title: Critical role of the astrocyte for functional remodeling in contralateral hemisphere of somatosensory cortex after stroke.
abstract: After ischemic stroke, the corresponding area contralateral to the lesion may partly compensate for the loss of function. We previously reported the remodeling of neuronal circuits in the contralateral somatosensory cortex (SSC) during the first week after infarction for processing bilateral information, resulting in functional compensation. However, the underlying processes in the contralateral hemisphere after stroke have not yet been fully elucidated. Recent studies have shown that astrocytes may play critical roles in synaptic reorganization and functional compensation after a stroke. Thus, we aim to clarify the contribution of astrocytes using a rodent stroke model. In vivo calcium imaging showed a significantly large number of astrocytes in the contralateral SSC responding to ipsilateral limb stimulation at the first week after infarction. Simultaneously, extracellular glutamine level increased, indicating the involvement of astrocytes in the conversion of glutamate to glutamine, which may be an important process for functional recovery. This hypothesis was supported further by the observation that application of (2S,3S)-3-{3-[4-(trifluoromethyl)benzoylamino]benzyloxy} aspartate, a glial glutamate transporter blocker, disturbed the functional recovery. These findings indicate the involvement of astrocytes in functional remodeling/recovery in the area contralateral to the lesion. Our study has provided new insights into the mechanisms underlying synaptic remodeling after cerebral infarction, which contributes to the development of effective therapeutic approaches for patients after a stroke.
authors.affiliation: Department of Integrative Physiology, and Institute of Experimental Animal Research, Gunma University Graduate School of Medicine, Maebashi, Gunma 371-8511, Japan. takatsur@med
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Takatsuru
authors.forename: Kei
authors.initials: K
authors.lastname: Eto
authors.forename: Ryosuke
authors.initials: R
authors.lastname: Kaneko
authors.forename: Hiroko
authors.initials: H
authors.lastname: Masuda
authors.forename: Noriaki
authors.initials: N
authors.lastname: Shimokawa
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Koibuchi
authors.forename: Junichi
authors.initials: J
authors.lastname: Nabekura
mesh_terms: D050960:Aminomethyltransferase / Q000235:genetics / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000627:therapeutic use; D001253:Astrocytes / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D004195:Disease Models, Animal; D027341:Excitatory Amino Acid Transporter 1 / Q000235:genetics / Q000378:metabolism; D027342:Excitatory Amino Acid Transporter 2 / Q000235:genetics / Q000378:metabolism; D007839:Functional Laterality / Q000502:physiology*; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism; D005998:Glycine / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D017551:Microdialysis; D009043:Motor Activity; D009474:Neurons / Q000378:metabolism; D010812:Physical Stimulation; D012333:RNA, Messenger / Q000378:metabolism; D013003:Somatosensory Cortex / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D020521:Stroke / Q000188:drug therapy / Q000473:pathology*; D013997:Time Factors; D014738:Vibrissae / Q000294:innervation
chemical_list: C508240:(2S,3S)-3-(3-(4-(trifluoromethyl)benzoylamino)benzyloxy)aspartate; D027341:Excitatory Amino Acid Transporter 1; D027342:Excitatory Amino Acid Transporter 2; D012333:RNA, Messenger; C493393:Slc1a3 protein, mouse; D001224:Aspartic Acid; D018698:Glutamic Acid; D050960:Aminomethyltransferase; D002118:Calcium; D005998:Glycine