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.
Highlights
Recovery after stroke is thought to be mediated by adaptive circuit plasticity, whereby surviving neurons assume the roles of those that died
We performed in vivo intrinsic signal imaging (ISI) and two-photon (2P) calcium imaging of sensory-evoked responses before and after a photothrombotic (PT) stroke that was targeted to a specific barrel (C1) in the barrel field of primary somatosensory cortex (S1BF)
To study neuronal plasticity and remapping at the local circuit level, before and after focal cortical lesions, we focused on the barrel field of primary somatosensory cortex (S1BF) for several reasons: (1) somatosensory deficits are common after stroke in humans[23,24]; (2) as nocturnal animals, mice preferentially rely on their whiskers to explore their surroundings; (3) S1BF exhibits significant experience-dependent plasticity, even in adult animals[8,25,26]; and (4) the dynamics of neuronal circuits in rodent S1BF are well characterized[27,28,29,30]
Summary
Recovery after stroke is thought to be mediated by adaptive circuit plasticity, whereby surviving neurons assume the roles of those that died. 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. Human studies with brain imaging or neurophysiology have revealed variable (and sometimes opposite) changes in brain activity or metabolism after stroke Some of these changes, such as the apparent reorganization of cortical sensorimotor maps or differences in resting state functional connectivity (reviewed elsewhere9), have been interpreted as evidence of remapping. Our results argue against the classic remapping model of stroke recovery (where surviving neurons/circuits can assume a new role), at least in the barrel cortex, and are instead more consistent with a model where spontaneous or rehabilitation-induced recovery involves potentiation of pre-existing circuits
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