Distinct Laminar Requirements for NMDA Receptors in Experience-Dependent Visual Cortical Plasticity

© 2020 Oxford University Press. All rights reserved. Primary visual cortex (V1) is the locus of numerous forms of experience-dependent plasticity. Restricting visual stimulation to one eye at a time has revealed that many such forms of plasticity are eye-specific, indicating that synaptic modificati...

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Main Authors: Fong, Ming-fai (Author), Finnie, Peter Sb (Author), Kim, Taekeun (Author), Thomazeau, Aurore (Author), Kaplan, Eitan S (Author), Cooke, Samuel F (Author), Bear, Mark F (Author)
Format: Article
Language:English
Published: Oxford University Press (OUP), 2021-11-05T18:56:51Z.
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Online Access:Get fulltext
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100 1 0 |a Fong, Ming-fai  |e author 
700 1 0 |a Finnie, Peter Sb  |e author 
700 1 0 |a Kim, Taekeun  |e author 
700 1 0 |a Thomazeau, Aurore  |e author 
700 1 0 |a Kaplan, Eitan S  |e author 
700 1 0 |a Cooke, Samuel F  |e author 
700 1 0 |a Bear, Mark F  |e author 
245 0 0 |a Distinct Laminar Requirements for NMDA Receptors in Experience-Dependent Visual Cortical Plasticity 
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520 |a © 2020 Oxford University Press. All rights reserved. Primary visual cortex (V1) is the locus of numerous forms of experience-dependent plasticity. Restricting visual stimulation to one eye at a time has revealed that many such forms of plasticity are eye-specific, indicating that synaptic modification occurs prior to binocular integration of thalamocortical inputs. A common feature of these forms of plasticity is the requirement for NMDA receptor (NMDAR) activation in V1.We therefore hypothesized that NMDARs in cortical layer 4 (L4), which receives the densest thalamocortical input, would be necessary for all forms of NMDAR-dependent and input-specific V1 plasticity.We tested this hypothesis in awake mice using a genetic approach to selectively delete NMDARs from L4 principal cells.We found, unexpectedly, that both stimulus-selective response potentiation and potentiation of open-eye responses following monocular deprivation (MD) persist in the absence of L4 NMDARs. In contrast, MD-driven depression of deprived-eye responses was impaired in mice lacking L4 NMDARs, as was L4 long-term depression in V1 slices. Our findings reveal a crucial requirement for L4 NMDARs in visual cortical synaptic depression, and a surprisingly negligible role for them in cortical response potentiation. These results demonstrate that NMDARs within distinct cellular subpopulations support different forms of experience-dependent plasticity. 
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655 7 |a Article 
773 |t 10.1093/cercor/bhz260 
773 |t Cerebral Cortex