Superior colliculus anatomy and neurochemistry remain intact following primary visual cortex lesion — The Association Specialists
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Superior colliculus anatomy and neurochemistry remain intact following primary visual cortex lesion (21474)

Melissa Chong 1 , Katrina Worthy 1 , Marcello Rosa 1 , Nafiseh Atapour 1
  1. Monash University, Clayton, VIC, Australia

Visual input from retina to primary visual cortex (V1) is necessary for proper vision1. Induced lesions in V1 in non-human primates cause blindness2 and have been shown to lead to widespread damage to the structures along the visual pathway, including lateral geniculate nucleus (LGN) and retina3, 4. Both of them undergo neurodegeneration and volume loss post-V1 lesion3, 4, and LGN in particular displays additional neurochemical changes5. The superior colliculus (SC), a layered midbrain structure facilitating polysensory and sensorimotor integration, has direct and indirect V1 connections6-9. We investigated in adult marmoset monkeys (Callithrix jacchus) if degenerative changes could be extended to SC. We also investigated the expression of orthodenticle homeobox 2 protein (Otx2) – a retinal protein that can be transported across axons towards other visual structures10, 11 – as a measure of change in SC neurochemistry following V1 lesion. Our study revealed that ipsilateral lesioned SC volume was not significantly different from contralateral or control/healthy SC, and SC volume shrinkage had little correlation with that observed in LGN. Estimates of total neuronal density and density of Otx2-positive neurons were similar between lesioned and control SC. Lesion induction age had no impact on Otx2 expression in the SC. Our data supports the idea that SC may be protected from detectable degeneration and volume loss as a result of V1 lesion by its widespread connectivity with structures other than V1. The absence of any detectable change in Otx2 staining supports the idea that SC neurochemistry remains unaffected by V1 lesion.

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