Contrast gain control and cortical TrkB signaling shape visual acuity
Résumé
During development, aging and in amblyopia, visual acuity is much below the limitations set by the retina. Expression of brain-derived neurotrophic factor (BDNF) in the visual cortex is reduced in these situations. We have tested the hypothesis that TrkB/BDNF regulates cortical visual acuity in adult mice. We found that genetically interfering with TrkB/BDNF signaling in pyramidal cells in the mature visual cortex reduced synaptic strength and resulted in a loss of neural responses to high spatial frequency stimuli. Responses to low spatial frequency stimuli were unaffected. This selective loss was not accompanied by a change in receptive field sizes or plasticity but exclusively by a reduction in apparent contrast. We demonstrate that a dependence on spatial frequency in the Heeger normalization model explains this selective effect of contrast reduction on high resolution vision, and argue that it involves contrast gain control operating within the visual cortex.
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