RNA-seq of mouse primary somatosensory cortex (S1) in a neuropathic pain model after electroacupuncture stimulus
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB42405 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR5056100.fastq.gz | Fastqsanger.gz | |||
| ERR5056101.fastq.gz | Fastqsanger.gz | |||
| ERR5056102.fastq.gz | Fastqsanger.gz | |||
| ERR5056103.fastq.gz | Fastqsanger.gz | |||
| ERR5056095.fastq.gz | Fastqsanger.gz |
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Project description:This study aims to identify the molecular mechanism in the sensory cortex underlying pain-relief effect of electroacupuncture
2021-01-09 | E-MTAB-9987 | biostudies-arrayexpress
Project description:Single-Cell Transcriptomic Analysis of Somatosensory Neurons Uncovers Temporal Development of Neuropathic Pain
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Project description:Peripheral nerve injury could lead to chronic neuropathic pain. Understanding transcriptional changes induced by nerve injury could provide fundamental insights into the complex pathogenesis of neuropathic pain. Gene expression profiles of dorsal root ganglia (DRG) under neuropathic pain condition have been studied. However, little is known about transcriptomic changes in individual DRG neurons after peripheral nerve injury. Here we performed single-cell RNA sequencing on dissociated mouse DRG cells after spared nerve injury (SNI). In addition to DRG neuron types also found under normal conditions, we identified three SNI-induced neuron clusters (SNIICs) characterized by the expression of Atf3/Gfra3/Gal (SNIIC1), Atf3/Mrgprd (SNIIC2) and Atf3/S100b/Gal (SNIIC3). These SNIICs were originated from Cldn9+/Gal+, Mrgprd+ and Trappc3l+ DRG neuron types. Interestingly, SNIIC2 was switched to SNIIC1 by increasing Gal and reducing Mrgprd expression 2 days after nerve injury. Inferring the gene regulatory networks underlying nerve injury, we revealed that activated transcription factor Atf3 and Egr1 in SNIICs could enhance Gal expression while activated Cpeb1 in SNIIC2 might suppress Mrgprd expression within 2 days after SNI. Furthermore, we screened the transcriptomic changes in the development of neuropathic pain to identify the potential analgesic targets. We revealed that the expression of cardiotrophin-like cytokine factor 1, which could activate the astrocytes in the dorsal horn of spinal cord, was increased in SNIIC1 neurons and contributed to SNI-induced mechanical allodynia. Therefore, our results provide a new framework to understand the changes in neuron types and the dynamics of molecular and cellular mechanisms underlying the development of neuropathic pain.
2021-02-24 | GSE155622 | 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: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 mRNA in prelimbic cortex (PL) involved in NP rats. mRNA microarrays were applied in the present study.
2020-02-14 | GSE145226 | GEO
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:Electroacupuncture (EA) has been accepted to effectively relieve neuropathic pain. Current knowledge of its neural modulation mainly covers the spinal cord and subcortical nuclei, with little evidence from the cortical regions. Using in vivo two-photon imaging in mice with chronic constriction injury, we found that EA treatment systemically modulated the Ca2+ activity of neural circuits in the primary somatosensory cortex, including the suppression of excitatory pyramidal neurons, potentiation of GABAergic somatostatin-positive interneurons, and suppression of vasoactive intestinal peptide-positive interneurons. Furthermore, EA-mediated alleviation of pain hypersensitivity and cortical modulation were dependent on the activation of endocannabinoid receptor 1. These findings collectively reveal a cortical circuit involved in relieving mechanical or thermal hypersensitivity under neuropathic pain and identify one molecular pathway directing analgesic effects of EA.
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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.
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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:Neuropathic pain (NP), defined as a complex chronic pain state caused by somatosensory nervous system lesions or diseases, is currently the most challenging clinical neurological disorder in the world. The main signs and symptoms of NP include spontaneous pain, abnormal pain and hyperalgesia. It is generally believed that the specific pathological causes of NP include spinal cord or peripheral spinal cord injury, postherpetic neuralgia, trigeminal neuralgia, and tumor invasion. While the critical role of mRNA in NP is well recognized, the involvement of mRNA in the development of NP remains to be elucidated. Therefore, in this study, we explored changes in mRNA expression profiles through transcriptome sequencing to provide a landscape of mRNA dysregulation in the NP spinal cord.
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