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CSF-CN contributes to cancer-induced bone pain via the MKP-1-mediated MAPK pathway
Chen P, Pan M, Lin QS, Lin XZ, Lin Z (2021) CSF-CN contributes to cancer-induced bone pain via the MKP-1-mediated MAPK pathway. Biochem Biophys Res Commun 547:36-43. doi: 10.1016/j.bbrc.2021.02.010
Summary: Cerebrospinal fluid-contacting nucleus (CSF–CN) has been reported to be involved in the development of neuropathic pain and inflammatory pain. This study aimed to see whether it also has a role in cancer-induced bone pain (CIBP). Targeted ablation of CSF-CN dramatically aggravated pain sensitivity.
Usage: Injection via icv of CTB-SAP was performed to “knockout” the CSF-CN.
Related Products: CTB-SAP (Cat. #IT-14)
Targeting spinal neuropeptide Y1 receptor-expressing interneurons to alleviate chronic pain and itch
Nelson TS, Taylor BK (2021) Targeting spinal neuropeptide Y1 receptor-expressing interneurons to alleviate chronic pain and itch. Prog Neurobiol 196:101894. doi: 10.1016/j.pneurobio.2020.101894
Summary: Intrathecal administration of NPY-SAP reduced several operant and cognitive measures of Complete Freund’s adjuvant (CFA)-induced allodynia, including responsiveness to cold temperatures, feeding interference, and an escape task, but did not interfere with systemic morphine-induced analgesia. (Wiley et al.) Similar to the spared nerve injury (SNI) model of neuropathic pain, NPY-SAP dose-dependently reduced the development of mechanical allodynia (hindpaw withdrawal response to von Frey filaments), mechanical hyperalgesia (response to blunt pin), and cold allodynia (hindpaw withdrawal response duration to acetone droplet evaporation). (Nelson et al.) Together, these directed lesion studies support the idea that the Y1-IN subpopulation of dorsal horn neurons is necessary for the maintenance of both mechanical and cold modalities of nociceptive transmission in chronic pain states.
Related Products: NPY-SAP (Cat. #IT-28)
See Also:
- Wiley RG et al. Neuropeptide Y receptor-expressing dorsal horn neurons: role in nocifensive reflex responses to heat and formalin. Neuroscience 161:139-147, 2009.
- Nelson TS et al. Facilitation of neuropathic pain by the NPY Y1 receptor-expressing subpopulation of excitatory interneurons in the dorsal horn. Sci Rep 9(1):7248, 2019.
Spinal microglia-neuron interactions in chronic pain.
Ho IHT, Chan MTV, Wu WKK, Liu X (2020) Spinal microglia-neuron interactions in chronic pain. J Leukoc Biol 108:1575-1592. doi: 10.1002/JLB.3MR0520-695R
Summary: Spinal microglial activation is initiated shortly and persisted for more than 3 mo after partial sciatic nerve ligation. Intrathecal injection of Mac1-SAP, a saporin-conjugated anti-CD11b antibody to deplete microglia, abolished cold and mechanical allodynia for 2–12 wk after injury,92 supporting the role of activated microglia for chronic pain maintenance.
Related Products: Mac-1-SAP rat (Cat. #IT-33)
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Systems pathology of neuropathic pain and fibromyalgia.
Ueda H (2019) Systems pathology of neuropathic pain and fibromyalgia. Biol Pharm Bull 42(11):1773-1782. doi: 10.1248/bpb.b19-00535
Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)
Role of nociceptive afferent input on forelimb reaching and grasping behaviors in the spinal cord injured rat
Walker JR, Ong A, Detloff MR (2019) Role of nociceptive afferent input on forelimb reaching and grasping behaviors in the spinal cord injured rat. Neuroscience 2019 Abstracts 572.09. Society for Neuroscience, Chicago, IL.
Summary: Individuals with spinal cord injury (SCI) suffer a loss of motor and sensory function. The current standard of care to recover fine motor control is rehabilitation focused on a combination of range of motion, aerobic, and strength training (ST). However, limited research has been conducted to determine the role of nociceptive afferent inputs from muscle on spinal plasticity and/or recovery of function. Using a rodent model of SCI strength training rehabilitation, we determined that motor training not only improves forelimb strength and fine motor function but also can modulate the development of neuropathic pain, suggesting that improvements in reaching and grasping may be due, in part, to plasticity of nociceptive afferents. To further explore this, Sprague-Dawley rats received injections of rIB4-conjugated saporin, mu p75-conjugated saporin or unconjugated (vehicle) into the cervical dorsal root ganglia unilaterally to eliminate non-peptidergic and peptidergic nociceptors. There is an uninjured cohort and a group with unilateral C5 SCI. Von Frey and Hargreaves’ tests were performed at baseline and several time points post-injection to assess the effcacy of the nociceptive elimination. Several measures of forelimb strength were recorded over time including the isometric pull task, a single pellet retrieval task and the Montoya staircase test. To confirm the depletion of peptidergic and non-peptidergic nociceptors following saporin injection and/or SCI, cervical DRGs and spinal cords were stained with antibodies against CGRP and isolectin-B4. An understanding of the role of nociceptors in spinal plasticity and functional motor and sensory recovery of SCI patients will guide future research and refine rehabilitation strategies to further improve their quality of life.
Related Products: IB4-SAP (Cat. #IT-10), mu p75-SAP (Cat. #IT-16)
Neuropeptide Y release in the rat spinal cord measured with Y1 receptor internalization is increased after nerve injury.
Marvizon JC, Chen W, Fu W, Taylor BK (2019) Neuropeptide Y release in the rat spinal cord measured with Y1 receptor internalization is increased after nerve injury. Neuropharmacology 158:107732. doi: 10.1016/j.neuropharm.2019.107732
Summary: NPY is released from dorsal horn interneurons or primary afferent terminals by electrical stimulation and by activation of TRPV1, PKA or NMDA receptors in. Release evoked by noxious and tactile stimuli increases after peripheral nerve injury. Ablation of Y1-expressing dorsal horn neurons with NPY-saporin produced antinociception (Lemons and Wiley) and reduced mechanical and cold hypersensitivity in the spared nerve injury model (Nelson et al.), suggesting that they are pro-nociceptive neurons.
Related Products: NPY-SAP (Cat. #IT-28)
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Receptor dependence of BDNF actions in superficial dorsal horn: relation to central sensitization and actions of macrophage colony stimulating factor 1.
Boakye PA, Rancic V, Whitlock KH, Simmons D, Longo FM, Ballanyi K, Smith PA (2019) Receptor dependence of BDNF actions in superficial dorsal horn: relation to central sensitization and actions of macrophage colony stimulating factor 1. J Neurophysiol 121(6):2308-2322. doi: 10.1152/jn.00839.2018 PMID: 30995156
Objective: To find missing steps in understanding how peripheral injury instigates central sensitization and the onset of neuropathic pain.
Summary: Colony-stimulating factor 1 (CSF-1) increases excitatory drive to excitatory neurons via a BDNF-dependent mechanism and decreases excitatory drive to inhibitory neurons via BDNF-independent processes.
Usage: immunohistochemistry (1:500)
Related Products: NGFR (mu p75) Rabbit Polyclonal, affinity-purified (Cat. #AB-N01AP)
Facilitation of neuropathic pain by the NPY Y1 receptor-expressing subpopulation of excitatory interneurons in the dorsal horn.
Nelson TS, Fu W, Donahue RR, Corder GF, Hökfelt T, Wiley RG, Taylor BK (2019) Facilitation of neuropathic pain by the NPY Y1 receptor-expressing subpopulation of excitatory interneurons in the dorsal horn. Sci Rep 9(1):7248. doi: 10.1038/s41598-019-43493-z PMID: 31076578
Objective: To test the relevance of the NPYY1 spinal population to the development and/or maintenance of acute and neuropathic pain.
Summary: This neuroanatomical and behavioral characterization of Y1R-expressing excitatory interneurons provides compelling evidence for the development of spinally-directed Y1R agonists to reduce chronic neuropathic pain.
Usage: Selectively ablated Y1R-expressing interneurons while sparing the central terminals of primary afferents. Rats received intrathecal injections of either NPY-SAP or control Blank-SAP (1000 ng each).
Related Products: NPY-SAP (Cat. #IT-28), Blank-SAP (Cat. #IT-21)
Losartan, an angiotensin II type 1 receptor antagonist, alleviates mechanical hyperalgesia in a rat model of chemotherapy-induced neuropathic pain by inhibiting inflammatory cytokines in the dorsal root ganglia.
Kim E, Hwang S-H, Kim H-K, Abdi S, Kim HK (2019) Losartan, an angiotensin II type 1 receptor antagonist, alleviates mechanical hyperalgesia in a rat model of chemotherapy-induced neuropathic pain by inhibiting inflammatory cytokines in the dorsal root ganglia. Mol Neurobiol 56(11):7408-7419. doi: 10.1007/s12035-019-1616-0 PMID: 31037647
Objective: To assess losartan’s analgesic effect on paclitaxel-induced neuropathic pain (PINP) in rats and its mechanism of action in dorsal root ganglion (DRG).
Summary: The mechanical thresholds, protein levels of inflammatory cytokines, and cellular location of AT1R and interleukin 1β (IL-1β) in the DRG were assessed with behavioral testing, Western blotting, and immunohistochemistry, respectively.
Usage: western blot (1:100)
Related Products: Angiotensin II receptor (AT-1R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N27AP)
Spinal α2-adrenoceptors and neuropathic pain modulation; therapeutic target.
Bahari Z, Meftahi GH (2019) Spinal α2-adrenoceptors and neuropathic pain modulation; therapeutic target. Br J Pharmacol 176(14):2366-2381. doi: 10.1111/bph.14580
Objective: To provide an an overview of the cellular mechanisms through which brainstem adrenergic descending inhibitory processing can alter spinal pain transmission to the higher centres, and how these pathways change in neuropathic pain conditions focusing on the role of spinal α2‐adrenoceptors in the spinal dorsal horn.
Summary: The α2‐adrenoceptor agonist may be useful to treat neuropathic pain.
Related Products: Anti-DBH-SAP (Cat. #IT-03)