Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.expneurol.2011.02.003
Title: Increased synapsin expression and neurite sprouting in lamprey brain after spinal cord injury
Authors: Lau, B.Y.B.
Foldes, A.E.
Alieva, N.O. 
Oliphint, P.A.
Busch, D.J.
Morgan, J.R.
Keywords: Petromyzon marinus
Phospho-synapsin
PKA
Synapsin
Synaptic vesicle
Synaptogyrin
Synaptoporin
VAMP
Issue Date: Apr-2011
Source: Lau, B.Y.B., Foldes, A.E., Alieva, N.O., Oliphint, P.A., Busch, D.J., Morgan, J.R. (2011-04). Increased synapsin expression and neurite sprouting in lamprey brain after spinal cord injury. Experimental Neurology 228 (2) : 283-293. ScholarBank@NUS Repository. https://doi.org/10.1016/j.expneurol.2011.02.003
Abstract: Spinal cord injury induces structural plasticity throughout the mammalian nervous system, including distant locations in the brain. Several types of injury-induced plasticity have been identified, such as neurite sprouting, axon regeneration, and synaptic remodeling. However, the molecular mechanisms involved in injury-induced plasticity are unclear as is the extent to which injury-induced plasticity in brain is conserved across vertebrate lineages. Due to its robust roles in neurite outgrowth and synapse formation during developmental processes, we examined synapsin for its potential involvement in injury-induced plasticity. We used lamprey, a vertebrate that undergoes robust anatomical plasticity and functional recovery after spinal cord injury. At 3 and 11. weeks after spinal cord transection, synapsin I mRNA was upregulated > 2-fold in lamprey brain, as assayed by semi-quantitative RT-PCR. Other synaptic vesicle-associated genes remained unchanged. In situ hybridization revealed that synapsin I mRNA was increased globally throughout the lamprey brain. Immunolabeling for synapsin I protein revealed a significant increase in both the intensity and density of synapsin I-positive structures in lamprey hindbrain at 11. weeks post-transection, relative to controls. Moreover, the number of structures immunolabeled for phospho-synapsin (serine 9) increased after injury, suggestive of neurite sprouting. Indeed, at the ultrastructural level, there was an increase in neurite density at 11. weeks post-transection. Taken together, these data show that neurite sprouting in the brain is an evolutionarily conserved response to a distant spinal cord injury and suggest that synapsin and its phosphorylation at serine 9 play key roles in the sprouting mechanism. © 2011 Elsevier Inc.
Source Title: Experimental Neurology
URI: http://scholarbank.nus.edu.sg/handle/10635/128528
ISSN: 00144886
DOI: 10.1016/j.expneurol.2011.02.003
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