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Updated: Jul 26, 2026
10:05
A Large Lateral Craniotomy Procedure for Mesoscale Wide-field Optical Imaging of Brain Activity
Published on: May 7, 2017
Topographic plasticity in primary visual cortex is mediated by local corticocortical connections
Mike B Calford1, Layne L Wright, Andrew B Metha
1Psychobiology Laboratory, School of Psychology, The Australian National University, ACT 0200, Australia. mike.calford@newcastle.edu.au
Summary
Long-range horizontal connections in the visual cortex (V1) are crucial for developing ectopic receptive fields after retinal lesions. This neuroplasticity allows the brain to adapt to visual damage by reorganizing neural pathways.
Area of Science:
- Neuroscience
- Visual System Research
- Cortical Plasticity
Background:
- Monocular retinal lesions in cats create a lesion projection zone (LPZ) in the primary visual cortex (V1).
- Neurons in the LPZ exhibit normal receptive fields (RFs) for the intact eye and ectopic RFs for the lesioned eye.
- Long-range horizontal connections within V1 were hypothesized to mediate these ectopic RFs.
Purpose of the Study:
- To investigate the role of long-range horizontal connections in V1 in the formation of ectopic RFs following retinal lesions.
- To determine if deactivating these connections would abolish the ectopic RFs.
Main Methods:
- Adult cats with monocular retinal lesions were studied using neurophysiological recording techniques.
- Kainic acid, a neurotoxin, was used to selectively deactivate neurons at specific sites in V1.
- Responses to stimulation of both intact and lesioned eyes were recorded to assess RF locations and responsiveness.
Main Results:
- Deactivation of neurons via kainic acid injection at sites corresponding to ectopic RFs significantly blocked responses to lesioned-eye stimulation.
- Responses to intact-eye stimulation remained intact, serving as a control for direct kainic acid effects.
- Six out of seven cases showed a blockade of ectopic RF responsiveness.
Conclusions:
- Long-range horizontal projections within V1 are a dominant input contributing to retinal lesion-induced plasticity.
- These connections play a critical role in the brain's ability to reorganize visual processing after damage.
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