Transcriptomics

Dataset Information

3

Expression data from adult rat tail MNs after spinal cord transection


ABSTRACT: Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearence of plateau potentials in motor neurons and the development of spasticity after spinalization. To understand the molecular mechanism behind this phenomenon we examined the transcriptional response of the motor neurons after spinal cord injury. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immidate flaccid paralysis of the tail and a subsequent appearence of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurons 21 and 60 days after complete spinal transection where the tail exhibits clear signs of spasticity. Tail MNs were retorgradely labelled with flourogold injected into the muscle and intra peritoneally. 5-7 days after tracer injections the spinal cord was dissected out, snab frozen in liquid nitrogen, sliced in 10 um thick slices and fluorescent motor neurons were laser dissected into a collector tube to a total of ca. 50-200 cells pr sample. RNA was then extracted, two round amplified and hybridized to Affymetrix rat 230 2.0 arays. 27 samples were hybridized onto chips, 8 Spi-21, 8 Spi-60, 6 ShamC-21 and 5 ShamC-60.

ORGANISM(S): Rattus norvegicus  

SUBMITTER: Jacob Wienecke   Hans Hultborn  Ole Kiehn  Jesper Ryge  Ann-Charlotte Westerdahl 

PROVIDER: E-GEOD-16710 | ArrayExpress | 2009-10-31

SECONDARY ACCESSION(S): GSE16710PRJNA117361

REPOSITORIES: GEO, ArrayExpress

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Publications

Global gene expression analysis of rodent motor neurons following spinal cord injury associates molecular mechanisms with development of postinjury spasticity.

Wienecke J J   Westerdahl A-C AC   Hultborn H H   Kiehn O O   Ryge J J  

Journal of neurophysiology 20091125 2


Spinal cord injury leads to severe problems involving impaired motor, sensory, and autonomic functions. After spinal injury there is an initial phase of hyporeflexia followed by hyperreflexia, often referred to as spasticity. Previous studies have suggested a relationship between the reappearance of endogenous plateau potentials in motor neurons and the development of spasticity after spinalization. To unravel the molecular mechanisms underlying the increased excitability of motor neurons and th  ...[more]

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