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Visual Agnosia

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Visual agnosia is a condition characterized by the inability to recognize visually presented objects despite having normal vision. For instance, a person with visual agnosia can describe the shape and color of an object but cannot identify or name it. This impairment does not affect their visual field, acuity, color vision, brightness discrimination, language, or memory. An example of this condition in a social setting is someone at a dinner party asking for "that silver thing with a round...

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Related Experiment Video

Updated: Aug 20, 2025

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

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

Published on: February 8, 2020

Neuromodulation in the developing visual cortex after long-term monocular deprivation.

Anju Malik¹, Abdelrahman B M Eldaly^1,2, Stephen K Agadagba¹

¹Department of Electrical Engineering, City University of Hong Kong, Hong Kong SAR, P. R. China.

Cerebral Cortex (New York, N.Y. : 1991)

|November 17, 2022

Summary

This summary is machine-generated.

Long-term monocular deprivation (LTMD) in juvenile mice alters neural dynamics in the non-deprived eye, while adult mice show changes in the deprived eye. These findings reveal age-dependent plasticity in the visual cortex.

Keywords:

fiber photometry local field potential (LFP)long-term monocular deprivation (LTMD)ocular dominance plasticity (ODP)

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Area of Science:

Neuroscience
Developmental Neuroscience
Visual System Research

Background:

Neural dynamics in the primary visual cortex (V1) are altered by critical period monocular deprivation (MD).
Previous research highlights chronic disruptions in V1 function (e.g., ocular dominance, acuity) after long-term monocular deprivation (LTMD).
Neuromodulation and neural synchrony alterations following LTMD remain less explored.

Purpose of the Study:

To investigate age-dependent differences in experience-dependent plasticity following LTMD.
To examine intracellular calcium signals and local field potential (LFP) alterations in juvenile versus adult mice.
To explore changes in brain oscillation power bands and phase-amplitude coupling (PAC) after LTMD.

Main Methods:

Utilized intracellular calcium imaging with fluorescent indicators to assess neuromodulatory changes.
Recorded local field potentials to analyze power spectrum of brain oscillations.
Quantified phase-amplitude coupling (PAC) to understand neural synchrony alterations.

Main Results:

Juvenile mice subjected to LTMD exhibited greater neuromodulatory changes in the non-deprived eye (NDE).
Adult mice subjected to LTMD showed a more pronounced response in the deprived eye (DE).
LTMD in juveniles altered delta, theta, and gamma oscillation power, enhancing delta-gamma PAC in the NDE; adult LTMD altered delta power and enhanced delta-gamma PAC in the DE.

Conclusions:

LTMD induces distinct age-dependent neuromodulatory and neural synchrony alterations in the primary visual cortex.
Juvenile plasticity is characterized by NDE-dominant changes, while adult plasticity shows DE-dominant responses.
Observed oscillatory and PAC markers are intrinsic to cortical processing and relevant across various nested oscillatory patterns during LTMD.