Impact of neural cell adhesion molecule deletion on regeneration after mouse spinal cord injury. (31st May 2016)
- Record Type:
- Journal Article
- Title:
- Impact of neural cell adhesion molecule deletion on regeneration after mouse spinal cord injury. (31st May 2016)
- Main Title:
- Impact of neural cell adhesion molecule deletion on regeneration after mouse spinal cord injury
- Authors:
- Saini, Vedangana
Loers, Gabriele
Kaur, Gurcharan
Schachner, Melitta
Jakovcevski, Igor - Editors:
- Kirik, Deniz
- Abstract:
- Abstract: The neural cell adhesion molecule (NCAM) plays important functional roles in development of the nervous system. We investigated the influence of a constitutive ablation of NCAM on the outcome of spinal cord injury. Transgenic mice lacking NCAM (NCAM −/− ) were subjected to severe compression injury of the lower thoracic spinal cord using wild‐type (NCAM+/+) littermates as controls. According to the single‐frame motion analysis, the NCAM −/− mice showed reduced locomotor recovery in comparison to control mice at 3 and 6 weeks after injury, indicating an overall positive impact of NCAM on recovery after injury. Also the Basso Mouse Scale score was lower in NCAM −/− mice at 3 weeks after injury, whereas at 6 weeks after injury the difference between genotypes was not statistically significant. Worse locomotor function was associated with decreased monoaminergic and cholinergic innervation of the spinal cord caudal to the injury site and decreased axonal regrowth/sprouting at the site of injury. Astrocytic scar formation at the injury site, as assessed by immunohistology for glial fibrillary acidic protein at and around the lesion site was increased in NCAM −/− compared with NCAM+/+ mice. Migration of cultured monolayer astrocytes from NCAM −/− mice was reduced as assayed by scratch wounding. Numbers of Iba‐1 immunopositive microglia were not different between genotypes. We conclude that constitutive NCAM deletion in young adult mice reduces recovery after spinal cordAbstract: The neural cell adhesion molecule (NCAM) plays important functional roles in development of the nervous system. We investigated the influence of a constitutive ablation of NCAM on the outcome of spinal cord injury. Transgenic mice lacking NCAM (NCAM −/− ) were subjected to severe compression injury of the lower thoracic spinal cord using wild‐type (NCAM+/+) littermates as controls. According to the single‐frame motion analysis, the NCAM −/− mice showed reduced locomotor recovery in comparison to control mice at 3 and 6 weeks after injury, indicating an overall positive impact of NCAM on recovery after injury. Also the Basso Mouse Scale score was lower in NCAM −/− mice at 3 weeks after injury, whereas at 6 weeks after injury the difference between genotypes was not statistically significant. Worse locomotor function was associated with decreased monoaminergic and cholinergic innervation of the spinal cord caudal to the injury site and decreased axonal regrowth/sprouting at the site of injury. Astrocytic scar formation at the injury site, as assessed by immunohistology for glial fibrillary acidic protein at and around the lesion site was increased in NCAM −/− compared with NCAM+/+ mice. Migration of cultured monolayer astrocytes from NCAM −/− mice was reduced as assayed by scratch wounding. Numbers of Iba‐1 immunopositive microglia were not different between genotypes. We conclude that constitutive NCAM deletion in young adult mice reduces recovery after spinal cord injury, validating the hypothesized beneficial role of this molecule in recovery after injury. Abstract : Transgenic mice lacking neural cell adhesion molecule (NCAM −/− ) were subjected to severe compression injury of the lower thoracic spinal cord. NCAM −/− mice showed reduced motor recovery in comparison to control mice at 6 weeks after injury, associated with decreased monoaminergic (TH + ) and cholinergic (ChAT + ) innervation and decreased axonal regrowth/sprouting (NF200 + axons). Astrocytic scar formation at the injury site, assessed by the expression of glial fibrillary acidic protein was increased in NCAM −/− mice. … (more)
- Is Part Of:
- European journal of neuroscience. Volume 44:Number 1(2016:Jul.)
- Journal:
- European journal of neuroscience
- Issue:
- Volume 44:Number 1(2016:Jul.)
- Issue Display:
- Volume 44, Issue 1 (2016)
- Year:
- 2016
- Volume:
- 44
- Issue:
- 1
- Issue Sort Value:
- 2016-0044-0001-0000
- Page Start:
- 1734
- Page End:
- 1746
- Publication Date:
- 2016-05-31
- Subjects:
- astrocyte -- cholinergic system -- locomotor recovery -- microglia -- monoaminergic system
Nervous system -- Periodicals
612.8 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1460-9568 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/ejn.13271 ↗
- Languages:
- English
- ISSNs:
- 0953-816X
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3829.731700
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 2821.xml