Monocular Visual Deprivation and Ocular Dominance Plasticity Measurement in the Mouse Primary Visual Cortex

Monocular visual deprivation is an excellent experimental paradigm to induce primary visual cortical response plasticity. In general, the response of the cortex to the contralateral eye to a stimulus is much stronger than the response of the ipsilateral eye in the binocular segment of the mouse prim...

Full description

Saved in:
Bibliographic Details
Published inJournal of visualized experiments no. 156
Main Authors Chen, Ke, Zhao, Yilei, Liu, Ting, Su, Zhaohao, Yu, Huiliang, Chan, Leanne Lai Hang, Liu, Tiejun, Yao, Dezhong
Format Journal Article
LanguageEnglish
Published United States 08.02.2020
Online AccessGet full text

Cover

Loading…
More Information
Summary:Monocular visual deprivation is an excellent experimental paradigm to induce primary visual cortical response plasticity. In general, the response of the cortex to the contralateral eye to a stimulus is much stronger than the response of the ipsilateral eye in the binocular segment of the mouse primary visual cortex (V1). During the mammalian critical period, suturing the contralateral eye will result in a rapid loss of responsiveness of V1 cells to contralateral eye stimulation. With the continuing development of transgenic technologies, more and more studies are using transgenic mice as experimental models to examine the effects of specific genes on ocular dominance (OD) plasticity. In this study, we introduce detailed protocols for monocular visual deprivation and calculate the change in OD plasticity in mouse V1. After monocular deprivation (MD) for 4 days during the critical period, the orientation tuning curves of each neuron are measured, and the tuning curves of layer four neurons in V1 are compared between stimulation of the ipsilateral and contralateral eyes. The contralateral bias index (CBI) can be calculated using each cell's ocular OD score to indicate the degree of OD plasticity. This experimental technique is important for studying the neural mechanisms of OD plasticity during the critical period and for surveying the roles of specific genes in neural development. The major limitation is that the acute study cannot investigate the change in neural plasticity of the same mouse at a different time.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Undefined-1
ObjectType-Feature-3
content type line 23
ISSN:1940-087X
1940-087X
DOI:10.3791/60600