Visually driven activation in macaque areas V2 and V3 without input from the primary visual cortex.

Creating focal lesions in primary visual cortex (V1) provides an opportunity to study the role of extra-geniculo-striate pathways for activating extrastriate visual cortex. Previous studies have shown that more than 95% of neurons in macaque area V2 and V3 stop firing after reversibly cooling V1. Ho...

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Main Authors: Michael C Schmid, Theofanis Panagiotaropoulos, Mark A Augath, Nikos K Logothetis, Stelios M Smirnakis
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2009-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC2677457?pdf=render
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author Michael C Schmid
Theofanis Panagiotaropoulos
Mark A Augath
Nikos K Logothetis
Stelios M Smirnakis
author_facet Michael C Schmid
Theofanis Panagiotaropoulos
Mark A Augath
Nikos K Logothetis
Stelios M Smirnakis
author_sort Michael C Schmid
collection DOAJ
description Creating focal lesions in primary visual cortex (V1) provides an opportunity to study the role of extra-geniculo-striate pathways for activating extrastriate visual cortex. Previous studies have shown that more than 95% of neurons in macaque area V2 and V3 stop firing after reversibly cooling V1. However, no studies on long term recovery in areas V2, V3 following permanent V1 lesions have been reported in the macaque. Here we use macaque fMRI to study area V2, V3 activity patterns from 1 to 22 months after lesioning area V1. We find that visually driven BOLD responses persist inside the V1-lesion projection zones (LPZ) of areas V2 and V3, but are reduced in strength by approximately 70%, on average, compared to pre-lesion levels. Monitoring the LPZ activity over time starting one month following the V1 lesion did not reveal systematic changes in BOLD signal amplitude. Surprisingly, the retinotopic organization inside the LPZ of areas V2, V3 remained similar to that of the non-lesioned hemisphere, suggesting that LPZ activation in V2, V3 is not the result of input arising from nearby (non-lesioned) V1 cortex. Electrophysiology recordings of multi-unit activity corroborated the BOLD observations: visually driven multi-unit responses could be elicited inside the V2 LPZ, even when the visual stimulus was entirely contained within the scotoma induced by the V1 lesion. Restricting the stimulus to the intact visual hemi-field produced no significant BOLD modulation inside the V2, V3 LPZs. We conclude that the observed activity patterns are largely mediated by parallel, V1-bypassing, subcortical pathways that can activate areas V2 and V3 in the absence of V1 input. Such pathways may contribute to the behavioral phenomenon of blindsight.
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spelling doaj.art-9501b91297a34c4d8a02bf222c435eee2022-12-22T03:13:11ZengPublic Library of Science (PLoS)PLoS ONE1932-62032009-01-0145e552710.1371/journal.pone.0005527Visually driven activation in macaque areas V2 and V3 without input from the primary visual cortex.Michael C SchmidTheofanis PanagiotaropoulosMark A AugathNikos K LogothetisStelios M SmirnakisCreating focal lesions in primary visual cortex (V1) provides an opportunity to study the role of extra-geniculo-striate pathways for activating extrastriate visual cortex. Previous studies have shown that more than 95% of neurons in macaque area V2 and V3 stop firing after reversibly cooling V1. However, no studies on long term recovery in areas V2, V3 following permanent V1 lesions have been reported in the macaque. Here we use macaque fMRI to study area V2, V3 activity patterns from 1 to 22 months after lesioning area V1. We find that visually driven BOLD responses persist inside the V1-lesion projection zones (LPZ) of areas V2 and V3, but are reduced in strength by approximately 70%, on average, compared to pre-lesion levels. Monitoring the LPZ activity over time starting one month following the V1 lesion did not reveal systematic changes in BOLD signal amplitude. Surprisingly, the retinotopic organization inside the LPZ of areas V2, V3 remained similar to that of the non-lesioned hemisphere, suggesting that LPZ activation in V2, V3 is not the result of input arising from nearby (non-lesioned) V1 cortex. Electrophysiology recordings of multi-unit activity corroborated the BOLD observations: visually driven multi-unit responses could be elicited inside the V2 LPZ, even when the visual stimulus was entirely contained within the scotoma induced by the V1 lesion. Restricting the stimulus to the intact visual hemi-field produced no significant BOLD modulation inside the V2, V3 LPZs. We conclude that the observed activity patterns are largely mediated by parallel, V1-bypassing, subcortical pathways that can activate areas V2 and V3 in the absence of V1 input. Such pathways may contribute to the behavioral phenomenon of blindsight.http://europepmc.org/articles/PMC2677457?pdf=render
spellingShingle Michael C Schmid
Theofanis Panagiotaropoulos
Mark A Augath
Nikos K Logothetis
Stelios M Smirnakis
Visually driven activation in macaque areas V2 and V3 without input from the primary visual cortex.
PLoS ONE
title Visually driven activation in macaque areas V2 and V3 without input from the primary visual cortex.
title_full Visually driven activation in macaque areas V2 and V3 without input from the primary visual cortex.
title_fullStr Visually driven activation in macaque areas V2 and V3 without input from the primary visual cortex.
title_full_unstemmed Visually driven activation in macaque areas V2 and V3 without input from the primary visual cortex.
title_short Visually driven activation in macaque areas V2 and V3 without input from the primary visual cortex.
title_sort visually driven activation in macaque areas v2 and v3 without input from the primary visual cortex
url http://europepmc.org/articles/PMC2677457?pdf=render
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