title: Neuronal circuit remodeling in the contralateral cortical hemisphere during functional recovery from cerebral infarction.
abstract: Recent advances in functional imaging of human brain activity in stroke patients, e.g., functional magnetic resonance imaging, have revealed that cortical hemisphere contralateral to the infarction plays an important role in the recovery process. However, underlying mechanisms occurring in contralateral hemisphere during functional recovery have not been elucidated. We experimentally induced a complete infarction of somatosensory cortex in right hemisphere of mice and examined the neuronal changes in contralateral (left) somatosensory cortex during recovery. Both basal and ipsilateral somatosensory stimuli-evoked neuronal activity in left (intact) hemisphere transiently increased 2 d after stroke, followed by an increase in the turnover rate of usually stable mushroom-type synaptic spines at 1 week, observed by using two-photon imaging in vivo. At 4 weeks after stroke, when functional recovery had occurred, a new pattern of electrical circuit activity in response to somatosensory stimuli was established in intact ipsilateral hemisphere. Thus, the left somatosensory cortex can compensate for the loss of the right somatosensory cortex by remodeling neuronal circuits and establishing new sensory processing. This finding could contribute to establish the effective clinical treatments targeted on the intact hemisphere for the recovery of impaired functions and to achieve better quality of life of patients.
authors.affiliation: Japan Science and Technology Agency, Kawaguchi, Japan.
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Takatsuru
authors.forename: Dai
authors.initials: D
authors.lastname: Fukumoto
authors.forename: Miki
authors.initials: M
authors.lastname: Yoshitomo
authors.forename: Tomomi
authors.initials: T
authors.lastname: Nemoto
authors.forename: Hideo
authors.initials: H
authors.lastname: Tsukada
authors.forename: Junichi
authors.initials: J
authors.lastname: Nabekura
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000200:Action Potentials; D000818:Animals; D020520:Brain Infarction / Q000503:physiopathology*; D049229:Dendritic Spines / Q000187:drug effects / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D007839:Functional Laterality; D008164:Luminescent Proteins / Q000235:genetics; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D010812:Physical Stimulation; D020127:Recovery of Function / Q000187:drug effects / Q000502:physiology; D013003:Somatosensory Cortex / Q000187:drug effects / Q000503:physiopathology*; D020521:Stroke / Q000503:physiopathology*; D013569:Synapses / Q000187:drug effects / Q000502:physiology; D013997:Time Factors
chemical_list: D018691:Excitatory Amino Acid Antagonists; D008164:Luminescent Proteins; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione
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