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Barrel cortex plasticity after photothrombotic stroke involves potentiating responses of pre-existing circuits but not functional remapping to new circuits

William A. Zeiger (), Máté Marosi, Satvir Saggi, Natalie Noble, Isa Samad and Carlos Portera-Cailliau ()
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William A. Zeiger: University of California Los Angeles
Máté Marosi: University of California Los Angeles
Satvir Saggi: University of California Los Angeles
Natalie Noble: University of California Los Angeles
Isa Samad: University of California Los Angeles
Carlos Portera-Cailliau: University of California Los Angeles

Nature Communications, 2021, vol. 12, issue 1, 1-14

Abstract: Abstract Recovery after stroke is thought to be mediated by adaptive circuit plasticity, whereby surviving neurons assume the roles of those that died. However, definitive longitudinal evidence of neurons changing their response selectivity after stroke is lacking. We sought to directly test whether such functional “remapping” occurs within mouse primary somatosensory cortex after a stroke that destroys the C1 barrel. Using in vivo calcium imaging to longitudinally record sensory-evoked activity under light anesthesia, we did not find any increase in the number of C1 whisker-responsive neurons in the adjacent, spared D3 barrel after stroke. To promote plasticity after stroke, we also plucked all whiskers except C1 (forced use therapy). This led to an increase in the reliability of sensory-evoked responses in C1 whisker-responsive neurons but did not increase the number of C1 whisker-responsive neurons in spared surround barrels over baseline levels. Our results argue against remapping of functionality after barrel cortex stroke, but support a circuit-based mechanism for how rehabilitation may improve recovery.

Date: 2021
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-24211-8

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DOI: 10.1038/s41467-021-24211-8

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