Motor cortex after C3 lesion
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE76679 | GEO | 2016/07/01
SECONDARY ACCESSION(S): PRJNA308308
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression analysis of motor cortex after spinal C3 lesion Dorsal column wire knife lesions: Adult female Fischer 344 rats weighing 150-200 gm were used. Animals underwent a laminectomy at spinal level C3. Dorsal funiculus lesions were made in the middle of C3 using a Kopf microwire device (Kopf Instruments, Tujunga, CA). After fixation in a spinal stereotaxic unit, a small dural incision was made. The wire knife was lowered into the spinal cord to a depth of 1.1 mm ventral to the dorsal cord surface and 1.1 mm to the left of the midline. The tip of the wireknife was extruded, forming a 2.25 mm-wide arc that was raised to the dorsal surface of the cord. To ensure complete axotomy of the dorsal funiculus, spinal tissue was compressed against the microwire knife surface using a microaspiration pipette until all visible white matter was transected. Cortical microdissection: The forelimb and hindlimb motor cortex were microdisected from rat cortices: Rostral to Bregma: an area from 2.0 to 4.5 mm mediolateral and from 0 to 2 mm anterior-posterior Caudal to Bregma: an area from 2.0 to 3.5 mediolateral and from 0 to 3 mm caudal to Bregma. Only the inferior half of the cortex containing layer V corticospinal motor neurons was sampled in each region.
2016-07-01 | E-GEOD-76679 | biostudies-arrayexpress
Project description:Patients with spinal cord injuries often suffer from multiple complications, including cognitive impairments after recovering from the primary wound. The molecular mechanism linking spinal cord injury and brain abnormality, however, remains elusive and has been largely attributed to neuroinflammation. In this work, we assessed persistent compositional and molecular changes in the motor cortex at 30 days post injury, a commonly perceived chronic stage, using a rat T10 contusion injury model. Brain slices and neurons isolated from the motor cortex were assessed using immunohistochemistry and RNA-sequencing, respectively. We observed significant changes in cellular compositions in the motor cortex including a decreased neuron to astrocyte ratio, and alterations in the morphology of neurons and astrocytes, indicating changes in functionality. Comparison of transcriptomic data collected at a sub-acute stage, namely 7 days post injury, with that at 30 days post injury, identified persistent and de novo (genes uniquely altered at 30 dpi.) changes that occur primarily after recovery of the spinal cord injury, enriched for neuronal and synaptic function related pathways. Strikingly, male and female rats showed distinct transcriptomic alterations at 30 days post-injury, with males showing neuron-related changes and females showing alterations in metabolism- and extracellular matrix–related pathways. These molecular differences were accompanied by better functional recovery in females, as reflected by significantly higher BBB scores, suggesting sex-dependent molecular changes induced in the motor cortex. Collectively, our study lays the foundation for understanding sexual dimorphism in brains after spinal cord injury and provides a plausible connection between spinal cord injury and increased risk for neurodegeneration later in life.
2026-04-06 | GSE326470 | GEO
Project description:The present study aimed to assess the molecular bases of cortical compensatory mechanisms following spinal cord injury in primates. To accomplish this, comprehensive changes in gene expression were investigated in the bilateral primary motor cortex (M1), dorsal premotor cortex (PMd), and ventral premotor cortex (PMv) after a unilateral lesion of the lateral corticospinal tract (l-CST). At 2 weeks after the lesion, a large number of genes exhibited altered expression levels in the contralesional M1, which is directly linked to the lesioned l-CST. Gene ontology and network analyses indicated that these changes in gene expression are involved in the atrophy and plasticity changes observed in neurons. Orchestrated gene expression changes were present when behavioral recovery was attained 3 months after the lesion, particularly among the bilateral premotor areas, and a large number of these genes are involved in plasticity. Moreover, several genes abundantly expressed in M1 of intact monkeys were upregulated in both the PMd and PMv after the l-CST lesion. These area-specific and time-dependent changes in gene expression may underlie the molecular mechanisms of functional recovery following a lesion of the l-CST.
2018-03-31 | GSE81264 | GEO
Project description:We performed micrarrays to investigate neuronal gene expression changes during acute inflammatory CNS axon injury using the murine myelin oligodendrocyte glycoprotein 35-55 (MOG35-55)-induced experimental autoimmune encephalomyelitis (EAE) model. The present study was assigned to assess the direct and indirect endogenous neuronal response to spinal axonal injury in the motor and sensory cortex. Gene expression in motor and sensory cortex enriched tissue was assessed from four healthy and six EAE female mice. Tissue was collected from mice with paraplegia or monoplegia, with contralateral hindlimb paresis (EAE day 18-21). The gene expression profiles of the EAE mice were compared to the motor or sensory cortex of healthy control mice, resulting in a list of differentially expressed genes in healthy and EAE mice.
2014-10-01 | E-GEOD-47900 | biostudies-arrayexpress
Project description:Corticothalamic Neurons in Motor Cortex Have a Permissive Role in Motor Execution
| PRJNA1241835 | ENA
Project description:Gene expression profiling has been performed previously on motor cortex and spinal cord homogenates and of sporadic ALS cases and controls, to identify genes and pathways differentially expressed in ALS. More recent studies have combined the use of laser capture microdissection (LCM) with gene expression profiling to isolate the motor neurons from the surrounding cells, such as microglia and astrocytes, in order to determine those genes differentially expressed in the vulnerable cell population – i.e. motor neuron. The aim of the present study is to combine LCM and microarray analysis to determine those genes and pathways differentially expressed in MNs from human SOD1-related MND and to establish potential pathways for therapeutic intervention. Keywords: Human motor neurons The aim of this study was to determine the gene expression profiles from a small subset of cases which all carry mutations in the SOD1 gene. Expression profiles from isolated motor neurons in SOD1-related ALS cases were compared to those from control motor neurons, in order to establish the pathways implicated in SOD1-related motor neuronal cell death. The 'control' samples were originally submitted to GEO as GSE19332.
2011-01-01 | E-GEOD-20589 | biostudies-arrayexpress
Project description:Molecular mechanisms over differentiation and differential axonal targeting of distinct neuron subtypes in the cerebral cortex are beginning to be elucidated. These studies have focused on controls that specifically distinguish one subtype of neocortical projection neurons, e.g. corticospinal motor neurons (CSMN), from closely related corticothalamic projection neurons (CThPN) or intracortical callosal projection neurons (CPN). CSMN are located in layer V of the neocortex and make synaptic connections to motor output circuitry in the spinal cord and brainstem. CSMN axons form the corticospinal tract (CST), which is the major motor output pathway from the motor cortex and critically controls voluntary movement. CSMN somatotopically and precisely target specific segments along the rostrocaudal axis of the spinal cord, the molecular basis for which remains unknown. We used microarrays to examine gene expression differences between two CSMN subpopulations that target different levels of the spinal cord - CSMN-C (which extend axons to the brainstem and cervical spinal cord) and CSMN-L (which preferrrentially extend axons to the thoracic and lumbar spinal cord). We compared CSMN-C vs CSMN-L gene expression at 3 critical developmental time points (previously described in Arlotta et a., 2005)
2018-12-31 | GSE77311 | GEO
Project description:RNA-seq analysis of mature mouse primary motor cortex in response to conditional knockdown of Fezf2. Analysis of M1 transcriptomes identifies significant changes to gene expression with the knockdown of Fezf2 in mature tissue.
2017-10-31 | GSE102365 | GEO
Project description:Gene expression profiling has been performed previously on motor cortex and spinal cord homogenates and of sporadic ALS cases and controls, to identify genes and pathways differentially expressed in ALS. More recent studies have combined the use of laser capture microdissection (LCM) with gene expression profiling to isolate the motor neurons from the surrounding cells, such as microglia and astrocytes, in order to determine those genes differentially expressed in the vulnerable cell population – i.e. motor neuron. The aim of the present study is to combine LCM and microarray analysis to determine those genes and pathways differentially expressed in MNs from human SOD1-related MND and to establish potential pathways for therapeutic intervention. Keywords: Human motor neurons
2011-01-01 | GSE20589 | GEO