Recovery of evoked potentials, metabolic activity and behavior in a mouse model of somatosensory cortex lesion: role of the neural cell adhesion molecule (NCAM)

Details

Ressource 1Download: serval:BIB_BF80269F8EDB.P001 (1145.50 [Ko])
State: Public
Version: author
License: Not specified
It was possible to publish this article open access thanks to a Swiss National Licence with the publisher.
Serval ID
serval:BIB_BF80269F8EDB
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Recovery of evoked potentials, metabolic activity and behavior in a mouse model of somatosensory cortex lesion: role of the neural cell adhesion molecule (NCAM)
Journal
Cerebral Cortex
Author(s)
Troncoso  E., Muller  D., Korodi  K., Steimer  T., Welker  E., Kiss  J. Z.
ISSN
1047-3211 (Print)
Publication state
Published
Issued date
03/2004
Volume
14
Number
3
Pages
332-41
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Mar
Abstract
Understanding the processes that underlie functional recovery after cortical injury is a major challenge for neurobiology and clinical neurology. The aim of the present study was to establish a mouse model of functional recovery that would facilitate the investigation of the molecular and cellular events involved in cortical dynamics. We show that a focal injury of approximately 0.5 mm of diameter and 1 mm depth made in the barrel cortex of adult mice induced a transitory deficit that could be characterized using somatosensory evoked potential (SEP), metabolic mapping and a behavioral test. SEP recordings of short latency responses using an epicranial multi-array system showed a decreased cortical activity in the peri-lesion regions 2 weeks after the injury and a partial recovery to normal pattern 6 weeks after the lesion. Delayed SEP signals over the motor cortex were not altered by the injury. Metabolic mapping with [14C]deoxyglucose uptake in the surround of the injury reproduced the time course of deficit and recovery. Finally, a deficit in vibrissae related performance in a gap-crossing test 1 week after injury was followed by a functional recovery in the following 2 weeks. We show in addition that the recovery process is deficient and significantly delayed in NCAM knockout mice lacking all isoforms of NCAM (neural cell adhesion molecule)and PSA-NCAM. These results support the hypothesis that impairment and recovery of functions after focal cortical lesion involves remodeling of intact circuits surrounding the lesion and that the NCAM molecule participate in this process. The model opens new possibilities for investigating the role of candidate molecules in functional recovery using genetically modified mice.
Keywords
Animals Antimetabolites/metabolism Behavior, Animal/*physiology Deoxyglucose/metabolism Evoked Potentials, Somatosensory/*physiology Male Mice Mice, Inbred C57BL Mice, Knockout Neural Cell Adhesion Molecules/genetics/*physiology Physical Stimulation Psychomotor Performance/physiology Somatosensory Cortex/*injuries/*metabolism/pathology Vibrissae/innervation
Pubmed
Web of science
Open Access
Yes
Create date
24/01/2008 14:41
Last modification date
25/09/2019 6:10
Usage data