Ocular dominance columns in V1 are more susceptible than associated callosal patches to imbalance of eye input during precritical and critical periods

2021 ◽  
Author(s):  
Jaime F. Olavarria ◽  
Robyn J. Laing ◽  
Adrian K. Andelin
Keyword(s):  
Ocular Dominance ◽  
Critical Periods ◽  
Ocular Dominance Columns

Critical periods for functional and anatomical compensation in lateral suprasylvian visual area following removal of visual cortex in cats

1984 ◽  
Vol 52 (5) ◽  
pp. 941-960 ◽  
Author(s):  
L. Tong ◽  
R. E. Kalil ◽  
P. D. Spear
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Ocular Dominance ◽  
Direction Selectivity ◽  
Visual Area ◽  
Critical Periods ◽  
Cortex Lesion ◽  
Thalamic Projections ◽  
Adult Cats ◽  
Visual Cortical

Previous experiments have found that neurons in the cat's lateral suprasylvian (LS) visual area of cortex show functional compensation following removal of visual cortical areas 17, 18, and 19 on the day of birth. Correspondingly, an enhanced retino-thalamic pathway to LS cortex develops in these cats. The present experiments investigated the critical periods for these changes. Unilateral lesions of areas 17, 18, and 19 were made in cats ranging in age from 1 day postnatal to 26 wk. When the cats were adult, single-cell recordings were made from LS cortex ipsilateral to the lesion. In addition, transneuronal autoradiographic methods were used to trace the retino-thalamic projections to LS cortex in many of the same animals. Following lesions in 18- and 26-wk-old cats, there is a marked reduction in direction-selective LS cortex cells and an increase in cells that respond best to stationary flashing stimuli. These results are similar to those following visual cortex lesions in adult cats. In contrast, the percentages of cells with these properties are normal following lesions made from 1 day to 12 wk of age. Thus the critical period for development of direction selectivity and greater responses to moving than to stationary flashing stimuli in LS cortex following a visual cortex lesion ends between 12 and 18 wk of age. Following lesions in 26-wk-old cats, there is a decrease in the percentage of cells that respond to the ipsilateral eye, which is similar to results following visual cortex lesions in adult cats. However, ocular dominance is normal following lesions made from 1 day to 18 wk of age. Thus the critical period for development of responses to the ipsilateral eye following a lesion ends between 18 and 26 wk of age. Following visual cortex lesions in 2-, 4-, or 8-wk-old cats, about 30% of the LS cortex cells display orientation selectivity to elongated slits of light. In contrast, few or no cells display this property in normal adult cats, cats with lesions made on the day of birth, or cats with lesions made at 12 wk of age or later. Thus an anomalous property develops for many LS cells, and the critical period for this property begins later (between 1 day and 2 wk) and ends earlier (between 8 and 12 wk) than those for other properties.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Correlation model for joint development of refined retinotopic map and ocular dominance columns

2002 ◽  
Vol 42 (19) ◽  
pp. 2295-2310 ◽  
Author(s):  
Greg A. Woodbury ◽  
Rick van der Zwan ◽  
William G. Gibson
Keyword(s):  
Ocular Dominance ◽  
Correlation Model ◽  
Ocular Dominance Columns ◽  
Joint Development ◽  
Retinotopic Map

scholarly journals Critical periods in amblyopia

2018 ◽  
Vol 35 ◽  
Author(s):  
TAKAO K. HENSCH ◽  
ELIZABETH M. QUINLAN
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Molecular Mechanisms ◽  
Ocular Dominance ◽  
Molecular Genetic ◽  
Monocular Deprivation ◽  
Critical Periods ◽  
Developmental Constraints ◽  
Early Postnatal Development ◽  
Visual Cortical

AbstractThe shift in ocular dominance (OD) of binocular neurons induced by monocular deprivation is the canonical model of synaptic plasticity confined to a postnatal critical period. Developmental constraints on this plasticity not only lend stability to the mature visual cortical circuitry but also impede the ability to recover from amblyopia beyond an early window. Advances with mouse models utilizing the power of molecular, genetic, and imaging tools are beginning to unravel the circuit, cellular, and molecular mechanisms controlling the onset and closure of the critical periods of plasticity in the primary visual cortex (V1). Emerging evidence suggests that mechanisms enabling plasticity in juveniles are not simply lost with age but rather that plasticity is actively constrained by the developmental up-regulation of molecular ‘brakes’. Lifting these brakes enhances plasticity in the adult visual cortex, and can be harnessed to promote recovery from amblyopia. The reactivation of plasticity by experimental manipulations has revised the idea that robust OD plasticity is limited to early postnatal development. Here, we discuss recent insights into the neurobiology of the initiation and termination of critical periods and how our increasingly mechanistic understanding of these processes can be leveraged toward improved clinical treatment of adult amblyopia.

scholarly journals Monocular Cells Without Ocular Dominance Columns

2006 ◽  
Vol 96 (5) ◽  
pp. 2253-2264 ◽  
Author(s):  
Daniel L. Adams ◽  
Jonathan C. Horton
Keyword(s):  
Squirrel Monkey ◽  
Visual Processing ◽  
Striate Cortex ◽  
Single Cells ◽  
Ocular Dominance ◽  
Squirrel Monkeys ◽  
Ocular Dominance Columns ◽  
Receptive Field Property ◽  
Field Property ◽  
Made In

In many regions of the mammalian cerebral cortex, cells that share a common receptive field property are grouped into columns. Despite intensive study, the function of the cortical column remains unknown. In the squirrel monkey, the expression of ocular dominance columns is variable, with columns present in some animals and not in others. By searching for differences between animals with and without columns, it should be possible to infer how columns contribute to visual processing. Single-cell recordings outside layer 4C were made in nine squirrel monkeys, followed by labeling of ocular dominance columns in layer 4C. In the squirrel monkey, compared with the macaque, cells outside layer 4C were more likely to respond to stimulation of either eye whether ocular dominance columns were present or not. In three animals lacking ocular dominance columns, single cells were recorded from layer 4C. Remarkably, 20% of cells in layer 4C were monocular despite the absence of columns. This observation means that ocular dominance columns are not necessary for monocular cells to occur in striate cortex. In macaques each row of cytochrome oxidase (CO) patches is aligned with an ocular dominance column and receives koniocellular input serving one eye only. In squirrel monkeys this was not true: CO patches and ocular dominance columns had no spatial correlation and the koniocellular input to CO patches was binocular. Thus even when ocular dominance columns occur in the squirrel monkey, they do not transform the functional architecture to resemble that of the macaque.

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