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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

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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 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

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

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

Gene expression of pdgfrb+ cells in the intact and injured spinal cord.

Project description:Spinal cord injury (SCI) leads to fibrotic scar formation at the lesion site, which finally affects axon regeneration and motor functional recovery. Myofibroblasts have been regarded as the main cell types that filled in the fibrotic scar, however, the cell source of myofibroblasts in transection and crush SCI model remain to be elusive. Here we used lineage tracing or single cell transcription sequencing to investigate the cell origin of fibrotic scar. We found fibrotic scars were filled from PDGFRβ+ daughter cells in spinal cord in crush SCI or transection SCI. The parenchyma perivascular-derived and meninges-derived PDGFRβ+ fibroblasts, but not PDGFRβ+ pericytes, proliferated and contributed to fibrotic cells in the lesion core. The percentage of meninges-derived fibroblasts specifically was higher than parenchyma perivascular-derived fibroblasts in transection model, which might contribute to the more fibrotic scar in transection model than crush model. These findings may provide theoretical support for the treatment of spinal cord injury.

2024-06-07 | GSE218584 | GEO

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