Alterations of Both Dendrite Morphology and Weaker Electrical Responsiveness in the Cortex of Hip Area Occur Before Rearrangement of the Motor Map in Neonatal White Matter Injury Model

Hypoxia-ischemia (H-I) in rats at postnatal day 3 causes disorganization of oligodendrocyte development in layers II/III of the sensorimotor cortex without apparent neuronal loss, and shows mild hindlimb dysfunction with imbalanced motor coordination. However, the mechanisms by which mild motor dysf...

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Main Authors: Yoshitomo Ueda, Yoshio Bando, Sachiyo Misumi, Shino Ogawa, Akimasa Ishida, Cha-Gyun Jung, Takeshi Shimizu, Hideki Hida
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-06-01
Series:Frontiers in Neurology
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fneur.2018.00443/full
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spelling doaj-7d3b62adf69449c793438cffa1e840a12020-11-24T23:12:59ZengFrontiers Media S.A.Frontiers in Neurology1664-22952018-06-01910.3389/fneur.2018.00443347914Alterations of Both Dendrite Morphology and Weaker Electrical Responsiveness in the Cortex of Hip Area Occur Before Rearrangement of the Motor Map in Neonatal White Matter Injury ModelYoshitomo Ueda0Yoshio Bando1Sachiyo Misumi2Shino Ogawa3Shino Ogawa4Akimasa Ishida5Cha-Gyun Jung6Takeshi Shimizu7Hideki Hida8Department of Neurophysiology and Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, JapanDepartment of Functional Anatomy and Neuroscience, Asahikawa Medical University, Asahikawa, JapanDepartment of Neurophysiology and Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, JapanDepartment of Neurophysiology and Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, JapanDepartment of Obstetrics and Gynecology, Nagoya City University Graduate School of Medical Sciences, Nagoya, JapanDepartment of Neurophysiology and Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, JapanDepartment of Neurophysiology and Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, JapanDepartment of Neurophysiology and Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, JapanDepartment of Neurophysiology and Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, JapanHypoxia-ischemia (H-I) in rats at postnatal day 3 causes disorganization of oligodendrocyte development in layers II/III of the sensorimotor cortex without apparent neuronal loss, and shows mild hindlimb dysfunction with imbalanced motor coordination. However, the mechanisms by which mild motor dysfunction is induced without loss of cortical neurons are currently unclear. To reveal the mechanisms underlying mild motor dysfunction in neonatal H-I model, electrical responsiveness and dendrite morphology in the sensorimotor cortex were investigated at 10 weeks of age. Responses to intracortical microstimulation (ICMS) revealed that the cortical motor map was significantly changed in this model. The cortical area related to hip joint movement was reduced, and the area related to trunk movement was increased. Sholl analysis in Golgi staining revealed that layer I–III neurons on the H-I side had more dendrite branches compared with the contralateral side. To investigate whether changes in the motor map and morphology appeared at earlier stages, ICMS and Sholl analysis were also performed at 5 weeks of age. The minimal ICMS current to evoke twitches of the hip area was higher on the H-I side, while the motor map was unchanged. Golgi staining revealed more dendrite branches in layer I–III neurons on the H-I side. These results revealed that alterations of both dendrite morphology and ICMS threshold of the hip area occurred before the rearrangement of the motor map in the neonatal H-I model. They also suggest that altered dendritic morphology and altered ICMS responsiveness may be related to mild motor dysfunction in this model.https://www.frontiersin.org/article/10.3389/fneur.2018.00443/fullhypoxia-ischemia in premature infantswhite matter injuryintracortical microstimulation (ICMS)golgi stainingcortical layer I-IIIhip area
collection DOAJ
language English
format Article
sources DOAJ
author Yoshitomo Ueda
Yoshio Bando
Sachiyo Misumi
Shino Ogawa
Shino Ogawa
Akimasa Ishida
Cha-Gyun Jung
Takeshi Shimizu
Hideki Hida
spellingShingle Yoshitomo Ueda
Yoshio Bando
Sachiyo Misumi
Shino Ogawa
Shino Ogawa
Akimasa Ishida
Cha-Gyun Jung
Takeshi Shimizu
Hideki Hida
Alterations of Both Dendrite Morphology and Weaker Electrical Responsiveness in the Cortex of Hip Area Occur Before Rearrangement of the Motor Map in Neonatal White Matter Injury Model
Frontiers in Neurology
hypoxia-ischemia in premature infants
white matter injury
intracortical microstimulation (ICMS)
golgi staining
cortical layer I-III
hip area
author_facet Yoshitomo Ueda
Yoshio Bando
Sachiyo Misumi
Shino Ogawa
Shino Ogawa
Akimasa Ishida
Cha-Gyun Jung
Takeshi Shimizu
Hideki Hida
author_sort Yoshitomo Ueda
title Alterations of Both Dendrite Morphology and Weaker Electrical Responsiveness in the Cortex of Hip Area Occur Before Rearrangement of the Motor Map in Neonatal White Matter Injury Model
title_short Alterations of Both Dendrite Morphology and Weaker Electrical Responsiveness in the Cortex of Hip Area Occur Before Rearrangement of the Motor Map in Neonatal White Matter Injury Model
title_full Alterations of Both Dendrite Morphology and Weaker Electrical Responsiveness in the Cortex of Hip Area Occur Before Rearrangement of the Motor Map in Neonatal White Matter Injury Model
title_fullStr Alterations of Both Dendrite Morphology and Weaker Electrical Responsiveness in the Cortex of Hip Area Occur Before Rearrangement of the Motor Map in Neonatal White Matter Injury Model
title_full_unstemmed Alterations of Both Dendrite Morphology and Weaker Electrical Responsiveness in the Cortex of Hip Area Occur Before Rearrangement of the Motor Map in Neonatal White Matter Injury Model
title_sort alterations of both dendrite morphology and weaker electrical responsiveness in the cortex of hip area occur before rearrangement of the motor map in neonatal white matter injury model
publisher Frontiers Media S.A.
series Frontiers in Neurology
issn 1664-2295
publishDate 2018-06-01
description Hypoxia-ischemia (H-I) in rats at postnatal day 3 causes disorganization of oligodendrocyte development in layers II/III of the sensorimotor cortex without apparent neuronal loss, and shows mild hindlimb dysfunction with imbalanced motor coordination. However, the mechanisms by which mild motor dysfunction is induced without loss of cortical neurons are currently unclear. To reveal the mechanisms underlying mild motor dysfunction in neonatal H-I model, electrical responsiveness and dendrite morphology in the sensorimotor cortex were investigated at 10 weeks of age. Responses to intracortical microstimulation (ICMS) revealed that the cortical motor map was significantly changed in this model. The cortical area related to hip joint movement was reduced, and the area related to trunk movement was increased. Sholl analysis in Golgi staining revealed that layer I–III neurons on the H-I side had more dendrite branches compared with the contralateral side. To investigate whether changes in the motor map and morphology appeared at earlier stages, ICMS and Sholl analysis were also performed at 5 weeks of age. The minimal ICMS current to evoke twitches of the hip area was higher on the H-I side, while the motor map was unchanged. Golgi staining revealed more dendrite branches in layer I–III neurons on the H-I side. These results revealed that alterations of both dendrite morphology and ICMS threshold of the hip area occurred before the rearrangement of the motor map in the neonatal H-I model. They also suggest that altered dendritic morphology and altered ICMS responsiveness may be related to mild motor dysfunction in this model.
topic hypoxia-ischemia in premature infants
white matter injury
intracortical microstimulation (ICMS)
golgi staining
cortical layer I-III
hip area
url https://www.frontiersin.org/article/10.3389/fneur.2018.00443/full
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