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Publication : Metaplasticity in the Visual Cortex: Crosstalk Between Visual Experience and Reactive Oxygen Species.

First Author  Francis-Oliveira J Year  2018
Journal  J Neurosci Volume  38
Issue  25 Pages  5649-5665
PubMed ID  29789380 Mgi Jnum  J:263546
Mgi Id  MGI:6164406 Doi  10.1523/JNEUROSCI.2617-17.2018
Citation  Francis-Oliveira J, et al. (2018) Metaplasticity in the Visual Cortex: Crosstalk Between Visual Experience and Reactive Oxygen Species. J Neurosci 38(25):5649-5665
abstractText  Metaplasticity is the regulation of synaptic plasticity based on the history of previous synaptic activation. This concept was formulated after observing that synaptic changes in the visual cortex are not fixed, but dynamic and dependent on the history of visual information flux. In visual cortical neurons, sustained synaptic stimulation activate the enzymatic complex NOX2, resulting in the generation of reactive oxygen species (ROS). NOX2 is the main molecular structure responsible for translating neural activity into redox modulation of intracellular signaling pathways involved in plastic changes. Here, we studied the interaction between NOX2 and visual experience as metaplastic factors regulating synaptic plasticity at the supergranular layers of the mouse visual cortex. We found that genetic inhibition of NOX2 reverses the polarizing effects of dark rearing from LTP to LTD. In addition, we demonstrate that this process relies on changes in the NMDA receptor functioning. Altogether, this work indicates a role of ROS in the activity-dependent regulation of cortical synaptic plasticity.SIGNIFICANCE STATEMENT Synaptic plasticity in the visual cortex is modulated by the history of sensory experience and this modulation has been defined as metaplasticity. Dark rearing facilitates synaptic potentiation as a mechanism optimizing the range of synaptic modification. This process requires the production of reactive oxygen species mediated by the enzymatic complex NOX2. If the activity of NOX2 is inhibited, then visual deprivation results in synaptic depression. These findings increase our knowledge about metaplasticity and help in our understanding of how neural activity modulates cellular mechanisms of synaptic change.
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