ratio of NR2A/B NMDA receptor subunits determines the qualities of ocular dominance plasticity in visual cortex
Bidirectional synaptic plasticity during development ensures that appropriate synapses in the brain are strengthened and maintained while inappropriate connections are weakened and eliminated. This plasticity is well illustrated in mouse visual cortex, where monocular deprivation during early postna...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 106; no. 13; pp. 5377 - 5382 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
31.03.2009
National Acad Sciences |
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| Online Access | Get full text |
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| Abstract | Bidirectional synaptic plasticity during development ensures that appropriate synapses in the brain are strengthened and maintained while inappropriate connections are weakened and eliminated. This plasticity is well illustrated in mouse visual cortex, where monocular deprivation during early postnatal development leads to a rapid depression of inputs from the deprived eye and a delayed strengthening of inputs from the non-deprived eye. The mechanisms that control these bidirectional synaptic modifications remain controversial. Here we demonstrate, both in vitro and in vivo, that genetic deletion or reduction of the NR2A NMDA receptor subunit impairs activity-dependent weakening of synapses and enhances the strengthening of synapses. Although brief monocular deprivation in juvenile WT mice normally causes a profound depression of the deprived-eye response without a change in the non-deprived eye response, NR2A-knockout mice fail to exhibit deprivation-induced depression and instead exhibit precocious potentiation of the non-deprived eye inputs. These data support the hypothesis that a reduction in the NR2A/B ratio during monocular deprivation is permissive for the compensatory potentiation of non-deprived inputs. |
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| AbstractList | Bidirectional synaptic plasticity during development ensures that appropriate synapses in the brain are strengthened and maintained while inappropriate connections are weakened and eliminated. This plasticity is well illustrated in mouse visual cortex, where monocular deprivation during early postnatal development leads to a rapid depression of inputs from the deprived eye and a delayed strengthening of inputs from the non-deprived eye. The mechanisms that control these bidirectional synaptic modifications remain controversial. Here we demonstrate, both in vitro and in vivo, that genetic deletion or reduction of the NR2A NMDA receptor subunit impairs activity-dependent weakening of synapses and enhances the strengthening of synapses. Although brief monocular deprivation in juvenile WT mice normally causes a profound depression of the deprived-eye response without a change in the non-deprived eye response, NR2A-knockout mice fail to exhibit deprivation-induced depression and instead exhibit precocious potentiation of the non-deprived eye inputs. These data support the hypothesis that a reduction in the NR2A/B ratio during monocular deprivation is permissive for the compensatory potentiation of non-deprived inputs. Bidirectional synaptic plasticity during development ensures that appropriate synapses in the brain are strengthened and maintained while inappropriate connections are weakened and eliminated. This plasticity is well illustrated in mouse visual cortex, where monocular deprivation during early postnatal development leads to a rapid depression of inputs from the deprived eye and a delayed strengthening of inputs from the non-deprived eye. The mechanisms that control these bidirectional synaptic modifications remain controversial. Here we demonstrate, both in vitro and in vivo, that genetic deletion or reduction of the NR2A NMDA receptor subunit impairs activity-dependent weakening of synapses and enhances the strengthening of synapses. Although brief monocular deprivation in juvenile WT mice normally causes a profound depression of the deprived-eye response without a change in the non-deprived eye response, NR2A-knockout mice fail to exhibit deprivation-induced depression and instead exhibit precocious potentiation of the non-deprived eye inputs. These data support the hypothesis that a reduction in the NR2A/B ratio during monocular deprivation is permissive for the compensatory potentiation of non-deprived inputs. [PUBLICATION ABSTRACT] |
| Author | Khibnik, Lena Philpot, Benjamin D Bear, Mark F Cho, Kathleen K.A |
| Author_xml | – sequence: 1 fullname: Cho, Kathleen K.A – sequence: 2 fullname: Khibnik, Lena – sequence: 3 fullname: Philpot, Benjamin D – sequence: 4 fullname: Bear, Mark F |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19276107$$D View this record in MEDLINE/PubMed |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 1K.K.A.C. and L.K. contributed equally to this work. Edited by Richard L. Huganir, Johns Hopkins University School of Medicine, Baltimore, MD, and approved February 4, 2009 |
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| Snippet | Bidirectional synaptic plasticity during development ensures that appropriate synapses in the brain are strengthened and maintained while inappropriate... |
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| SubjectTerms | Animals Biological Sciences Brain Dominance, Ocular Eyes Genetics Long term depression Long term potentiation Mice Mice, Knockout N methyl D aspartate receptors Neuronal Plasticity Neurons Neuroscience Neurosciences Ocular dominance Receptors, N-Methyl-D-Aspartate - analysis Rodents Synapses Theory Vision, Monocular Visual Cortex Visual deprivation |
| Title | ratio of NR2A/B NMDA receptor subunits determines the qualities of ocular dominance plasticity in visual cortex |
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