Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.expneurol.2011.02.003
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dc.titleIncreased synapsin expression and neurite sprouting in lamprey brain after spinal cord injury
dc.contributor.authorLau, B.Y.B.
dc.contributor.authorFoldes, A.E.
dc.contributor.authorAlieva, N.O.
dc.contributor.authorOliphint, P.A.
dc.contributor.authorBusch, D.J.
dc.contributor.authorMorgan, J.R.
dc.date.accessioned2016-10-18T06:27:22Z
dc.date.available2016-10-18T06:27:22Z
dc.date.issued2011-04
dc.identifier.citationLau, 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
dc.identifier.issn00144886
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/128528
dc.description.abstractSpinal 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.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.expneurol.2011.02.003
dc.sourceScopus
dc.subjectPetromyzon marinus
dc.subjectPhospho-synapsin
dc.subjectPKA
dc.subjectSynapsin
dc.subjectSynaptic vesicle
dc.subjectSynaptogyrin
dc.subjectSynaptoporin
dc.subjectVAMP
dc.typeArticle
dc.contributor.departmentMECHANOBIOLOGY INSTITUTE
dc.description.doi10.1016/j.expneurol.2011.02.003
dc.description.sourcetitleExperimental Neurology
dc.description.volume228
dc.description.issue2
dc.description.page283-293
dc.description.codenEXNEA
dc.identifier.isiut000288829900016
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