Remodeling of synaptic structures in the motor cortex following spinal cord injury.
After spinal cord injury (SCI), structural reorganization occurs at multiple levels of the motor system including the motor cortex, and this remodeling may underlie recovery of motor function. The present study determined whether SCI leads to a remodeling of synaptic structures in the motor cortex. Dendritic spines in the rat motor cortex were visualized by confocal microscopy in fixed slices, and their density and morphology were analyzed after an overhemisection injury at C4 level. Spine density decreased at 7 days and partially recovered by 28 days. Spine head diameter significantly increased in a layer-specific manner. SCI led to a higher proportion of longer spines especially at 28 days, resulting in a roughly 10% increase in mean spine length. In addition, filopodium-like long dendritic protrusions were more frequently observed after SCI, suggesting an increase in synaptogenic events. This spine remodeling was accompanied by increased expression of polysialylated neural cell adhesion molecule, which attenuates adhesion between the pre- and postsynaptic membranes, in the motor cortex from as early as 3 days to 2 weeks after injury, suggesting a decrease in synaptic adhesion during the remodeling process. These results demonstrate time-dependent changes in spine density and morphology in the motor cortex following SCI. This synaptic remodeling seems to proceed with a time scale ranging from days to weeks. Elongation of dendritic spines may indicate a more immature and modifiable pattern of synaptic connectivity in the motor cortex being reorganized following SCI.
Kim
Byung G
BG
Department of Neuroscience, NRB Rm EP-04, Georgetown University Medical Center, 3970 Reservoir Rd., NW, Washington, DC 20007, USA.
Dai
Hai-Ning
HN
McAtee
Marietta
M
Vicini
Stefano
S
Bregman
Barbara S
BS
D000596:Amino Acids; D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western / Q000379:methods; D049229:Dendritic Spines / Q000473:pathology / Q000502:physiology; D003952:Diagnostic Imaging; D004195:Disease Models, Animal; D000076122:Disks Large Homolog 4 Protein; D005260:Female; D066298:In Vitro Techniques; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D008565:Membrane Proteins / Q000378:metabolism; D009044:Motor Cortex / Q000473:pathology*; D039842:Neural Cell Adhesion Molecule L1 / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology*; D011554:Pseudopodia / Q000473:pathology / Q000502:physiology; D051381:Rats; D012794:Sialic Acids / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000473:pathology* / Q000503:physiopathology*; D013569:Synapses / Q000473:pathology* / Q000502:physiology*; D013997:Time Factors
D000596:Amino Acids; D000076122:Disks Large Homolog 4 Protein; C501449:Dlg4 protein, rat; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D039842:Neural Cell Adhesion Molecule L1; D012794:Sialic Acids; C098463:dolaisoleucine; C103469:polysialyl neural cell adhesion molecule