A {Role} for {Retinal} {Brain}-{Derived} {Neurotrophic} {Factor} in {Ocular} {Dominance} {Plasticity}

Mandolesi, Georgia, Elisabetta Menna, Alexey Harauzov, Christopher S. von Bartheld, Matteo Caleo, and Lamberto Maffei. "A {Role} for {Retinal} {Brain}-{Derived} {Neurotrophic} {Factor} in {Ocular} {Dominance} {Plasticity}." Current Biology. 15 (2005): 2119-2124.


Visual deprivation is a classical tool to study the plasticity of visual cortical connections. After eyelid closure in young animals (monocular deprivation, MD), visual cortical neurons become dominated by the open eye, a phenomenon known as ocular dominance (OD) plasticity [1]. It is commonly held that the molecular mediators of OD plasticity are cortically derived and that the retina is immune to the effects of MD 2, 3 and 4. Recently, it has been reported that visual deprivation induces neurochemical, structural, and functional changes in the retina 5, 6 and 7, but whether these retinal changes contribute to the effects of MD in the cortex is unknown. Here, we provide evidence that brain-derived neurotrophic factor (BDNF) produced in the retina influences OD plasticity. We found a reduction of BDNF expression in the deprived retina of young rats. We compensated this BDNF imbalance between the two eyes by either injecting exogenous BDNF in the deprived eye or reducing endogenous BDNF expression in the nondeprived eye. Both treatments were effective in counteracting the OD shift induced by MD. Retinal BDNF could also influence OD distribution in normal animals. These results show for the first time that OD plasticity is modulated by BDNF produced in the retina.




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