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Contrast adaptation
Published in Pablo Artal, Handbook of Visual Optics, 2017
The underlying pathways are illustrated in Figure 21.23 in simplified fashion. The (already perhaps partially adapted) output of the retina provides input to the contralateral and ipsilateral cortex. There are no known efferent back projections from there to the fellow eye. Therefore, binocular neurons in visual cortex must merge the adapted and the nonadapted inputs from both eyes, and a mixed signal must be forwarded to higher centers where the interocular transfer becomes apparent to the subject.
Normal and Abnormal Development of the Neuronal Response Properties in Primate Visual Cortex
Published in Jon H. Kaas, Christine E. Collins, The Primate Visual System, 2003
Yuzo M. Chino, Hua Bi, Bin Zhang
adultlike monocular tuning properties and responsiveness.24,31,32 As a result, small imbalances in the signals between the two eyes are more readily detected by binocular neurons and are more effective in disrupting the normal development of binocular response properties of V1 neurons. It is remarkable that during this critical time of development, only 7 days of strabismus is sufficient to cause significant damage to the binocular signal processing mechanisms in primate V1, and that periods of strabismus longer than 2 weeks result in little additional loss of disparity sensitivity. Another important difference is that strabismus causes substantial binocular suppression in V1 neurons soon after misalignment occurs, whereas, as described previously, monocular form deprivation rarely generates interocular suppression in cortical units.112
The Role of Binocularity in Anisometropic Amblyopia
Published in Journal of Binocular Vision and Ocular Motility, 2019
Sarah J. Murray, Charlotte J. Codina
Farivar et al.32 compared the multifocal functional magnetic resonance images (fMRIs) of 20 pure anisometropic amblyopes with 10 controls and reported that amblyopic visual cortices appeared more ‘disordered’ with reduced blood-oxygen-level-dependent percentages and increased ‘scatter’ in the areas V1, V2, and V3. The deficits were greater in the extrastriate areas and correlated with the depth of amblyopia. This is likely a reflection of altered synaptic thresholds caused by long-term depression of the weak post-synaptic activity of the amblyopic eye.31 However, there is still uncertainty as to whether the increased V2 deficit is merely a passive continuation of V1 deficits (the increase due to the higher number of binocular neurons) or an active amplification.33