Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE16710 | GEO | 2009/11/01

SECONDARY ACCESSION(S): PRJNA117361

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data from adult rat tail MNs after spinal cord transection

Project description: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.

2009-10-31 | E-GEOD-16710 | biostudies-arrayexpress

Time series gene expression data from adult rat tail MNs following spinal cord transection

2010-05-01 | GSE19701 | GEO

Time series gene expression data from adult rat tail MNs following spinal cord transection

Project description: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 reappearance of plateau potentials in motor neurons and the development of spasticity after spinalization. To understand the molecular mechanism behind this phenomena we examined the transcriptional response of the motor neurons after spinal cord injury as it progress over time. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immediate flaccid paralysis of the tail and a subsequent appearance of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurones 0, 2, 7, 21 and 60 days after complete spinal transection. Tail MNs were retrogradely labelled with Fluoro-Gold injected into the muscle and intra peritoneally. 5-7 days after tracer injections the spinal cord was dissected out, snap-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. 31 samples were hybridized onto chips, 4 Spi-0 (Control), 6 Spi-2, 5 Spi-7, 8 Spi-21 and 8 Spi-60.

2010-05-27 | E-GEOD-19701 | biostudies-arrayexpress

Changes in miRNAs in the dorsal root ganglion after CNS injury and intramuscular neurotrophin-3 treatment

Project description:Brain and spinal injury often impair sensorimotor processing in the spinal cord and reduce mobility. We established that complete transection of corticospinal pathways in the pyramids leads to increased spasms, excessive mono- and polysynaptic spinal reflexes and impaired locomotion in rats. Intramuscular neurotrophin-3 treatment at a clinically-feasible time-point after injury reduced these signs of spasticity. We found Neurotrophin-3 reduced spastic movements and improved neurophysiological sensorimotor control. Furthermore, the balance of inhibitory and excitatory synapses in the cord and the level of an ion transporter in motor neuron membranes required for normal reflexes were normalized. We discovered that Neurotrophin-3 is transported in sensory afferents from muscles to the dorsal root ganglia. Using genome-wide small RNA sequencing of the whole cervical level 6-8 dorsal root ganglia, we explored miRNA changes in afferent neurons that were present 10 weeks after bilateral pyramidotomy. Many of the dysregulated genes are involved in axon guidance and plasticity. Intramuscular neurotrophin-3 treatment normalized many of those gene changes and may be one of the mechanisms how reflexes, functional recovery and molecular markers in the spinal cord are restored. This identifies neurotrophin-3 as a therapy that treats the underlying causes of spasticity and not only its symptoms.

2018-05-29 | GSE82196 | GEO

Changes in mRNA in the dorsal root ganglion after CNS injury and intramuscular neurotrophin-3 treatment

Project description:Brain and spinal injury often impair sensorimotor processing in the spinal cord and reduce mobility. We established that complete transection of corticospinal pathways in the pyramids leads to increased spasms, excessive mono- and polysynaptic spinal reflexes and impaired locomotion in rats. Intramuscular neurotrophin-3 treatment at a clinically-feasible time-point after injury reduced these signs of spasticity. We found Neurotrophin-3 reduced spastic movements and improved neurophysiological sensorimotor control. Furthermore, the balance of inhibitory and excitatory synapses in the cord and the level of an ion transporter in motor neuron membranes required for normal reflexes were normalized. We discovered that Neurotrophin-3 is transported in sensory afferents from muscles to the dorsal root ganglia. Using genome-wide RNA sequencing of the whole cervical level 6-8 dorsal root ganglia, we explored mRNA changes in afferent neurons that were present 10 weeks after bilateral pyramidotomy. Many of the dysregulated genes are involved in axon guidance and plasticity. Intramuscular neurotrophin-3 treatment normalized many of those gene changes and may be one of the mechanisms how reflexes, functional recovery and molecular markers in the spinal cord are restored. This identifies neurotrophin-3 as a therapy that treats the underlying causes of spasticity and not only its symptoms.

2018-05-29 | GSE82195 | GEO

NMLF response to spinal cord injury in Zebrafish

Project description:The study was designed to identify genes regulated after spinal transection that might contribute to regenerative growth of neurons projecting from the NMLF in Zebrafish. Zebrafish were injured by surgical transection of the spinal cord at 1 mm caudal to the brainstem-spinal cord junction (Injured). Animals receiving sham surgery (identical surgical procedures without transection) served as control (Control). The nucleus of the medial longitudinal fascicle (NMLF) was laser capture microdissected from approximately 30 frozen sections. RNA was prepared, amplified, and run on Affymetrix Zebrafish arrays. Zebrafish were used because they recover swimming function after spinal transection in about 6 weeks. The NMLF has been identified as a prominent group of neurons that descend through the site of injury in the spinal cord and that regenerate after injury. Times were selected to distinguish early events from those in the timeframe of regenerative growth.

2011-12-01 | E-GEOD-28470 | biostudies-arrayexpress

Regulation of stem cell identity by miR-200a during spinal cord regeneration

Project description:Salamanders have the remarkable ability to functionally regenerate after spinal cord transection. In response to injury, GFAP+ glial cells in the axolotl spinal cord proliferate and migrate to replace the missing neural tube and create a permissive environment for axon regeneration. In this paper we show that miR-200a acts to repress expression of Brachyury in sox2 positive progenitor cells in the axoltol spinal cord after spinal cord injury but after tail amputation when multiple tissue types must be regenerated then mir-200a is downregualted allowing progenitor cells in the spinal cord to naturally become bipotent progenitors which can give rise to muscle and neural cell types. When miR-200a is inhibited after spinal cord injury then these cells also express BRachyury cna can form muscle.

2022-02-10 | GSE196098 | GEO

Gene profiling of intermediolateral column, medial, and lateral motoneuron after spinal cord transection

Project description:To determine spinal cord injury (SCI) induced changes in gene expression, laser capture microscopy (LCM) and Affymetrix microarrays were used to profiles three distinct populations of motor neurons (MNs) in five sets of littermates. In each set, one littermate received a lamenectomy (sham operated), and the other received a complete spinal cord transection. Each MN population was caudal to the transection and not axotomized. Thus, MNs in transected animals were responding to two major insults: deafferentation and changing microenvironments due to spreading immune and inflammatory responses. A total of 30 expression profiles from sham operated control animals have been uploaded to GEO database with accession number GSE2595. The current series contains 32 motoneuron expression profiles from spinalized mice. All chips (30 sham + 32 transection) were generated together using RMA in 2004.

2009-09-23 | GSE18179 | GEO

Intrinsic response of thoracic propriospinal neurons to axotomy

Project description:Analysis of expression changes in prelabeled laser-microdissected thoracic propriospinal neurons at different times after low-thoracic spinal cord transection in adult rats. Propriospinal neurons projecting to the lumbar enlargement were captured at various time points following no lesion or low thoracic spinal cord transection.

2010-05-05 | E-GEOD-20907 | biostudies-arrayexpress

Transcription profiling of mouse laser capture microdissected SOD1 G93A motor neurons reveals cellular pathways involved in the adaptation and progression of motor neuron injury in the mouse model of familial ALS

Project description:Microarray analysis has been applied to the study of ALS in order to investigate gene expression in whole spinal cord homogenates of SOD1 G93A mice and human ALS cases, although the massive presence of glial cells and inflammatory factors has made it difficult to define which gene expression changes were motor neuron specific. Recently, laser capture microdissection (LCM), combined with microarray analysis, has allowed the identification of motor neuron specific changes in gene expression in human ALS cases. The aim of the present study is to combine LCM and microarray analysis to study how motor neurons in the spinal cord of transgenic SOD1 G93A mice and transgenic SOD1 WT respond to stimuli determined by the presence of the human mutant protein throughout the evolution of the stages in motor neuron injury Experiment Overall Design: Motor neurons have been isolated from the spinal cord of G93A mice and non transgenic littermates at different time points and the transcription expression profile of the isolated motor neurons has been analysed

2008-06-11 | E-GEOD-10953 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data