2, Peixian Hou2
1Department of Ophthalmology, West China Hospital, Sichuan University, 37 Guoxue Xiang, Chengdu 610041, China; Department of Ophthalmology, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Luzhou 646000, China.
Background:
This study aimed to examine the role of the p38 mitogen-activated protein kinase (MAPK)/ activating transcription factor 2 (ATF2) signaling in visual function impairment and visual cortical plasticity in mice with monocular deprivation (MD).
Methods:
Visual behavioral tests, including visual water task, visual cliff test, and flash visual evoked potential, were performed on each group. We studied the density of dendritic spines and the synaptic ultrastructure by Golgi staining and transmission electron microscope. We performed Western blot and immunohistochemistry and detected the expression of ATF2, PSD-95, p38 MAPK, and phosphor-p38 MAPK in the left visual cortex.
Results:
In the MD + SB group, the visual acuity in deprived eyes substantially improved, the impairment of visual depth perception was alleviated, and the P wave amplitude and C/I ratio increased. The density of dendritic spines and the numerical density of synapses increased significantly, the width of the synaptic cleft decreased significantly, and the length of the active synaptic zone and the thickness of post-synaptic density (PSD) increased substantially. The protein expression of phosphor-p38 MAPK decreased, whereas that of PSD-95 and ATF2 increased significantly.
Conclusions:
Inhibiting the phosphorylation of p38 MAPK and negative feedback upregulated ATF2 expression, alleviated damage to visual function, and protected against synaptic plasticity in mice with MD.
