Ontology highlight
ABSTRACT:
PROVIDER: PRJNA825413 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18710026_1.fastq.gz | Fastqsanger.gz | |||
| SRR18710026_2.fastq.gz | Fastqsanger.gz | |||
| SRR18710027_1.fastq.gz | Fastqsanger.gz | |||
| SRR18710027_2.fastq.gz | Fastqsanger.gz | |||
| SRR18710028_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
Similar Datasets
Project description:Ongoing nociceptive inputs from peripheral tissues and nerve injuries lead to maladaptive alterations in central nervous system, which drive the transition from acute to chronic pain. Although astrocytes act as dynamic and active players in neuropathic pain states, the contribution of astrocytes in upper brain nucleus in this process remains unclear. Here, we revealed that prolonged neuronal inputs induced by periphery injury leads to astrocyte reactive and downregulation of inward rectifying potassium channel protein 4.1 (Kir4.1) in paraventricular thalamus（PVT）. In turn, reactive PVT astrocytes could maintain the hyperexcitability of neurons, and enhanced projections from PVT to medial prefrontal cortex (mPFC) in the chronicity of neuropathic pain. Notably, we identify a neuro-glial interaction mediating pain chronification in PVT, and clarified Kir4.1 channels as a potential therapeutic target for neuropathic pain treatment.
2025-05-20 | GSE297165 | GEO
Project description:Chronic pain is one of the most significant and costly medical problems throughout the world. Recent evidence has confirmed the hippocampus as an active modulator of pain chronicity but the underlying mechanisms remain poorly defined. By means of in vivo electrophysiology together with chemogenetic and optogenetic manipulations in freely behaving mice, we identified a neural ensemble in the ventral hippocampal CA1 (vCA1) that showed inhibitory responses to noxious external stimuli, but not to innocuous stimuli. Following peripheral inflammation, this neuronal ensemble became responsive to innocuous stimuli and causally contributed to sensory hypersensitivity in inflammatory animals. Mimicking this inhibition of vCA1 neurons using chemogenetics in naïve mice induced chronic pain-like behavioral changes, whereas activating these vCA1 neurons in mice with chronic peripheral inflammation resulted in a striking reduction of pain-related behaviors. Pathway-specific manipulation of vCA1 projections to the basolateral amygdala (BLA) and infralimbic cortex (IL) showed that these pathways were differentially involved in pain modulation at different temporal stages of chronic inflammatory pain. These results confirm a crucial role of the ventral hippocampus and its circuits in modulating the development of chronic pain in mice.
2022-12-19 | PXD038416 | Pride
Project description:Post-surgical pain causes significant suffering. Extracts of the human amniotic membrane (AM) may be novel regenerative matrices, but little is known about their use in pain treatment. Locally applying FLO (particulates of AM) in mice acutely attenuated post-surgical pain hypersensitivity and inhibited its transition to a prolonged state after plantar-incision. Mechanistically, this was achieved through direct nociceptive neuronal inhibition via CD44-dependent mechanisms and indirect anti-pain effect by attenuating immune cell recruitment and promoting wound healing. We purified heavy chain-hyaluronic acid/pentraxin 3 (HC-HA/PTX3) from human AM as a major bioactive matrix component for pain relief, as it mirrored FLO-induced analgesia and nociceptive neuronal inhibition. Strikingly, HC-HA/PTX3 triggered acute cytoskeleton rearrangement to inhibit ion channels on nociceptive neurons, presenting a novel cellular mechanism for pain control. Moreover, long-term drug treatment broadly changed neuronal gene expression. Our study demonstrated the potential and mechanisms of a naturally occurring biologic from human birth tissues as non-opioid treatments for post-surgical pain.
2024-06-25 | GSE242389 | GEO
Project description:A genetically defined mPFC-thalamic circuit underlies pain chronicity
| PRJNA1016417 | ENA
Project description:We report global distribution of trimethylated Histone H3 Lysine 4 (H3K4me3) in human prefrontal cortex neurons at different ages Neuronal nuclei from human prefrontal cortex were isolated by FACS. Regions marked by H3K4me3 were identified by chromatin immunoprecipiation followed by deep sequencing.
2010-04-20 | E-GEOD-21172 | biostudies-arrayexpress
Project description:Distinct representation of visceral and somatic pain by unique PVH neuronal ensembles and suggested that PVH as a pain sorting center that distinctly processes visceral and somatic pain, providing a new framework for comprehending how the brain processes nociceptive information and identifying potential molecular targets for specific pain processing.
2024-09-23 | GSE254504 | GEO
Project description:Reliable representations of information regarding complex behaviors including social interactions require the coordinated activity of heterogeneous cell types within distributed brain regions. Activity in the medial prefrontal cortex is critical in regulating social behavior, but our understanding of the specific cell types which comprise the social ensemble has been limited by available mouse lines and molecular tagging strategies which rely on the expression of a single marker gene. Here we sought to quantify the heterogeneous neuronal populations which are recruited during social interaction in parallel in a non-biased manner and determine how distinct cell types are differentially active during social interactions. We identify distinct populations of prefrontal neurons activated by social interaction by quantification of immediate early gene (IEG) expression in transcriptomically clustered neurons. This approach revealed variability in the recruitment of different excitatory and inhibitory populations within the medial prefrontal cortex. Furthermore, evaluation of the populations of IEGs recruited following social interaction revealed both cell-type and region-specific transcriptional programs, suggesting that reliance on a single molecular marker is insufficient to quantify activation across all cell types. Our findings provide a comprehensive description of cell-type specific transcriptional programs invoked by social interactions and reveal new insights into the heterogeneous neuronal populations which compose the social ensemble
2024-06-14 | GSE269499 | GEO
Project description:We search for developmental changes specific to humans by examining gene expression profiles in the human, chimpanzee and rhesus macaque prefrontal and cerebellar cortex. In both brain regions, developmental patterns were more evolved in humans than in chimpanzees. The major human specific genes in prefrontal cortex was enriched in neuronal functions and regulated by several transcription factors, which were previously implicated in regulation of neuronal functions. To confirm neuronal function of the human prefrontal cortex specific genes, we identifed response genes upon neuronal activation in mouse cortical neurons. Our results show that human specific genes are enriched in the response genes upon neuronal activation, implying the function of human prefrontal cortex specific genes in synaptic development. The cortical neurons from E15 mouse were isolated and cultured. We then exposed neurons to bicuculline (Bic), or potassium chloride (KCl), or without treatment. The cultured neurons under each group were hybridized to Agilent whole mouse genome oligo microarray (4x44k).
2012-02-02 | E-GEOD-29139 | biostudies-arrayexpress
Project description:Chronic pain can be a debilitating condition, leading to profound changes in nearly every aspect of life. However, the reliance on opioids such as oxycodone for pain management is thought to initiate dependence and addiction liability. The neurobiological intersection at which opioids relieve pain and possibly transition to addiction is poorly understood. Using RNA sequencing pathway analysis in rats with complete Freund's adjuvant (CFA)-induced chronic inflammation, we found that the transcriptional signatures in the medial prefrontal cortex (mPFC; a brain region where pain and reward signals integrate) elicited by CFA in combination with oxycodone differed from those elicited by CFA or oxycodone alone. However, the expression of Egr3 was augmented in all animals receiving oxycodone. Furthermore, virus-mediated overexpression of EGR3 in the mPFC increased mechanical pain relief but not the affective aspect of pain in animals receiving oxycodone, whereas pharmacological inhibition of EGR3 via NFAT attenuated mechanical pain relief. Egr3 overexpression also increased the motivation to obtain oxycodone infusions in a progressive ratio test without altering the acquisition or maintenance of oxycodone self-administration. Taken together, these data suggest that EGR3 in the mPFC is at the intersection of nociceptive and addictive-like behaviors.
2023-05-18 | GSE232804 | GEO
Project description:Trimethylated histone H3-lysine 4 is primarily distributed in the form of sharp peaks, extending in neuronal chromatin on average only across 500-1500 base pairs mostly in close proximity to annotated transcription start sites. To explore whether H3K4me3 peaks could also extend across much broader domains, we undertook a detailed analysis of broadest domain cell-type specific H3K4me3 peaks in ChIP-seq datasets from sorted neuronal and non-neuronal nuclei in human, non-human primate and mouse prefrontal cortex (PFC), and blood for comparison. In this GEO submission, we list six newly generated ChIP-seq data sets. FACS sorted Neuronal (NeuN+) nuclei and non-neuronal (NeuN-) nuclei collected from prefrontal cortex (PFC) and processed by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-Seq). In addition we collected nucleated blood cells from 3 control subjects. These are additional subjects unrelated to brain cohort.
2016-07-21 | E-GEOD-72929 | biostudies-arrayexpress