Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis by RNA sequencing of the cortical brain in a mouse model of early life pain

ABSTRACT: Transcriptome analysis by RNA sequencing of the cortical brain in a mouse model of early life pain

PROVIDER: PRJNA823048 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18604307.fastq.gz	Fastqsanger.gz
	SRR18604308.fastq.gz	Fastqsanger.gz
	SRR18604309.fastq.gz	Fastqsanger.gz
	SRR18604310.fastq.gz	Fastqsanger.gz
	SRR18604311.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 64

Similar Datasets

Transcriptome analysis by RNA sequencing of the cortical brain in a mouse model of early life pain

Project description:Preterm children are frequently exposed to various painful stimuli in the early days of life. Early-life-pain (ELP) may affect cortical development and reduce the fitness and resilience in during youth and adult life. We developed an optogenetic Cre/loxP mouse model of "early-life-pain" (ELP) using mice with transgenic expression of an improved channelrhodopsin-2 (ChR2)/Td-Tomato fusion protein under control of the advillin promoter, that drives expression of ChR2/td-Tomato specifically in primary somatosensory neurons of the dorsal root ganglia (Avil-ChR2 mice). Floxed ChR2/td-Tomato littermates (ChR2-flfl) were used as controls. Mice were exposed to blue light in a chamber once daily from postnatal day P1-P5. Cortical gene expression was analyzed at P7 via RNA-sequencing in eight biological replicates per group. Cortices were rapidly excised and snap froze in liquid nitrogen. Total RNA was extracted from with Qiagen RNeays spin columns and quantified on a Nanodrop. Sequencing libraries were prepared using Illumina TruSeq stranded mRNA library preparation kit, and sequencing was performed on an Illumina NGS platform. The alignment was performed with SeqMan NGen 17 (Lasergene) using the reference genome mm10 provided from UCSC (GRCm38) as template, a minimum read length of 35 bp and automatic adapter trimming. Sequence reads were normalized with EdgeR and analyzed in ArrayStar 17 (Lasergene). Differential gene expression was assessed with general linear models and adjusted according to Benjamini Hochberg.

2023-09-06 | GSE200140 | GEO

Highly synchronized cortical circuit dynamics revealed by a new mouse model of neuropathic pain

Project description:The cerebral cortex plays a key role in the multi-dimensional human pain experience. However, the neural mechanisms mediating pain-related cortical activity remain largely unknown, particularly in primary somatosensory cortex (S1). We therefore developed a new animal model of trigeminal neuralgia, a prototypical neuropathic pain, which allowed us to evaluate pain-related cortical dynamics with unprecedented translational relevance. Our novel model (FLIT: Foramen Lacerum Impingement of Trigeminal-nerve) displayed robust clinically relevant trigeminal neuralgia-like behaviors, including asymmetric facial grimacing, dental pain-like behaviors, anxiety-like behavior, and sexual dysfunction, capturing many features of the human pain experience. Awake FLIT mice exhibited highly synchronized spontaneous population activity in S1, due to GABAergic interneuron hypoactivity. Remarkably, clinically effective treatments including carbamazepine and trigeminal nerve root decompression abrogated S1 synchronization and alleviated trigeminal neuralgia-like behaviors. These results reveal synchronized S1 activity as a new and important cortical substrate of neuropathic pain, which can be clinically targeted to provide effective therapy.

2023-02-10 | GSE162284 | GEO

Metagenomic signatures of early life brain damage

Project description:Metagenomic signatures of early life brain damage

| PRJNA1112760 | ENA

Cortical organoids model early brain development disrupted by 16p11.2 CNV in autism

Project description:Reciprocal deletion and duplication of 16p11.2 is the most common copy number variation (CNV) associated with Autism Spectrum Disorder (ASD) and other developmental disorders, and has significant effect on brain size. We used cortical organoids derived from ASD cases to investigate neurodevelopmental pathways dysregulated by dosage changes of 16p11.2 CNV. We show that organoids recapitulate patients’ macrocephaly and microcephaly phenotypes. Deletions and duplications have “mirror” effects on cell proliferation, maturation and synapse number, consistent with “mirror” effects on brain development in humans. Neuronal migration was decreased in both, deletion and duplication organoids. Transcriptomic and proteomic profiling revealed synaptic defects and neuronal migration as key drivers of 16p11.2 functional effect. We implicate upregulation of small GTPase RhoA involved in regulation of cytoskeletal dynamics, neuron migration and neurite outgrowth as one of the pathways impacted by the 16p11.2 CNV in ASD. Treatment with the RhoA inhibitor Rhosin rescued neuron migration, but not synaptic defects. This study identifies pathways dysregulated by the 16p11.2 CNV during early neocortical development using cortical organoid models. Grant ID: Simons Foundation, #345469 Grant Title: Translational dysregulation of the RhoA pathway in autism Affiliation: University of California San Diego Name: Lilia M. Iakoucheva; Alysson R. Muotri

2021-07-31 | GSE142174 | GEO

Cortical organoids model early brain development disrupted by 16p11.2 CNV in autism

Project description:Cortical organoids model early brain development disrupted by 16p11.2 CNV in autism

| PRJNA596197 | ENA

Nested oscillatory dynamics in cortical organoids model early human brain network development

Project description:Nested oscillatory dynamics in cortical organoids model early human brain network development

| PRJNA534424 | ENA

Infant Pain Vs. Pain with Parental Suppression: Immediate and Enduring Impact on Brain, Pain and Affect

Project description:Infant Pain Vs. Pain with Parental Suppression: Immediate and Enduring Impact on Brain, Pain and Affect

| PRJNA917311 | ENA

Early life cisplatin exposure induces nerve growth factor mediated neuroinflammation and chemotherapy induced neuropathic pain

Project description:Chemotherapy-induced neuropathic pain (CINP) is a common adverse health related comorbidity that manifests later in life in paediatric cancer patients. Current analgesia is ineffective, aligning closely with our lack of understanding of CINP. The aim of this study was to investigate how cisplatin induces nerve growth factor mediated neuroinflammation and nociceptor sensitisation. In a rodent model of cisplatin induced survivorship pain, cisplatin induced a neuroinflammatory environment in the dorsal root ganglia (DRG) demonstrated by nerve growth factor (NGF) positive macrophages infiltrating into the DRG. Cisplatin treated CD11b/F480 positive macrophages expressed more NGF compared to vehicle treated. Primary DRG sensory neuronal cultures demonstrated enhanced NGF-dependent TRPV1 mediated nociceptor activity after cisplatin treatment. Increased nociceptor activity was also observed when cultured DRG neurons were treated with conditioned media from cisplatin activated macrophages. Elevated nociceptor activity was dose-dependently inhibited by a neutralising NGF antibody. Intraperitoneal administration of a NGF neutralising antibody reduced cisplatin-induced mechanical hypersensitivity and aberrant nociceptor intraepidermal nerve fibre density. These findings identify that a monocyte/macrophage driven NGF/TrkA pathway is a novel analgesic target for adult survivors of childhood cancer.

2024-11-25 | GSE281897 | GEO

Nested oscillatory dynamics in cortical organoids model early human brain network development

Project description:We characterized the different cell types and their differential gene expression patterns in 1, 3, 6, and 10 month-old cortical organoids.

2019-04-25 | GSE130238 | GEO

Neuropathic pain promotes gene expression adaptations in brain networks involved in stress and depression

Project description:Neuropathic pain is a complex chronic condition, characterized by a wide range of sensory, cognitive, and affective symptoms. Indeed, a large percentage of neuropathic pain patients are also afflicted with depression and anxiety disorders -- a pattern that is reliably replicated in animal models. Mounting evidence from clinical and preclinical studies indicates that chronic pain corresponds with adaptations in several brain networks involved in mood, motivation, and reward. Chronic stress is also a major determinant for depression. However, whether chronic pain and chronic stress affect similar mechanisms, and whether chronic pain can affect gene expression patterns known to be involved in depression, remains poorly understood. We employed the spared nerve injury model (SNI) of neuropathic pain in adult C57BL\6 mice and performed next-generation RNA-sequencing in order to monitor changes in gene expression in three brain regions known to be implicated in the pathophysiology of depression and in the modulation of pain: the nucleus accumbens (NAc), the medial prefrontal cortex (mPFC), and the periaqueductal grey (PAG). We observed mostly unique transcriptome profiles across the three brain regions but found common intracellular signal transduction pathways and biological functions were affected. A large amount of genes showing SNI-induced altered expression have been implicated in depression, anxiety, or chronic pain. In addition, we identified genes that are similarly regulated in a murine model of depression: chronic unpredictable stress. Our study provides the first unbiased characterization of neuropathic pain-induced long-term gene expression changes in three distinct brain regions, and presents evidence that neuropathic pain affects the expression of several genes that are also regulated by chronic stress.

2017-09-06 | GSE91396 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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