A Small Motor Cortex Lesion Abolished Ocular Dominance Plasticity in the Adult Mouse Primary Visual Cortex and Impaired Experience-Dependent Visual Improvements.

Justyna Pielecka-Fortuna,Siegrid Löwel,Evgenia Kalogeraki,Franziska Greifzu

doi:10.1371/journal.pone.0137961

Abstract

It was previously shown that a small lesion in the primary somatosensory cortex (S1) prevented both cortical plasticity and sensory learning in the adult mouse visual system: While 3-month-old control mice continued to show ocular dominance (OD) plasticity in their primary visual cortex (V1) after monocular deprivation (MD), age-matched mice with a small photothrombotically induced (PT) stroke lesion in S1, positioned at least 1 mm anterior to the anterior border of V1, no longer expressed OD-plasticity. In addition, in the S1-lesioned mice, neither the experience-dependent increase of the spatial frequency threshold (“visual acuity”) nor of the contrast threshold (“contrast sensitivity”) of the optomotor reflex through the open eye was present. To assess whether these plasticity impairments can also occur if a lesion is placed more distant from V1, we tested the effect of a PT-lesion in the secondary motor cortex (M2). We observed that mice with a small M2-lesion restricted to the superficial cortical layers no longer expressed an OD-shift towards the open eye after 7 days of MD in V1 of the lesioned hemisphere. Consistent with previous findings about the consequences of an S1-lesion, OD-plasticity in V1 of the nonlesioned hemisphere of the M2-lesioned mice was still present. In addition, the experience-dependent improvements of both visual acuity and contrast sensitivity of the open eye were severely reduced. In contrast, sham-lesioned mice displayed both an OD-shift and improvements of visual capabilities of their open eye. To summarize, our data indicate that even a very small lesion restricted to the superficial cortical layers and more than 3mm anterior to the anterior border of V1 compromised V1-plasticity and impaired learning-induced visual improvements in adult mice. Thus both plasticity phenomena cannot only depend on modality-specific and local nerve cell networks but are clearly influenced by long-range interactions even from distant brain regions.

Highlights

Brain plasticity and learning are especially important after a brain lesion, such as a stroke, to enable rehabilitation
We showed that a photothrombotic lesion in primary somatosensory cortex (S1) completely abolished ocular dominance (OD)-plasticity in the binocular zone of V1, and abolished sensory learning in adult mice: neither the spatial frequency threshold (“visual acuity”) nor the contrast threshold (“contrast sensitivity”) of the open eye improved after monocular deprivation (MD) and daily testing in the optomotor setup [6]
We observed that 3-month-old mice with a small lesion in M2 had impaired visual cortex plasticity and reduced sensory learning

Summary

Introduction

Brain plasticity and learning are especially important after a brain lesion, such as a stroke, to enable rehabilitation. We showed that a photothrombotic lesion in primary somatosensory cortex (S1) completely abolished OD-plasticity in the binocular zone of V1, and abolished sensory learning in adult mice: neither the spatial frequency threshold (“visual acuity”) nor the contrast threshold (“contrast sensitivity”) of the open eye improved after MD and daily testing in the optomotor setup [6]. To investigate whether plasticity impairments from outside V1 are spatially restricted or can be triggered from more distant brain regions, we induced a small lesion in the motor cortex region M2. The learning-induced increases in both “visual acuity” and “contrast sensitivity” of the open eye were severely impaired in the lesioned animals. Even a small, superficial and distant cortical lesion can affect plasticity in V1 of the same hemisphere and impair learning-induced visual improvements in adult mice

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