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https://www.readbyqxmd.com/read/28722693/ikk-nf-%C3%AE%C2%BAb-dependent-satellite-glia-activation-induces-spinal-cord-microglia-activation-and-neuropathic-pain-after-nerve-injury
#1
Hyoungsub Lim, Hyunkyoung Lee, Kyungchul Noh, Sung Joong Lee
Increasing evidence indicates that both microglia and satellite glial cell (SGC) activation play causal roles in neuropathic pain development after peripheral nerve injury; however, the activation mechanisms and their contribution to neuropathic pain remain elusive. To address this issue, we generated Ikkβ conditional knockout mice (Cnp-Cre/Ikkβ; cIkkβ) in which IKK/NF-κB-dependent proinflammatory SGC activation was abrogated. In these mice, nerve injury-induced spinal cord microglia activation and pain hypersensitivity were significantly attenuated compared to those in control mice...
May 30, 2017: Pain
https://www.readbyqxmd.com/read/28701953/astrocyte-activation-in-locus-coeruleus-is-involved-in-neuropathic-pain-exacerbation-mediated-by-maternal-separation-and-social-isolation-stress
#2
Kazuo Nakamoto, Fuka Aizawa, Megumi Kinoshita, Yutaka Koyama, Shogo Tokuyama
Our previous studies demonstrated that emotional dysfunction associated with early life stress exacerbated nerve injury-induced mechanical allodynia. Sex differences were observed in several anxiety tests, but not in mechanical allodynia. To elucidate the mechanism underlying these findings, we have now investigated the involvement of astrocytes in emotional dysfunction and enhancement of nerve injury-induced mechanical allodynia in mice subjected to maternal separation combined with social isolation (MSSI) as an early life stress...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28688296/effects-of-ibudilast-on-oxycodone-induced-analgesia-and-subjective-effects-in-opioid-dependent-volunteers
#3
Z D Cooper, K W Johnson, S K Vosburg, M A Sullivan, J Manubay, D Martinez, J D Jones, P A Saccone, S D Comer
Opioid-induced glial activation is hypothesized to contribute to the development of tolerance to opioid-induced analgesia. This inpatient, double-blind, placebo-controlled, within-subject and between-groups pilot study investigated the dose-dependent effects of ibudilast, a glial cell modulator, on oxycodone-induced analgesia. Opioid-dependent volunteers were maintained on morphine (30mg, PO, QID) for two weeks and received placebo ibudilast (0mg, PO, BID) during the 1st week (days 1-7). On day 8, participants (N=10/group) were randomized to receive ibudilast (20 or 40mg, PO, BID) or placebo for the remainder of the study...
June 17, 2017: Drug and Alcohol Dependence
https://www.readbyqxmd.com/read/28685641/sleep-disturbances-and-severe-stress-as-glial-activators-key-targets-for-treating-central-sensitization-in-chronic-pain-patients
#4
Jo Nijs, Marco L Loggia, Andrea Polli, Maarten Moens, Eva Huysmans, Lisa Goudman, Mira Meeus, Luc Vanderweeën, Kelly Ickmans, Daniel Clauw
The mechanism of sensitization of the central nervous system partly explains the chronic pain experience in many patients, but the etiological mechanisms of this central nervous system dysfunction are poorly understood. Recently, an increasing number of studies suggest that aberrant glial activation takes part in the establishment and/or maintenance of central sensitization. Areas covered: This review focused on preclinical work and mostly on the neurobiochemistry studied in animals, with limited human studies available...
July 12, 2017: Expert Opinion on Therapeutic Targets
https://www.readbyqxmd.com/read/28680400/a-novel-small-molecule-gdnf-receptor-ret-agonist-bt13-promotes-neurite-growth-from-sensory-neurons-in-vitro-and-attenuates-experimental-neuropathy-in-the-rat
#5
Yulia A Sidorova, Maxim M Bespalov, Agnes W Wong, Oleg Kambur, Viljami Jokinen, Tuomas O Lilius, Ilida Suleymanova, Gunnar Karelson, Pekka V Rauhala, Mati Karelson, Peregrine B Osborne, Janet R Keast, Eija A Kalso, Mart Saarma
Neuropathic pain caused by nerve damage is a common and severe class of chronic pain. Disease-modifying clinical therapies are needed as current treatments typically provide only symptomatic relief; show varying clinical efficacy; and most have significant adverse effects. One approach is targeting either neurotrophic factors or their receptors that normalize sensory neuron function and stimulate regeneration after nerve damage. Two candidate targets are glial cell line-derived neurotrophic factor (GDNF) and artemin (ARTN), as these GDNF family ligands (GFLs) show efficacy in animal models of neuropathic pain (Boucher et al...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28670835/role-of-the-spinal-trkb-nmda-receptor-link-in-the-bdnf-induced-long-lasting-mechanical-hyperalgesia-in-the-rat-a-behavioural-study
#6
J L Marcos, D Galleguillos, T Pelissier, A Hernández, L Velásquez, L Villanueva, L Constandil
BACKGROUND: Intrathecal/intracisternal BDNF in rodents produces long-lasting hyperalgesia/allodynia, which implies BDNF plays a role in the establishment and maintenance of central sensitization. Both self-regeneration of endogenous BDNF and neuroplastic modifications of spinal NMDA receptors downstream TrkB signalling could be involved in such enduring hyperalgesia. We investigated to what extent BDNF by itself could participate in the generation and maintenance of mechanical hyperalgesia using pharmacological tools...
July 3, 2017: European Journal of Pain: EJP
https://www.readbyqxmd.com/read/28669596/role-of-microglia-in-mechanical-allodynia-in-the-anterior-cingulate-cortex
#7
Keisuke Miyamoto, Kazuhiko Kume, Masahiro Ohsawa
Plastic changes that increase nociceptive transmission are observed in several brain regions under conditions of chronic pain. Synaptic plasticity in the anterior cingulate cortex (ACC) is particularly associated with neuropathic pain. Glial cells are considered candidates for the modulation of neural plastic changes in the central nervous system. In this study, we aimed to investigate the role of ACC glial cells in the development of neuropathic pain. First, we examined the expression of glial cells in the ACC of nerve-ligated mice...
June 21, 2017: Journal of Pharmacological Sciences
https://www.readbyqxmd.com/read/28654797/simvastatin-prevents-morphine-induced-tolerance-and-dependence-in-mice
#8
Nasim Sadat Pajohanfar, Ehsan Mohebbi, Ahmad Hosseini-Bandegharaei, Mohamadraza Amin, Golnaz Vaseghi, Bahareh Amin
BACKGROUND: Tolerance to analgesic effects of opioids and dependence to them are main concerns in the treatment of chronic pain conditions, limiting clinical application of these drugs. This study aimed to evaluate the effect of simvastatin on the morphine-induced tolerance and dependence in mice. MATERIAL AND METHODS: For this purpose, mice were treated with either daily morphine (20 mg/kg, s.c.) alone, or in combination with simvastatin (2.5, 5 and 10mg/kg, i...
June 24, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28649222/highly-selective-cyclooxygenase-1-inhibitors-p6-and-mofezolac-counteract-inflammatory-state-both-in-vitro-and-in-vivo-models-of-neuroinflammation
#9
Rosa Calvello, Dario Domenico Lofrumento, Maria Grazia Perrone, Antonia Cianciulli, Rosaria Salvatore, Paola Vitale, Francesco De Nuccio, Laura Giannotti, Giuseppe Nicolardi, Maria Antonietta Panaro, Antonio Scilimati
Activated microglia secrete an array of pro-inflammatory factors, such as prostaglandins, whose accumulation contributes to neuronal damages. Prostaglandin endoperoxide synthases or cyclooxygenases (COX-1 and COX-2), which play a critical role in the inflammation, are the pharmacological targets of non-steroidal anti-inflammatory drugs, used to treat pain and inflammation. Since it was reported that COX-1 is the major player in mediating the brain inflammatory response, the aim of this study was to evaluate the effects of highly selective COX-1 inhibitors, such as P6 and mofezolac, in neuroinflammation models...
2017: Frontiers in Neurology
https://www.readbyqxmd.com/read/28647288/gap-junctions-pannexins-and-pain
#10
REVIEW
David C Spray, Menachem Hanani
Enhanced expression and function of gap junctions and pannexin (Panx) channels has been associated with both peripheral and central mechanisms of pain sensitization. At the level of the sensory ganglia, evidence includes augmented gap junction and pannexin1 expression in glial cells and neurons in inflammatory and neuropathic pain models and increased synchrony and enhanced cross-excitation among sensory neurons by gap junction-mediated coupling. In spinal cord and in suprapinal areas, evidence is largely limited to increased expression of relevant proteins, although in several rodent pain models, hypersensitivity is reduced by treatment with gap junction/Panx1 channel blocking compounds...
June 21, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28645297/interleukin-1-receptor-type-1-is-overexpressed-in-neurons-but-not-in-glial-cells-within-the-rat-superficial-spinal-dorsal-horn-in-complete-freund-adjuvant-induced-inflammatory-pain
#11
Krisztina Holló, László Ducza, Zoltán Hegyi, Klaudia Dócs, Krisztina Hegedűs, Erzsébet Bakk, Ildikó Papp, Gréta Kis, Zoltán Mészár, Zsuzsanna Bardóczi, Miklós Antal
BACKGROUND: All known biological functions of the pro-inflammatory cytokine interleukin-1β (IL-1β) are mediated by type 1 interleukin receptor (IL-1R1). IL-1β-IL-1R1 signaling modulates various neuronal functions including spinal pain processing. Although the role of IL-1β in pain processing is generally accepted, there is a discussion in the literature whether IL-1β exerts its effect on spinal pain processing by activating neuronal or glial IL-1R1. To contribute to this debate, here we investigated the expression and cellular distribution of IL-1R1 in the superficial spinal dorsal horn in control animals and also in inflammatory pain...
June 23, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28638088/chemokine-receptor-cxcr4-regulates-camkii-creb-pathway-in-spinal-neurons-that-underlies-cancer-induced-bone-pain
#12
Xue-Ming Hu, Hui Zhang, Heng Xu, Hai-Long Zhang, Li-Ping Chen, Wen-Qiang Cui, Wei Yang, Wen Shen
We previously demonstrated that the chemokine receptor CXCR4 plays an important role in cancer-induced bone pain by activating spinal neurons and glial cells. However, the specific neuronal mechanism of CXCR4 signaling is not clear. We further report that CXCR4 contributes to the activation of the neuronal CaMKII/CREB pathway in cancer-induced bone pain. We used a tumor cell implantation (TCI) model and observed that CXCR4, p-CaMKII and p-CREB were persistently up-regulated in spinal neurons. CXCR4 also co-expressed with p-CaMKII and p-CREB, and mediated p-CaMKII and p-CREB expression after TCI...
June 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28637974/neuron-glia-interaction-is-a-key-mechanism-underlying-persistent-orofacial-pain
#13
Koichi Iwata, Ayano Katagiri, Masamichi Shinoda
Excitability of neurons in the trigeminal ganglion (TG), trigeminal spinal subnucleus caudalis (Vc), and upper cervical spinal cord (C1-C2) is greatly enhanced after orofacial inflammation and trigeminal nerve injury, and TG, Vc, and C1-C2 neurons remain sensitized long after such episodes. Sensitized neurons generate various molecules, which are released from nociceptive neurons in these areas and are involved in modulating the excitability of TG, Vc, and C1-C2 nociceptive neurons. Hyperexcitable nociceptive neurons also activate satellite glial cells in the TG and microglial cells and astrocytes in the Vc and C1-C2...
2017: Journal of Oral Science
https://www.readbyqxmd.com/read/28625489/diosmin-reduces-chronic-constriction-injury-induced-neuropathic-pain-in-mice
#14
Mariana M Bertozzi, Ana C Rossaneis, Victor Fattori, Daniela T Longhi-Balbinot, Andressa Freitas, Fernando Q Cunha, José C Alves-Filho, Thiago M Cunha, Rubia Casagrande, Waldiceu A Verri
Injury or dysfunction of somatosensory system induces a complex syndrome called neuropathic pain, which still needs adequate pharmacological control. The current pharmacological treatments were in part developed from natural compounds. Flavonoids are natural polyphenolic molecules presenting varied biological activities and low toxicity. The flavonoid diosmin is a safe compound with good tolerability and low toxicity. This study evaluated the antinociceptive effect of diosmin in the sciatic nerve chronic constriction injury (CCI)-induced neuropathic pain model...
June 15, 2017: Chemico-biological Interactions
https://www.readbyqxmd.com/read/28618070/morin-suppresses-astrocyte-activation-and-regulates-cytokine-release-in-bone-cancer-pain-rat-models
#15
Wei Jiang, Ying Wang, Wei Sun, Mengyuan Zhang
As inflammatory and immune responses are involved in pathophysiology of debilitating neuropathic pain, reagents that can modulate these two responses may have therapeutic potential. Morin, derived from the moraceae family of plants, benefits inflammation-related diseases, but its antinociceptive effects on cancer pain remain elusive. In the present study, we investigated antinociceptive effects of morin on bone cancer pain using a rat model, where rats were subject to implantation of Walker 256 mammary gland carcinoma cells into the tibia...
June 15, 2017: Phytotherapy Research: PTR
https://www.readbyqxmd.com/read/28617705/liver-x-receptor-%C3%AE-is-involved-in-counteracting-mechanical-allodynia-by-inhibiting-neuroinflammation-in-the-spinal-dorsal-horn
#16
Jing Xu, Yi-Wei Feng, Ling Liu, Wei Wang, Xiong-Xiong Zhong, Xu-Hong Wei, Xian-Guo Liu
BACKGROUND: Liver X receptors, including α and β isoforms, are ligand-activated transcription factors. Whether liver X receptor α plays a role in neuropathic pain is unknown. METHODS: A spared nerve injury model was established in adult male rats and mice. Von Frey tests were performed to evaluate the neuropathic pain behavior; Western blot and immunohistochemistry were performed to understand the underlying mechanisms. RESULTS: Intrathecal injection of a specific liver X receptor agonist T0901317 or GW3965 could either prevent the development of mechanical allodynia or alleviate the established mechanical allodynia, both in rats and wild-type mice...
June 15, 2017: Anesthesiology
https://www.readbyqxmd.com/read/28615336/prevention-and-reversal-of-latent-sensitization-of-dorsal-horn-neurons-by-glial-blockers-in-a-model-of-low-back-pain-in-male-rats
#17
Juanjuan Zhang, Siegfried Mense, Rolf-Detlef Treede, Ulrich Hoheisel
In an animal model of non-specific low back pain, recordings from dorsal horn neurons were made to investigate the influence of glial cells in the central sensitization process. To induce a latent sensitization of the neurons, nerve growth factor (NGF) was injected into the multifidus muscle; the manifest sensitization to a second NGF injection 5 days later was used as a read-out. The sensitization manifested in increased resting activity and in an increased proportion of neurons responding to stimulation of deep somatic tissues...
June 14, 2017: Journal of Neurophysiology
https://www.readbyqxmd.com/read/28598070/-helminth-derived-immunomodulatory-glycan-lnfp3-impairs-pathogenesis-of-peripheral-neuropathic-pain-and-spinal-glial-activation
#18
You-Quan Ding, Hhong-Yi Ren, Xia Xiao, Xuan-Yang Li, Jian-Guo Qi
OBJECTIVES: To investigate the effect of helminth-derived immunomodulatory glycan lacto-N-fucopentaose3(LNFP3) on the pathogenesis of neuropathic pain and spinal glial activation in the corresponding time windows after adult rat tibial nerve permanent transection (modified spared nerve injury, mSNI). METHODS: Ten weeks old male adult Sprague-Dawley (SD) rats weighing 250-300 g were randomly grouped into four groups: sham-operated group (n =6), mSNI group (n =6), mSNI plus bovine serum albumin (BSA) group (n =12) and mSNI plus LNFP3 group (n=12)...
September 2016: Sichuan da Xue Xue Bao. Yi Xue Ban, Journal of Sichuan University. Medical Science Edition
https://www.readbyqxmd.com/read/28589150/tempol-a-superoxide-dismutase-mimetic-agent-inhibits-superoxide-anion-induced-inflammatory-pain-in-mice
#19
Catia C F Bernardy, Ana C Zarpelon, Felipe A Pinho-Ribeiro, Cássia Calixto-Campos, Thacyana T Carvalho, Victor Fattori, Sergio M Borghi, Rubia Casagrande, Waldiceu A Verri
The present study evaluated the anti-inflammatory and analgesic effects of the superoxide dismutase mimetic agent tempol in superoxide anion-induced pain and inflammation. Mice were treated intraperitoneally with tempol (10-100 mg/kg) 40 min before the intraplantar injection of a superoxide anion donor, potassium superoxide (KO2, 30 μg). Mechanical hyperalgesia and thermal hyperalgesia, paw edema, and mRNA expression of peripheral and spinal cord mediators involved in inflammatory pain, TNFα, IL-1β, IL-10, COX-2, preproET-1, gp91(phox), Nrf2, GFAP, and Iba-1, were evaluated...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28587280/levo-corydalmine-alleviates-neuropathic-cancer-pain-induced-by-tumor-compression-via-the-ccl2-ccr2-pathway
#20
Yahui Hu, Nandani Darshika Kodithuwakku, Lin Zhou, Chengyuan Li, Dan Han, Weirong Fang, Jihua Liu, Yunman Li
Background: Tumor compression-induced pain (TCIP) is a complex pathological cancer pain. Spinal glial cells play a critical role in maintenance of cancer pain by releasing proinflammatory cytokines and chemokines. In this study, we verified the role of levo-corydalmine (l-CDL) on TCIP. Methods: Spontaneous pain, paw withdrawal threshold and latency were assessed using TCIP mouse model. Immunofluorescence was used to identify the reactions of glia. RT-PCR and western blot or ELISA were used to determine mRNA or protein expression of tumor necrosis factor-α (TNF-α), interlukin-1β (IL-1β), CC chemokine ligand 2 (CCL2) and chemotactic cytokine receptor 2 (CCR2) in vivo and in vitro...
June 6, 2017: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
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