gms | German Medical Science

70. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Skandinavischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

12.05. - 15.05.2019, Würzburg

Formation of somatosensory detourcircuits after spinal cord injury in mice

Die Entstehung von somatosensiblen Signalwegen zur Überbrückung von Rückenmarksverletzungen im Mausmodell

Meeting Abstract

  • presenting/speaker Julian Schwarting - Klinikum der Universität München, Neurochirurgische Klinik und Poliklinik, München, Deutschland; Klinikum der Universität München, Institut für Klinische Neuroimmunologie, München, Deutschland
  • Charlene Granier - Klinikum der Universität München, Institut für Klinische Neuroimmunologie, München, Deutschland
  • Fabian Laage-Gaupp - Klinikum der Universität München, Institut für Klinische Neuroimmunologie, München, Deutschland
  • Karl-Klaus Conzelmann - Klinikum der Universität München, Max von Pettenkofer-Institut & Gene Center, München, Deutschland
  • Alexander Gahnem - Klinikum der Universität München, Max von Pettenkofer-Institut & Gene Center, München, Deutschland
  • Martin Kerschensteiner - Klinikum der Universität München, Institut für Klinische Neuroimmunologie, München, Deutschland
  • Florence Bareyre - Klinikum der Universität München, Institut für Klinische Neuroimmunologie, München, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 70. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Skandinavischen Gesellschaft für Neurochirurgie. Würzburg, 12.-15.05.2019. Düsseldorf: German Medical Science GMS Publishing House; 2019. DocV246

doi: 10.3205/19dgnc265, urn:nbn:de:0183-19dgnc2655

Published: May 8, 2019

© 2019 Schwarting et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.


Outline

Text

Objective: Spinal cord injury results in the transection of sensory ascending and motor descending tracts causing sensorymotor dysfunction below the injury site. While complete transections of the spinal cord always lead to permanent disabilities, smaller injuries can be followed by substantial functional recovery. This recovery is mediated at least in part by axonal remodeling, the formation of new intraspinal detour circuits that circumvent the lesions site. Detour circuits have so far only been shown to occur in motor systems. Using a combination of different viral tracing techniques we asked whether such remodeling events occur in the somatosensory system after spinal cord injury in mice.

Methods: Mice received a dorsal column lesion and the formation of somatosensory detour circuits was compared to control animals at early (21d) and chronic (84d) timepoints after injury. To analyze the formation of collaterals from the sensory fibers, we injected an AAV-virus expressing the yellow fluorescent protein into the dorsal root ganglion (DRG) at C6. To label monosynaptic spinal interneurons projecting to the cuneate nucleus, we made use of a retrograde monosynaptic virus and injected a pseudotyped rabies viruses using a stereotactic ventral approach into the cuneate nucleus. Animals were dissected and imaged by confocal microscopy. We quantified the amount and the location of sprouting, contacts of sprouts to labelled relay interneurons and described the distribution of relay neurons before and after injury.

Results: We observed that sprouting is increased at 21d (p<0.001) after dorsal column lesion and remains increased chronically (84d) after injury (p<0.01). Interneurons monosynaptically connected to the cuneate nucleus are located in the intermediate layers of the spinal cord. Compared to the control group we saw that the contacts of sensory axons with labelled interneurons were increased 21d (p<0.001) and 84d after injury (p<0.05). The contact per neuron was also significantly increased (p<0.01) after 21d and after 84d (p<0.05).

Conclusion: Our results clearly show that the formation of detour circuits is not limited to motor systems but also occurs in somatosensory tracts. This is an interesting observation as functional recovery from spinal cord injury not only relies on the recovery of motor function but also of sensory feedback. Our work suggests that increasing remodeling of motor and sensory axons could be the key to efficient rehabilitation following incomplete spinal cord injury.