| First Author | Heimel JA | Year | 2010 |
| Journal | Nat Neurosci | Volume | 13 |
| Issue | 5 | Pages | 642-8 |
| PubMed ID | 20400960 | Mgi Jnum | J:159845 |
| Mgi Id | MGI:4452547 | Doi | 10.1038/nn.2534 |
| Citation | Heimel JA, et al. (2010) Contrast gain control and cortical TrkB signaling shape visual acuity. Nat Neurosci 13(5):642-8 |
| abstractText | During development and aging and in amblyopia, visual acuity is far below the limitations set by the retina. Expression of brain-derived neurotrophic factor (BDNF) in the visual cortex is reduced in these situations. We asked whether neurotrophic tyrosine kinase receptor, type 2 (TrkB) 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 apparent contrast was reduced. Our results indicate that a dependence on spatial frequency in the Heeger normalization model explains this selective effect of contrast reduction on high-resolution vision and suggest that it involves contrast gain control operating in the visual cortex. |
