Motor cortex after C3 lesion
Ontology highlight
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: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: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
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.
2014-10-01 | GSE47900 | GEO
Project description:Purpose: We applied polyA site sequencing (Passeq) to human Huntington's disease and control motor cortex and cerebellum to test if any genes change 3′UTR isoforms abundance. Methods: 3′ sequencing was performed on 6 motor cortices from grade 1 Huntington's patient brains, 4 motor cortices from grade 2 Huntington's patient brains, and 5 motor cortices from control brains. Cerebellum samples included 9 cerebella from grade 2-3 Huntington's patient brains, and 7 cerebella from control brains. To verify HTT isoforms in mice, sequencing was performed on 5 Q140 mouse striata and 3 wild-type mouse striata. Results: We report 11% of genes from Huntington's disease patient motor cortex exhibit a change in at least one of their 3′UTR isoforms, commensurate with the 11% of genes which show different total expression in HD motor cortex versus control. In contrast, gene isoform and expression changes are minimal (<5%) in Huntington's disease cerebellum versus controls. In the motor cortex, we show isoform and gene expression differs between between grade 1 and grade 2 brains. We identify a novel isoform of huntingtin mRNA which is conserved in wild-type and Huntington's model mice. Conclusions: This is the first study characterizing widespread alterations in 3′UTR isoform abundance in Huntington's disease. Alterations in isoform abundance may affect mRNA metabolism in Huntington's disease brains.
2017-09-21 | GSE96099 | GEO