2023
DOI: 10.1016/j.nicl.2023.103463
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An integrated measure of GABA to characterize post-stroke plasticity

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Cited by 8 publications
(3 citation statements)
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References 153 publications
(163 reference statements)
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“…We found that two types of GABA exist in PV-ChR2 group; GABA released from reactive astrocyte after Wallerian degeneration in the cortex and neuronal GABA released from PV-expressing neurons in capsular infarct model 21 . Astrocytic GABA seems to perturbate the neuronal function in ipsilesional cortex following capsular infarct, as mentioned before, whereas neuronal GABA is hypothesized to be involved to form post-stroke neuronal plasticity, mediated by Hebbian and homeostatic plasticity mechanism 56,57 . GABAergic modulation is reported to be important to shape spike-timing-dependent plasticity and operate as Hebbian/anti-Hebbian switch 58,59 .…”
Section: Discussionmentioning
confidence: 83%
“…We found that two types of GABA exist in PV-ChR2 group; GABA released from reactive astrocyte after Wallerian degeneration in the cortex and neuronal GABA released from PV-expressing neurons in capsular infarct model 21 . Astrocytic GABA seems to perturbate the neuronal function in ipsilesional cortex following capsular infarct, as mentioned before, whereas neuronal GABA is hypothesized to be involved to form post-stroke neuronal plasticity, mediated by Hebbian and homeostatic plasticity mechanism 56,57 . GABAergic modulation is reported to be important to shape spike-timing-dependent plasticity and operate as Hebbian/anti-Hebbian switch 58,59 .…”
Section: Discussionmentioning
confidence: 83%
“…37 Multiple studies have attempted to investigate the functional implications of this excitatory-inhibitory balance in post-stroke survivors and the implication for motor recovery, but findings remain still inconclusive. 38 Our study provides novel insights into the functional role of this excitatory-inhibitory balance by revealing the existence of two distinct intracortical excitability patterns underlying motor skill acquisition depending on lesion location. In individuals with cortical lesions, better acquisition rates were associated with greater inhibitory activity, suggesting that neurophysiological patterns similar to neurotypical individuals when lesions spare corticospinal pathways.…”
Section: Discussionmentioning
confidence: 85%
“…37,47 Changes in sleep architecture or enhanced sleep due to pharmacological effects (e.g., gabapentin improves slow wave sleep 48 and total sleep time 49 ) post-stroke may create a more conducive environment for offline motor learning compared with older controls. Finally, aging is associated with decreased neuroplasticity due to alterations in GABAergic activity, [50][51][52] which may impact the brain's ability to learn and consolidate motor memories during sleep. It is to be noted though that the differences in online and offline learning observed in this study occurred despite participants being in the chronic period of stroke recovery (i.e., when changes in neuroplasticity are believed to have plateaued), indicating that the enhancement in offline learning could be a sustained phenomenon.…”
Section: Discussionmentioning
confidence: 99%