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Peripheral deafferentation-driven functional somatosensory map shifts are associated with local, not large-scale dendritic structural plasticity.

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Publication date 2013
Author Schubert Vanessa, Lebrecht Daniel, Holtmaat Anthony,
Project Structure, Function and Plasticity of the Barrel Cortex
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Original article (peer-reviewed)

Journal The Journal of neuroscience : the official journal of the Society for Neuroscience
Volume (Issue) 33(22)
Page(s) 9474 - 87
Title of proceedings The Journal of neuroscience : the official journal of the Society for Neuroscience
DOI 10.1523/JNEUROSCI.1032-13.2013


Long-term peripheral deafferentation induces representational map changes in the somatosensory cortex. It has been suggested that dendrites and axons structurally rearrange in such paradigms. However, the extent and process of this plasticity remains elusive. To more precisely quantify deafferentation-induced structural plasticity of excitatory cells we repeatedly imaged GFP-expressing L2/3 and L5 pyramidal dendrites in the mouse barrel cortex over months after the removal of a subset of the whisker follicles (FR), a procedure that completely and permanently removes whisker-sensory input. In the same mice we imaged whisker-evoked intrinsic optical signals (IOS) to assess functional cortical map changes. FR triggered the expansion of spared whisker IOS responses, whereas they remained unchanged over months in controls. The gross structure and orientation of apical dendrite tufts remained stable over a two-month period, both in controls and after deprivation. However, terminal branch tip dynamics were slightly reduced after FR, and the formation of new dendritic spines was increased in a cell-type and location-dependent manner. Together, our data suggest that peripheral nerve lesion-induced cortical map shifts do not depend on the large scale restructuring of dendritic arbors but are rather associated with local cell-type and position-dependent changes in dendritic synaptic connectivity.