Recovery from the anatomical effects of long‐term monocular deprivation in cat lateral geniculate nucleus

Monocular deprivation (MD) imposed early in postnatal life elicits profound structural and functional abnormalities throughout the primary visual pathway. The ability of MD to modify neurons within the visual system is restricted to a so‐called critical period that, for cats, peaks at about one post...

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Bibliographic Details
Published in:Journal of comparative neurology (1911) 2018-02, Vol.526 (2), p.310-323
Main Authors: Duffy, Kevin R., Fong, Ming‐fai, Mitchell, Donald E., Bear, Mark F.
Format: Article
Language:English
Subjects:
Age Factors
Analysis of Variance
Anesthetics, Local - pharmacology
Animals
Animals, Newborn
Binocular vision
Cats
Critical period
dark exposure
Darkness
Developmental plasticity
Eye
Functional Laterality - physiology
Geniculate Bodies - anatomy & histology
Geniculate Bodies - physiology
Lateral geniculate nucleus
Monocular vision
Neural plasticity
neurofilament
Neurofilament Proteins - metabolism
Neurofilaments
Occlusion
Plastic properties
Recovery of Function - physiology
Retina
retinal inactivation
reverse occlusion
RRID:AB_509998
Sensory Deprivation - physiology
Structure-function relationships
Tetrodotoxin
Tetrodotoxin - pharmacology
Visual deprivation
Visual Pathways - drug effects
Visual Pathways - physiology
Visual system
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Summary:Monocular deprivation (MD) imposed early in postnatal life elicits profound structural and functional abnormalities throughout the primary visual pathway. The ability of MD to modify neurons within the visual system is restricted to a so‐called critical period that, for cats, peaks at about one postnatal month and declines thereafter so that by about 3 months of age MD has little effect. Recovery from the consequences of MD likewise adheres to a critical period that ends by about 3 months of age, after which the effects of deprivation are thought to be permanent and without capacity for reversal. The attenuation of plasticity beyond early development is a formidable obstacle for conventional therapies to stimulate recovery from protracted visual deprivation. In the current study we examined the efficacy of dark exposure and retinal inactivation with tetrodotoxin to promote anatomical recovery in the dorsal lateral geniculate nuclues (dLGN) from long‐term MD started at the peak of the critical period. Whereas 10 days of dark exposure or binocular retinal inactivation were not better at promoting recovery than conventional treatment with reverse occlusion, inactivation of only the non‐deprived (fellow) eye for 10 days produced a complete restoration of neuron soma size, and also reversed the significant loss of neurofilament protein within originally deprived dLGN layers. These results reveal a capacity for neural plasticity and recovery that is larger than anything previously observed following protracted MD in cat, and they highlight a possibility for alternative therapies applied at ages thought to be recalcitrant to recovery. The authors report an unprecedented level of recovery from the effects of long‐term monocular deprivation (MD) when the deprived eye was opened and the stronger eye's retina was inactivated for 10 days with tetrodotoxin. Neuron soma size in the dLGN recovered to match normal controls, and neurofilament labeling reduced by a long period of MD also recovered (arrows). Temporary inactivation of the stronger eye may offer a novel therapy for restoring visual function to the deprived eye.
ISSN:0021-9967
1096-9861
DOI:10.1002/cne.24336