Ontology highlight
ABSTRACT:
PROVIDER: PRJNA642748 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12107057_1.fastq.gz | Fastqsanger.gz | |||
| SRR12107057_2.fastq.gz | Fastqsanger.gz | |||
| SRR12107058_1.fastq.gz | Fastqsanger.gz | |||
| SRR12107058_2.fastq.gz | Fastqsanger.gz | |||
| SRR12107059_1.fastq.gz | Fastqsanger.gz |
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Project description:Painful diabetic neuropathy (PDN) is a debilitating complication of diabetes, yet its central nervous system pathogenesis remains poorly understood. We investigated transcriptomic alterations in the central amygdala (CeA) in a diabetic rat model exhibiting neuropathic pain behavior. Male Sprague-Dawley rats were intraperitoneally injected a single dose of streptozotocin to induce diabetes. Six weeks following administration, the development of neuropathic pain was confirmed by the von Frey filament test. Subsequently, RNA sequencing of the CeA tissues identified 157 differentially expressed genes. This RNA sequencing dataset of the CeA in a neuropathic pain-exhibiting diabetic rat model provides insights into central nervous system adaptations in PDN and highlights potential molecular targets for therapeutic intervention.
2026-03-03 | GSE322631 | GEO
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
Project description:This study investigated central transcriptional alterations associated with diabetic neuropathic pain and baclofen treatment. Whole-brain RNA sequencing was performed in control mice, untreated diabetic neuropathic pain mice, and baclofen-treated diabetic neuropathic pain mice. The dataset was used to assess GABAergic and inhibitory synaptic signaling, neuroinflammation, glial activation, and treatment-associated transcriptional modulation.
2026-08-13 | GSE343056 | GEO
Project description:Neuropathic pain is an apparently spontaneous experience triggered by abnormal physiology of the peripheral or central nervous system, which evolves with time. Neuropathic pain arising from peripheral nerve injury is characterized by a combination of spontaneous pain, hyperalgesia and allodynia. There is no evidence of this type of pain in human infants or rat pups; brachial plexus avulsion, which causes intense neuropathic pain in adults, is not painful when the injury is sustained at birth. Since infants are capable of nociception from before birth and display both acute and chronic inflammatory pain behaviour from an early neonatal age, it appears that the mechanisms underlying neuropathic pain are differentially regulated over a prolonged postnatal period. We used microarrays to detail the global programme of gene expression underlying the differences in nerve injury between along the postnatal development and identified distinct classes of regulated genes during the injury Experiment Overall Design: We have performed a microarray analysis of the rat L4/L5 dorsal root ganglia, 7 days post spared nerve injury, a model of neuropathic pain. Genes that are regulated in adult rats displaying neuropathic behaviour were compared to those regulated in young rats (10 days old) that did not show the same neuropathic behaviour.
2010-01-30 | E-GEOD-15041 | biostudies-arrayexpress
Project description:This program addresses the gene signature associated with DRG in the Chung rat model for neuropathic pain. The Chung neuropathic pain profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in DRG of the Sprague Dawley rats following spinal nerve ligation compared to the sham-operated controls.
2013-03-22 | E-GEOD-38038 | biostudies-arrayexpress
Project description:Peripheral nerve injury alters the expression of hundreds of proteins in dorsal root ganglia (DRG). Targeting some of these proteins has led to successful treatments for acute pain, but not for sustained postoperative neuropathic pain. The latter may require targeting multiple proteins. Since a single microRNA (miR) can affect the expression of multiple proteins, here, we describe an approach to identify chronic neuropathic pain-relevant miRs. We used two variants of the spared nerve injury (SNI): Sural-SNI and Tibial-SNI and found distinct pain phenotypes between the two. Both models induced strong mechanical allodynia, but only Sural-SNI rats maintained strong mechanical and cold allodynia, as previously reported. In contrast, we found that Tibial-SNI rats recovered from mechanical allodynia and never developed cold allodynia. Since both models involve nerve injury, we increased the probability of identifying differentially regulated miRs that correlated with the quality and magnitude of neuropathic pain and decreased the probability of detecting miRs that are solely involved in neuronal regeneration. We found seven such miRs in L3-L5 DRG. The expression of these miRs increased in Tibial-SNI. These miRs displayed a lower level of expression in Sural-SNI, with four having levels lower than those in sham animals. Bioinformatics analysis of how these miRs could affect the expression of some ion channels supports the view that, following a peripheral nerve injury, the increase of the 7 miRs may contribute to the recovery from neuropathic pain while the decrease of four of them may contribute to the development of chronic neuropathic pain. The approach used resulted in the identification of a small number of potentially neuropathic pain relevant miRs. Additional studies are required to investigate whether manipulating the expression of the identified miRs in primary sensory neurons can prevent or ameliorate chronic neuropathic pain following peripheral nerve injuries. To identify the miRs that were differentially dysregulated between Tibial-SNI and Sural-SNI, we first performed 12 microarrays in a limited number of samples (in four individual DRGs per group: Sham, Tibial-SNI and Sural-SNI; two L3-DRG and two L4-DRG). Then, miRs identified as having differential expression were corroborated with real time qRT-PCR in RNA isolated from individual DRGs (L3, L4 and L5) derived from 4 rats per group (not presented here, but in the manuscript).
2014-09-29 | E-GEOD-60033 | biostudies-arrayexpress
Project description:To investigate mechanisms underlying neuropathic pain, we established sciatic nerve chronic constriction injury (CCI) neuropathic pain model in rats, and performed RNA-seq on ipsilateral bulk L4-L6 dorsal root ganglia from CCI rats and sham rats 11 days after surgery. By comprehensive analysis, we identified several key mRNAs and miRNAs, especially those associated with inflammatory immune response, may serve as promising targets, facilitating further investigation and eventually developing better therapeutic strategies for NP.
2023-03-15 | GSE212311 | GEO
Project description:Neuropathic pain (NP) is a complex, chronic pain condition caused by injury or dysfunction affecting the somatosensory nervous system. This study aimed to identify crucial miRNA in prelimbic cortex (PL) involved in NP rats. miRNA microarrays were applied in the present study.
2020-02-13 | GSE145199 | GEO
Project description:Nerve injury-induced changes in pain-associated genes contribute to genesis of neuropathic pain and comorbid anxiety. Phosphorylated CTD interacting factor-1 (PCIF1)-triggered N6, 2′-O-dimethyladenosine (m6Am) mRNA modification represents an additional layer of gene regulation. However, the role of PCIF1 in these disorders is elusive. Here, we report PCIF1 is increased in glutamatergic neurons of primary somatosensory cortex hindlimb (S1HLGlu) in neuropathic pain mouse with anxiety, but not inflammatory pain or anxiety alone. Serpine-1 mRNA-binding protein-1 (SERBP1) is identified as a PCIF1 cofactor, their complex contributes to m6Am deposition onto mRNA. Blocking increase in SERBP1-PCIF1 in S1HLGlu abolishes m6Am gain in maf1 homolog, negative regulator of RNA polymerase III (Maf1), elevates MAF1 level, and mitigates neuropathic pain and anxiety. Conversely, mimicking this increase adds m6Am onto Maf1, reduces MAF1, leads to comorbidity symptoms. These findings highlight m6Am significance in neuropathic pain-anxiety comorbidity and identify S1HLGlu SERBP1–PCIF1 as a potential therapeutic target.
2025-06-30 | PXD065634 |
Project description:Clinical observations indicate that vitamin D is a pain alleviating molecule. In order to unveil the molecular mechanisms at play, we performed an experimental study on rats with a neuropathic pain. After three weeks of vitamin D treatment, the cerebrum, the spinal cord and the dorsal root ganglia were collected for a transcriptomic analysis, using cDNA microarrays.
2018-04-29 | E-MTAB-6801 | biostudies-arrayexpress