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Intra-articular injection of 2-pyridylethylamine produces spinal NPY-mediated antinociception in the formalin-induced rat knee-joint pain model
Souza-Silva E, Stein T, Mascarin LZ, Dornelles FN, Bicca MA, Tonussi CR (2020) Intra-articular injection of 2-pyridylethylamine produces spinal NPY-mediated antinociception in the formalin-induced rat knee-joint pain model. Brain Res 1735:146757. doi: 10.1016/j.brainres.2020.146757 PMID: 32135147
Objective: To investigate the participation of spinal NPY in the antinociceptive effect produced by 2-pyridylethylamine (2-PEA).
Summary: These data support the idea that antinociception induced by H1R agonists in the knee-joint of rats may be mediated by the spinal release of NPY, and this peptide seems to be acting via Y1R.
Usage: IT pretreatment with NPY-SAP (750 ng) reduced immunoblotting for Y1R in spinal cord homogenates.
Related Products: NPY-SAP (Cat. #IT-28)
Exploration of sensory and spinal neurons expressing gastrin-releasing peptide in itch and pain related behaviors.
Barry DM, Liu XT, Liu B, Liu XY, Gao F, Zeng X, Liu J, Yang Q, Wilhelm S, Yin J, Tao A, Chen ZF (2020) Exploration of sensory and spinal neurons expressing gastrin-releasing peptide in itch and pain related behaviors. Nat Commun 11(1):1397. doi: 10.1038/s41467-020-15230-y
Objective: To determine the role of GRP in sensory neurons.
Summary: GRP is a neuropeptide in sensory neurons for nonhistaminergic itch, and GRP sensory neurons are dedicated to itch transmission.
Usage: Bombesin-SAP (200 ng/5 μL, i.t.) was injected 2 weeks prior to optical stimulation.
Related Products: Bombesin-SAP (Cat. #IT-40)
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)
Nociceptors expressing TRPV1 and trigeminal nucleus neurons expressing NK1 mediate orthodontic pain
Wang S, Kim M, Ong K, Pae E-K, Chung M-K (2019) Nociceptors expressing TRPV1 and trigeminal nucleus neurons expressing NK1 mediate orthodontic pain. Neuroscience 2019 Abstracts 052.10. Society for Neuroscience, Chicago, IL.
Summary: Orthodontic force produces mechanical irritation and inflammation in periodontium, which inevitably accompanies pain. Despite its high prevalence, treatment of orthodontic pain is not effective. Determining detailed neural mechanisms involving peripheral and central nervous system should be critical to improve the management of orthodontic pain. Periodontal ligament is projected by peptidergic nociceptors, which is enriched with transient receptor potential vanilloid 1 (TRPV1), a receptor for capsaicin. Trigeminal subnucleus caudalis (Vc), is critical for relaying orofacial nociceptive signal into brain. A group of second- order neurons in the superficial dorsal horn of Vc express neurokinin 1 receptor (NK1), a receptor for substance P, and receive inputs from peptidergic nociceptors. However, the contribution of these nociceptive neurons to orthodontic pain has not been determined. Orthodontic force of 10g produced reliable tooth movement in mice. Orthodontic pain was evaluated by measuring mouse grimace scale (MGS) and bite force (BF), which could represent spontaneous pain and chewing-evoked pain, respectively. Orthodontic force increased MGS and decreased BF, which peaked at 1d and returned near to sham level at 7d. Using targeted chemical ablation of specific subsets of neurons, we determined the contribution of TRPV1+ nociceptors and NK1+ Vc neurons to orthodontic pain behaviors in mice. Ablation of TRPV1+ nociceptors by injecting resiniferatoxin into trigeminal ganglia significantly attenuated orthodontic force assessed by MGS and BF. Chemical ablation of NK1+ Vc neurons by injecting saporin conjugated with substance P into Vc also significantly reduced the extent of changes in MGS and BF by orthodontic force. These results suggest that TRPV1+ trigeminal nociceptors and NK1+ Vc neurons constitute a major neural pathway for transmission of orthodontic pain, which is a fundamental neural mechanism of orthodontic pain transmission. The new mouse model of orthodontic pain will be useful for mechanistic study to develop novel approaches for painless orthodontics.
Related Products: SSP-SAP (Cat. #IT-11)
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)
RGS4 maintains chronic pain symptoms in rodent models.
Avrampou K, Pryce KD, Ramakrishnan A, Sakloth F, Gaspari S, Serafini RA, Mitsi V, Polizu C, Swartz C, Ligas B, Richards A, Shen L, Carr FB, Zachariou V (2019) RGS4 maintains chronic pain symptoms in rodent models. J Neurosci 39(42):8291-8304. doi: 10.1523/JNEUROSCI.3154-18.2019 PMID: 31308097
Usage: western
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Spinal cord projection neurons: A superficial, and also deep, analysis.
Wercberger R, Basbaum AI (2019) Spinal cord projection neurons: A superficial, and also deep, analysis. Curr Opin Physiol 11:109-115. doi: 10.1016/j.cophys.2019.10.002
Summary: Modern approaches to map complex neural circuits require knowledge of the molecular language that defines cell type specificity. However, with few exceptions, NK1R remains the marker consistently used to define projection neurons and even to interrogate their contribution to pain and itch (Mantyh et al.) The first of two studies demonstrating that SP-SAP-mediated ablation of dorsal horn NK1R-expressing neurons reduces injury-induced hyperalgesia. (Carstens et al.) In this paper SP-SAP-mediated ablation of dorsal horn NK1R-expressing neurons reduced pruritogen-evoked scratching.
Related Products: SSP-SAP (Cat. #IT-11)
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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)