Publications by authors named "Maria I Rehermann"

The cytoskeleton of ependymal cells is fundamental to organize and maintain the normal architecture of the central canal (CC). However, little is known about the plasticity of cytoskeletal components after spinal cord injury. Here, we focus on the structural organization of the cytoskeleton of ependymal cells in the normal and injured spinal cord of mice (both females and males) using immunohistochemical and electron microscopy techniques.

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The ependyma of the adult spinal cord is a latent stem cell niche that is reactivated by spinal cord injury contributing new cells to the glial scar. The cellular events taking place in the early stages of the reaction of the ependyma to injury remain little understood. Ependymal cells are functionally heterogeneous with a mitotically active subpopulation lining the lateral domains of the central canal (CC) that are coupled via gap junctions.

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Plasticity of neural circuits takes many forms and plays a fundamental role in regulating behavior to changing demands while maintaining stability. For example, during spinal cord development neurotransmitter identity in neurons is dynamically adjusted in response to changes in the activity of spinal networks. It is reasonable to speculate that this type of plasticity might occur also in mature spinal circuits in response to injury.

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Article Synopsis
  • Traumatic spinal cord injuries affect about 2.5 million people globally and have limited natural healing capabilities in mammals.
  • Effective restoration of function requires replacing lost cells and fostering the growth and repair of nerve connections.
  • Research on regenerative species like salamanders and certain fish reveals that specific spinal progenitor cells have the potential for self-repair, which could inform strategies for enhancing recovery in mammals.
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The ependymal layer is a preserved structure across vertebrates but its functional significance remains poorly understood. Modern studies emphasize the role played by radial glia (RG) as neurogenic progenitors. We speculated that the cells lining the prosencephalon ventricles of freshwater turtles may have retained key features of RG.

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In fresh-water turtles, the bridge connecting the proximal and caudal stumps of transected spinal cords consists of regenerating axons running through a glial cellular matrix. To understand the process leading to the generation of the scaffold bridging the lesion, we analyzed the mitotic activity triggered by spinal injury in animals maintained alive for 20-30 days after spinal cord transection. Flow cytometry and bromodeoxyuridine (BrdU)-labeling experiments revealed a significant increment of cycling cells around the lesion epicenter.

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This paper provides the first evidence that freshwater turtles are able to reconnect their completely transected spinal cords, leading to some degree of recovery of the motor functions lost after injury. Videographic analysis showed that some turtles (5 of 11) surviving more than 20 days after injury were able to initiate stepping locomotion. However, the stepping movements were slower than those of normal animals, and swimming patterns were not restored.

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