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Neuroplasticity

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.

Vision

Vision

Vision is the result of light being detected and transduced into neural signals by the retina of the eye. This information is then further analyzed and interpreted by the brain. First, light enters the front of the eye and is focused by the cornea and lens onto the retina—a thin sheet of neural tissue lining the back of the eye. Because of refraction through the convex lens of the eye, images are projected onto the retina upside-down and reversed.

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Related Experiment Video

Updated: May 6, 2026

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

Evidence for metaplasticity in the human visual cortex.

Tommaso Bocci¹, Matteo Caleo, Silvia Tognazzi

¹Unit of Neurology, Department of Clinical and Experimental Medicine, Pisa University Medical School, Pisa, Italy.

Journal of Neural Transmission (Vienna, Austria : 1996)

|October 29, 2013

Summary

This summary is machine-generated.

Metaplasticity, the reversal of brain stimulation effects, was observed in the visual cortex. Transcranial direct current stimulation (tDCS) priming altered responses to repetitive transcranial magnetic stimulation (rTMS), demonstrating visual cortex metaplasticity.

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Area of Science:

Neuroscience
Electrophysiology
Brain Stimulation

Background:

Metaplasticity describes the modulation of neural plasticity by prior stimulation.
Previous studies demonstrated metaplasticity in the motor cortex using combined transcranial direct current stimulation (tDCS) and repetitive transcranial magnetic stimulation (rTMS).
The existence and mechanisms of metaplasticity in the human visual cortex remained largely unexplored.

Purpose of the Study:

To provide direct electrophysiological evidence for metaplasticity in the human visual cortex.
To investigate how tDCS priming influences the effects of subsequent rTMS on visual evoked potentials (VEPs).
To determine if metaplasticity mechanisms maintain synaptic homeostasis in the visual cortex.

Main Methods:

Healthy subjects received anodal or cathodal tDCS over the occipital cortex (priming).
Following tDCS, subjects underwent low- (1 Hz) or high-frequency (5 Hz) rTMS.
Visual evoked potentials (VEPs) were recorded at different contrasts before and after the combined tDCS-rTMS protocol.

Main Results:

Anodal tDCS increased VEP amplitude, which was paradoxically reduced by 5 Hz rTMS.
Cathodal tDCS decreased VEP amplitude, which was reversed by 1 Hz rTMS.
These effects were observed on both N1 and P1 VEP components, with no changes in motor thresholds, indicating spatial selectivity.

Conclusions:

Preconditioning the visual cortex with tDCS effectively modulates the direction and magnitude of plasticity induced by subsequent rTMS.
These findings provide direct electrophysiological evidence for metaplasticity in the human visual cortex.
Metaplasticity mechanisms may serve to maintain synaptic strengths within a functional dynamic range in the visual cortex.