Distinct laminar requirements for NMDA receptors in experience-dependent visual cortical plasticity
Autor: | Eitan S. Kaplan, Taekeun Kim, Peter S.B. Finnie, Ming-fai Fong, Mark F. Bear, Aurore Thomazeau, Sam F. Cooke |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
Male
genetic structures Cognitive Neuroscience Stimulation Mice Transgenic Biology Amblyopia Receptors N-Methyl-D-Aspartate Ocular dominance 03 medical and health sciences Cellular and Molecular Neuroscience Mice ocular dominance plasticity 0302 clinical medicine stimulus-selective response potentiation Neuroplasticity medicine Ocular Dominance Animals long-term depression Visual cortex visual cortex Long-term depression 030304 developmental biology amblyopia Mice Knockout 0303 health sciences Neuronal Plasticity Long-term potentiation NMDA receptor Mice Inbred C57BL Monocular deprivation medicine.anatomical_structure nervous system Evoked Potentials Visual Female Original Article Sensory Deprivation Neuroscience 030217 neurology & neurosurgery Photic Stimulation |
Zdroj: | Fong, M, Finnie, P S B, Kim, T, Thomazeau, A, Kaplan, E S, Cooke, S F & Bear, M F 2020, ' Distinct laminar requirements for NMDA receptors in experience-dependent visual cortical plasticity ', Cerebral Cortex, vol. 30, no. 4, pp. 2555–2572 . https://doi.org/10.1093/cercor/bhz260 Cerebral Cortex (New York, NY) |
DOI: | 10.1093/cercor/bhz260 |
Popis: | 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. |
Databáze: | OpenAIRE |
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