Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA222321 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:HDAC inhibitors attenuate the development of hypersensitivity in models of neuropathic pain [spinal cord tissue]
| PRJNA222323 | ENA
Project description:DRG from CCI and Seltzer models of neuropathic pain and sham operated animals
| PRJNA92277 | ENA
Project description:Comparison of L5 DRG gene expression profiles at day 14 from SNT treated animals vs. sham controls. This experiment is part of larger study, where the expression profiles of three disparate models of neuropathic pain (SNT, VZV infection and gp120+ddC) are compared in order to find genes that are responsible for mechanical hypersensitivity
2008-07-14 | E-MEXP-976 | biostudies-arrayexpress
Project description:Comparison of L5 DRG gene expression profiles at day 14 from gp120+ddC treated animals vs sham (SA + saline) treated animals.<br>This experiment is part of larger study, where the expression profiles of three disparate models of neuropathic pain (SNT, VZV infection and gp120+ddC) are compared in order to find genes that are responsible for mechanical hypersensitivity formation/maintenance.
2008-01-01 | E-MEXP-974 | biostudies-arrayexpress
Project description:Histone deacetylase inhibitors (HDACIs) interfere with the epigenetic process of histone acetylation and are known to have analgesic properties in models of chronic inflammatory pain. The aim of this study was to determine whether these compounds could also affect neuropathic pain. Different class I HDACIs were delivered intrathecally into rat spinal cord in models of traumatic nerve injury and antiretroviral drug-induced peripheral neuropathy (stavudine, d4T). Mechanical and thermal hypersensitivity was attenuated by 40% to 50% as a result of HDACI treatment, but only if started before any insult. The drugs globally increased histone acetylation in the spinal cord, but appeared to have no measurable effects in relevant dorsal root ganglia in this treatment paradigm, suggesting that any potential mechanism should be sought in the central nervous system. Microarray analysis of dorsal cord RNA revealed the signature of the specific compound used (MS-275) and suggested that its main effect was mediated through HDAC1. Taken together, these data support a role for histone acetylation in the emergence of neuropathic pain. n = 4, HDACi treated vs. vehicle treated. Injured ipsilateral DRG after L5 spinal nerve transection. Spinal cord tissue was run in a separate Affymetrix experiment.
2013-10-01 | E-GEOD-51295 | biostudies-arrayexpress
Project description:Histone deacetylase inhibitors (HDACIs) interfere with the epigenetic process of histone acetylation and are known to have analgesic properties in models of chronic inflammatory pain. The aim of this study was to determine whether these compounds could also affect neuropathic pain. Different class I HDACIs were delivered intrathecally into rat spinal cord in models of traumatic nerve injury and antiretroviral drug-induced peripheral neuropathy (stavudine, d4T). Mechanical and thermal hypersensitivity was attenuated by 40% to 50% as a result of HDACI treatment, but only if started before any insult. The drugs globally increased histone acetylation in the spinal cord, but appeared to have no measurable effects in relevant dorsal root ganglia in this treatment paradigm, suggesting that any potential mechanism should be sought in the central nervous system. Microarray analysis of dorsal cord RNA revealed the signature of the specific compound used (MS-275) and suggested that its main effect was mediated through HDAC1. Taken together, these data support a role for histone acetylation in the emergence of neuropathic pain. n = 4, HDACi treated vs. vehicle treated. Ipsilateral dorsal spinal cord tissue after L5 spinal nerve transection, DRG tissue was run in a separate Affymetrix experiment.
2013-10-01 | E-GEOD-51294 | biostudies-arrayexpress
Project description:Two out-bred rat selection lines were separated to produce different hypersensitivity phenotypes following nerve injury. These lines were termed High Pain and Low Pain (HP or LP). Each sub-strain was either subject to a Sham surgery or a Spinal Nerve Ligation (SNL) surgery to the L4 and L5 spinal nerves. Three days following surgery L4/L5 Dorsal Root Ganglia (DRG) were dissected from these animals. For the rat line separation protocol see: Devor M, Raber P (1990) Heritability of symptoms in an experimental model of neuropathic pain. Pain 42:51-67. 12 Hybridizations, 3 per condition; Sham HP DRG; 3 day SNL HP DRG; Sham LP DRG; 3 day SNL LP DRG.
2015-02-19 | E-GEOD-63442 | biostudies-arrayexpress
Project description:Chronic neuropathic pain is a major morbidity of neural injury, yet its mechanisms are incompletely understood. Hypersensitivity to previously non-noxious stimuli (allodynia) is a common symptom. Here, we demonstrate that the onset of cold hypersensitivity precedes tactile allodynia and this temporal divergence was associated with major differences in global gene expression in dorsal root ganglia (DRG). Transcripts whose expression correlate with the onset of cold allodynia were nociceptor-related, whereas those correlating with tactile hypersensitivity were enriched for immune cell activity. Selective ablation of TrpV1 lineage nociceptors resulted in mice that did not acquire cold allodynia but developed normal tactile hypersensitivity. Whereas, depletion of macrophages or T cells reduced neuropathic tactile allodynia but not cold hypersensitivity. We conclude that neuropathic pain is contributed to by reactive processes of sensory neurons and immune cells, each leading to distinct forms of pain hypersensitivity, potentially allowing effective drug development targeted to each pain modality.
2018-01-19 | GSE89224 | GEO
Project description:Neuropathic pain is a significant clinical challenge affecting patients treated with the chemotherapeutic paclitaxel. Current therapeutic options for paclitaxel-induced neuropathy are limited due to an incomplete understanding of its molecular mechanisms. Here, we demonstrate a critical role for the Integrated Stress Response (ISR) in paclitaxel-induced neuropathic pain. Paclitaxel robustly activates the ISR specifically in dorsal root ganglion (DRG) neurons via the upstream kinase GCN2. Activation of GCN2 alone is sufficient to sensitize DRG neurons to depolarization and produce pain-like behaviors in vivo. Critically, paclitaxel-induced DRG neuron sensitization and behavioral mechanical and cold hypersensitivity require GCN2 signaling. Finally, paclitaxel treatment reduces global tRNA charging and abundance, providing a mechanistic basis for GCN2 activation. These findings position GCN2 and the ISR as promising therapeutic targets for the management of paclitaxel-induced neuropathic pain.
2025-11-12 | GSE291827 | GEO