The Development of Hindlimb Postural Asymmetry Induced by Focal Traumatic Brain Injury Is Not Related to Serotonin 2A/C Receptor Expression in the Spinal Cord

Brain injury and stroke are leading causes of adult disability. Motor deficits are common problems, and their underlying pathological mechanisms remain poorly understood. The serotoninergic system is implicated in both functional recovery from and the occurrence of spasticity after injuries to the c...

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Main Authors: Marlene Storm Andersen, Dilârâ Bedriye Güler, Jonas Larsen, Karen Kalhøj Rich, Åsa Fex Svenningsen, Mengliang Zhang
Format: Article
Language:English
Published: MDPI AG 2022-05-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/10/5358
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author Marlene Storm Andersen
Dilârâ Bedriye Güler
Jonas Larsen
Karen Kalhøj Rich
Åsa Fex Svenningsen
Mengliang Zhang
author_facet Marlene Storm Andersen
Dilârâ Bedriye Güler
Jonas Larsen
Karen Kalhøj Rich
Åsa Fex Svenningsen
Mengliang Zhang
author_sort Marlene Storm Andersen
collection DOAJ
description Brain injury and stroke are leading causes of adult disability. Motor deficits are common problems, and their underlying pathological mechanisms remain poorly understood. The serotoninergic system is implicated in both functional recovery from and the occurrence of spasticity after injuries to the central nervous system. This study, which was conducted on rats, investigated the development of limb postural changes and their relationship to the expression of serotonin (5-HT) 2A and 2C receptors in the spinal cord in the 4 weeks after focal traumatic brain injury (TBI) to the right hindlimb sensorimotor cortex. The limb motor deficits were assessed by measuring gait pattern changes during walking and hindlimb postural asymmetry at different time intervals (3–28 days) after surgery. The expressions of the 5-HT2A and 2C receptors in the lumbar spinal cord were investigated using immunohistochemistry. The results showed that all the rats with TBI, independently of the duration of the interval, displayed postural asymmetry with flexion on the contralateral (left) side (>2 mm), while the sham-operated rats showed no apparent postural asymmetry. The TBI rats also had longer stride lengths during walking in both their hindlimbs and their forelimbs compared with the sham rats. For both the TBI and the sham rats, the hind-paw placement angles were larger on the contralateral side in some of the groups. Compared to the sham-operated rats, the 5-HT2A and 2C receptor expression did not significantly change on either side of the lumbar spinal cords of the TBI rats in any of the groups. These results suggest that focal TBI can induce motor deficits lasting a relatively long time, and that these deficits are not related to the expression of the 5-HT2A and 2C receptors in the spinal cord.
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spelling doaj.art-bb4628a5bf6548468eed5e0cce4fff902023-11-23T11:21:16ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-05-012310535810.3390/ijms23105358The Development of Hindlimb Postural Asymmetry Induced by Focal Traumatic Brain Injury Is Not Related to Serotonin 2A/C Receptor Expression in the Spinal CordMarlene Storm Andersen0Dilârâ Bedriye Güler1Jonas Larsen2Karen Kalhøj Rich3Åsa Fex Svenningsen4Mengliang Zhang5Department of Molecular Medicine, University of Southern Denmark, DK-5000 Odense, DenmarkDepartment of Molecular Medicine, University of Southern Denmark, DK-5000 Odense, DenmarkDepartment of Molecular Medicine, University of Southern Denmark, DK-5000 Odense, DenmarkDepartment of Molecular Medicine, University of Southern Denmark, DK-5000 Odense, DenmarkDepartment of Molecular Medicine, University of Southern Denmark, DK-5000 Odense, DenmarkDepartment of Molecular Medicine, University of Southern Denmark, DK-5000 Odense, DenmarkBrain injury and stroke are leading causes of adult disability. Motor deficits are common problems, and their underlying pathological mechanisms remain poorly understood. The serotoninergic system is implicated in both functional recovery from and the occurrence of spasticity after injuries to the central nervous system. This study, which was conducted on rats, investigated the development of limb postural changes and their relationship to the expression of serotonin (5-HT) 2A and 2C receptors in the spinal cord in the 4 weeks after focal traumatic brain injury (TBI) to the right hindlimb sensorimotor cortex. The limb motor deficits were assessed by measuring gait pattern changes during walking and hindlimb postural asymmetry at different time intervals (3–28 days) after surgery. The expressions of the 5-HT2A and 2C receptors in the lumbar spinal cord were investigated using immunohistochemistry. The results showed that all the rats with TBI, independently of the duration of the interval, displayed postural asymmetry with flexion on the contralateral (left) side (>2 mm), while the sham-operated rats showed no apparent postural asymmetry. The TBI rats also had longer stride lengths during walking in both their hindlimbs and their forelimbs compared with the sham rats. For both the TBI and the sham rats, the hind-paw placement angles were larger on the contralateral side in some of the groups. Compared to the sham-operated rats, the 5-HT2A and 2C receptor expression did not significantly change on either side of the lumbar spinal cords of the TBI rats in any of the groups. These results suggest that focal TBI can induce motor deficits lasting a relatively long time, and that these deficits are not related to the expression of the 5-HT2A and 2C receptors in the spinal cord.https://www.mdpi.com/1422-0067/23/10/5358traumatic brain injurypostural asymmetrygait deficitserotoninserotonin receptor
spellingShingle Marlene Storm Andersen
Dilârâ Bedriye Güler
Jonas Larsen
Karen Kalhøj Rich
Åsa Fex Svenningsen
Mengliang Zhang
The Development of Hindlimb Postural Asymmetry Induced by Focal Traumatic Brain Injury Is Not Related to Serotonin 2A/C Receptor Expression in the Spinal Cord
International Journal of Molecular Sciences
traumatic brain injury
postural asymmetry
gait deficit
serotonin
serotonin receptor
title The Development of Hindlimb Postural Asymmetry Induced by Focal Traumatic Brain Injury Is Not Related to Serotonin 2A/C Receptor Expression in the Spinal Cord
title_full The Development of Hindlimb Postural Asymmetry Induced by Focal Traumatic Brain Injury Is Not Related to Serotonin 2A/C Receptor Expression in the Spinal Cord
title_fullStr The Development of Hindlimb Postural Asymmetry Induced by Focal Traumatic Brain Injury Is Not Related to Serotonin 2A/C Receptor Expression in the Spinal Cord
title_full_unstemmed The Development of Hindlimb Postural Asymmetry Induced by Focal Traumatic Brain Injury Is Not Related to Serotonin 2A/C Receptor Expression in the Spinal Cord
title_short The Development of Hindlimb Postural Asymmetry Induced by Focal Traumatic Brain Injury Is Not Related to Serotonin 2A/C Receptor Expression in the Spinal Cord
title_sort development of hindlimb postural asymmetry induced by focal traumatic brain injury is not related to serotonin 2a c receptor expression in the spinal cord
topic traumatic brain injury
postural asymmetry
gait deficit
serotonin
serotonin receptor
url https://www.mdpi.com/1422-0067/23/10/5358
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