A pontine center in descending pain control
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA993642 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Our perception of pain changes according to expectation, context and mood illustrating how top-down-circuits affect sensory processing. Here we developed an intersectional platform for identifying supraspinal descending neurons that are engaged when an animal experiences pain. Amongst these, we identified a cluster of cells in the pontine micturition center (Barrington’s nucleus), expressing corticotropin-releasing-hormone (BarCrh) that detect painful but not innocuous stimuli. When activated, BarCrh-neurons attenuate nocifensive responses as well as tactile neuropathic pain. Mechanistically, pain related input from the ventrolateral periaqueductal gray activates BarCrh-neurons, which in turn project to the spinal dorsal horn to mediate analgesia. In combination, our data demonstrate that Barrington’s nucleus is not just a relay station dedicated to triggering micturition but also powerfully controls painful sensory input to the brain.
2025-02-17 | GSE237054 | GEO
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:Characterizing the proteomic profile of extracellular vesicles isolated from the descending colon of pediatric patients with inflammatory bowel disease and control participants
2018-09-11 | PXD007959 | Pride
Project description:Control ChIP-seq on mucosa of descending colon tissue male adult (40 years) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2021-05-23 | GSE175267 | GEO
Project description:HEAL PRECISION: INTERCEPT: Integrated Research Center for human Pain Tissues
| PRJNA1165342 | ENA
Project description:HEAL PRECISION: INTERCEPT: Integrated Research Center for human Pain Tissues
| PRJNA1165343 | ENA
Project description:Descending thoracic aortic aneurysms and dissections can go undetected until severe and catastrophic, and few clinical indices exist to screen for aneurysms or predict their risk of dissection or rupture. This study generated a plasma proteomic dataset from 150 patients with descending thoracic aortic disease and 52 controls to identify proteomic signatures capable of differentiating descending thoracic aortic disease from non-disease controls, as well as between cases with aneurysm versus descending ‘type B’ dissection. Of the 1,468 peptides and 195 proteins quantified across all samples, 853 peptides and 99 proteins were quantitatively different between disease and control patients (BH adjusted p-value < 0.01 from t-tests). Supervised machine learning (ML) methods were used to classify disease from control and aneurysm from descending dissection cases. The highest precision-recall area under the curve (PR AUC) was achieved on the held-out test set using significantly different proteins between disease and control patients (PR AUC 0.99), followed by input of significant peptides (PR AUC 0.96). Despite no statistically significant proteins between aneurysm and dissection cases, use of all proteins was able to modestly classify between the two disease states (PR AUC 0.77). To overcome correlation in the proteins and enable biological pathway analysis, a disease versus control classifier was optimized using only seven unique protein clusters, which achieved comparable performance to models trained on all/significant proteins (accuracy 0.88, F1-score 0.78, PR AUC 0.90). Model interpretation with permutation importance revealed that proteins in the most important clusters for differentiating disease and control function in coagulation, protein-lipid complex remodeling, and acute inflammatory response.
2024-06-16 | PXD041337 | Pride
Project description:The mechanism of chronic orofacial pain was investigated by examining the interaction between activated microglia, C1q and neurons in RVM of rats with orofacial pain caused by temporomandibular joint injection of CFA. The results demonstrated that the pain threshold in CFA group exhibited a continuous decline, reaching its lowest point on the third day. During the modeling process, administered daily stereotactic injections of ANX-005 and minocycline into the RVM, which resulted in a notable recovery in the rats' pain threshold and a significant increase in C1q/C3 and microglia in RVM of CFA rat. The application of ANX-005 or minocycline resulted in a reduction in the expression of C1q/C3 and microglia. Notably, the expression of excitatory presynaptic membrane markers reduced and the length and density of dendritic spines decreased on neurons in RVM. Additionally, C1q was abundantly localized on excitatory presynaptic membranes and expressed in microglial lysosomes. Treatment with ANX-005 or minocycline resulted in a reduced number of immunofluorescence colocalizations and an elevated dendritic spine density. These findings indicate that initial orofacial pain induced by CFA, microglia in RVM are involved in the pruning of excitatory presynaptic membranes through the complement C1q/C3-CR3 signaling pathway. This process results in a reduction in the proportion of excitatory synapses and a disruption in the physiological balance between RVM descending facilitation and descending inhibition. This leads to the predominance of descending facilitation in pain transmission in the RVM, which in turn facilitates the chronification of orofacial pain.
2025-01-27 | GSE287644 | GEO
Project description:Sensitization of spinal nociceptive circuits plays a cardinal role in neuropathic pain. This sensitization depends on new gene expression that is primarily regulated via transcriptional and translational control mechanisms. The relative roles of these mechanisms in regulating gene expression in the clinically relevant chronic phase of neuropathic pain are not well understood. Here, we show that changes in gene expression in the spinal cord during the chronic phase of neuropathic pain are substantially regulated at the translational level. Downregulating spinal translation at the chronic phase alleviated pain hypersensitivity. Cell-type-specific profiling revealed that spinal inhibitory neurons exhibited greater changes in translation after peripheral nerve injury compared to excitatory neurons. Notably, increasing translation selectively in all inhibitory neurons or parvalbumin-positive (PV + ) interneurons, but not excitatory neurons, promoted mechanical pain hypersensitivity. Furthermore, increasing translation in PV + neurons decreased their intrinsic excitability and spiking activity, whereas reducing translation in spinal PV + neurons prevented the nerve injury-induced decrease in excitability. Thus, translational control mechanisms in the spinal cord, primarily in inhibitory neurons, play a critical role in mediating neuropathic pain hypersensitivity.
2024-04-30 | GSE265957 | GEO
Project description:Fibulin-4 plays an essential role in elastic fiber formation, though it's exact function is unclear. Mice lacking the fibulin-4 gene develop cutis laxa with thoracic aortic aneurysms and have narrowed descending aortic diamaters, dying shortly after birth. Another model that disrupt elastic fiber formation, elastin gene knockeds, are also perinatally lethal and have narrowed descending aortas but do not develop thoracic aneurysms. We hypothesized that there may be altered gene expression to explain the altered anatomy based on aortic tissue location we observed, which may provide therapeutic target(s) Ascending and descending aortas of p0 mouse pups were dissected, pooled in groups of eight, and homogenized to isolate RNA and we used microarrays on the pooled samples to identify genes that had expression significantly changed.
2015-04-10 | E-GEOD-67707 | biostudies-arrayexpress