Peripheral Sensory Deprivation Restores Critical-Period-like Plasticity to 
Adult Somatosensory Thalamocortical Inputs

Chung, S; Jeong, J-H; Ko, S; Yu, X; Kim, Y-H; Isaac, JTR; Koretsky, AP

doi:10.1016/j.celrep.2017.06.018

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Peripheral Sensory Deprivation Restores Critical-Period-like Plasticity to Adult Somatosensory Thalamocortical Inputs

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Yu, X
Max Planck Institute for Biological Cybernetics, Max Planck Society;
Research Group Translational Neuroimaging and Neural Control, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Chung, S., Jeong, J.-H., Ko, S., Yu, X., Kim, Y.-H., Isaac, J., et al. (2017). Peripheral Sensory Deprivation Restores Critical-Period-like Plasticity to Adult Somatosensory Thalamocortical Inputs. Cell Reports, 19(13), 2707-2717. doi:10.1016/j.celrep.2017.06.018.

Zitierlink: https://hdl.handle.net/21.11116/0000-0000-C2FF-6

Zusammenfassung

Recent work has shown that thalamocortical (TC) inputs can be plastic after the developmental critical period has closed, but the mechanism that enables re-establishment of plasticity is unclear. Here, we find that long-term potentiation (LTP) at TC inputs is transiently restored in spared barrel cortex following either a unilateral infra-orbital nerve (ION) lesion, unilateral whisker trimming, or unilateral ablation of the rodent barrel cortex. Restoration of LTP is associated with increased potency at TC input and reactivates anatomical map plasticity induced by whisker follicle ablation. The reactivation of TC LTP is accompanied by reappearance of silent synapses. Both LTP and silent synapse formation are preceded by transient re-expression of synaptic GluN2B-containing N-methyl-D-aspartate (NMDA) receptors, which are required for the reappearance of TC plasticity. These results clearly demonstrate that peripheral sensory deprivation reactivates synaptic plasticity in the mature layer 4 barrel cortex with features similar to the developmental critical period.