2024-03-29T12:01:11Z
https://u-ryukyu.repo.nii.ac.jp/oai
oai:u-ryukyu.repo.nii.ac.jp:02019518
2022-10-06T06:17:49Z
1642838158423:1642838158860:1642838159351
1642838403551:1642838409905
Slow progression of sciatic nerve degeneration and regeneration after loose ligation through microglial activation and decreased KCC2 levels in the mouse spinal cord ventral horn
マウス脊髄前角におけるミクログリアの活性化とKCC2 の発現低下を介した緩い坐 骨神経結紮後の神経変性及び再生の緩徐な進行
屋富祖, 司
Peripheral nerve injury affects motor functions. To reveal the mechanisms underlying motor dysfunction and recoveryafter nerve compression, which have not been precisely examined, we investigated the temporal relationshipamong changes in motor function, nerve histopathology, and marker molecule expression in the spinal cordafter loose ligation of the mouse sciatic nerve. After ligation, sciatic motor function suddenly declined, and axonsgradually degenerated. During degeneration, galanin was localized in motor neuron cell bodies. Then, in the ventralhorn, microglia were activated, and expression of choline acetyltransferase (ChAT), a synthetic enzyme ofacetylcholine, and potassium chloride co-transporter 2 (KCC2), which shifts the action of γ-amino butyric acid(GABA) and glycine to inhibitory, decreased. Motor function recovery was insufficient although axonal regenerationwas complete. ChAT levels gradually recovered during axonal regeneration. When regeneration was nearlycomplete, microglial activation declined, and KCC2 expression started to increase. The KCC2 level sufficiently recoveredwhen axonal regeneration was complete, suggesting that the excitatory action of GABA/glycine mayparticipate in axonal regeneration. Furthermore, these changes proceeded slower than those after severance,suggesting that loose ligation, compression, may mediate slower progression of degeneration and regenerationthan severance, and these changes may cause the motor dysfunction and its recovery.
博士(医学)
http://purl.org/coar/resource_type/c_db06
琉球大学
琉球大学
2021-11-04
VoR
甲第536号
eng
open access