ePoster

STRUCTURAL PLASTICITY IN THE MAGNOCELLULAR LAYERS OF THE CAT LATERAL GENICULATE NUCLEUS FOLLOWING PERINATAL AUDITORY DEPRIVATION

Nick Murphyand 1 co-author

McGill University

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS07-10AM-509

Presentation

Date TBA

Board: PS07-10AM-509

Poster preview

STRUCTURAL PLASTICITY IN THE MAGNOCELLULAR LAYERS OF THE CAT LATERAL GENICULATE NUCLEUS FOLLOWING PERINATAL AUDITORY DEPRIVATION poster preview

Event Information

Poster Board

PS07-10AM-509

Abstract

The brain exhibits a remarkable capacity to structurally and functionally reorganize following abnormal sensory experience. It remains unclear how intact visual areas such as the lateral geniculate nucleus (LGN) develop and compensate for lost auditory input following deafness. Exuberant retinal projections to the LGN visualized with the antibody SMI-32 are pruned across development and are thought to be preserved following deafness. Y cells in the LGN relay motion information and are a promising substrate for investigating thalamic plasticity. Systematic random sampling was employed to quantify Y cell morphology in the LGN of hearing (N=5), perinatally deafened (N=4), and unilaterally deafened cats (N=1). Differences between hearing and deaf subjects were assessed using Mann-Whitney U tests. Within conditions, differences across layers were assessed using Kruskal-Wallis tests. In both conditions, neurons in A and A1 layers revealed an increase in dendrite number and length compared to the C-Complex. Dendrites were significantly longer in deaf subjects in layers A and A1. Deaf subjects exhibited increased higher-order branches in layers A and A1. In both conditions, neurons exhibited a higher branch order in layers A and A1. Deaf subjects revealed an increase in Y cell density in layers A and A1 compared to hearing subjects. Following unilateral deafness, there was an increase in Y cell density in layers corresponding to the contralaterally deafened ear. Overall, the present study reveals that the visual thalamus responds to the absence of auditory input to the brain.

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