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https://www.readbyqxmd.com/read/28812173/melatonin-attenuates-pain-hypersensitivity-and-decreases-astrocyte-mediated-spinal-neuroinflammation-in-a-rat-model-of-oxaliplatin-induced-pain
#1
Ye-Song Wang, Yuan-Yuan Li, Wei Cui, Li-Bin Li, Zhao-Cai Zhang, Bao-Ping Tian, Gen-Sheng Zhang
Neuroinflammatory response in spinal dorsal horn has been demonstrated to be a critical factor in oxaliplatin-induced pain. Melatonin has been shown to have anti-inflammatory and anti-allodynia effects in both preclinical and clinical studies. In the present study, we investigated the role of systemic administration of melatonin on oxaliplatin-induced pain. Intraperitoneal (i.p.) injection with oxaliplatin induced significantly mechanical allodynia and thermal hyperalgesia. Melatonin (i.p.) significantly alleviated mechanical allodynia and thermal hyperalgesia in the oxaliplatin but not sham-treated rats...
August 15, 2017: Inflammation
https://www.readbyqxmd.com/read/28801619/repetitive-motor-cortex-stimulation-reinforces-the-pain-modulation-circuits-of-peripheral-neuropathic-pain
#2
Myeounghoon Cha, Sun Woo Um, Minjee Kwon, Taick Sang Nam, Bae Hwan Lee
Recent evidence indicates that motor cortex stimulation (MCS) is a potentially effective treatment for chronic neuropathic pain. However, the neural mechanisms underlying the attenuated hyperalgesia after MCS are not completely understood. In this study, we investigated the neural mechanism of the effects of MCS using an animal model of neuropathic pain. After 10 daily sessions of MCS, repetitive MCS reduced mechanical allodynia and contributed to neuronal changes in the anterior cingulate cortex (ACC). Interestingly, inhibition of protein kinase M zeta (PKMζ), a regulator of synaptic plasticity, in the ACC blocked the effects of repetitive MCS...
August 11, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28797041/repeat-low-level-blast-exposure-increases-transient-receptor-potential-vanilloid-1-trpv1-and-endothelin-1-et-1-expression-in-the-trigeminal-ganglion
#3
Elaine D Por, Melody L Sandoval, Chiquita Thomas-Benson, Teresa A Burke, Allison Doyle Brackley, Nathaniel A Jeske, Jeffery M Cleland, Brian J Lund
Blast-associated sensory and cognitive trauma sustained by military service members is an area of extensively studied research. Recent studies in our laboratory have revealed that low-level blast exposure increased expression of transient receptor potential vanilloid 1 (TRPV1) and endothelin-1 (ET-1), proteins well characterized for their role in mediating pain transmission, in the cornea. Determining the functional consequences of these alterations in protein expression is critical to understanding blast-related sensory trauma...
2017: PloS One
https://www.readbyqxmd.com/read/28791431/glycine-receptors-and-glycine-transporters-targets-for-novel-analgesics
#4
REVIEW
Hanns Ulrich Zeilhofer, Mario A Acuña, Jacinthe Gingras, Gonzalo E Yévenes
Glycinergic neurotransmission has long been known for its role in spinal motor control. During the last two decades, additional functions have become increasingly recognized-among them is a critical contribution to spinal pain processing. Studies in rodent pain models provide proof-of-concept evidence that enhancing inhibitory glycinergic neurotransmission reduces chronic pain symptoms. Apparent strategies for pharmacological intervention include positive allosteric modulators of glycine receptors and modulators or inhibitors of the glial and neuronal glycine transporters GlyT1 and GlyT2...
August 8, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28769766/breakthrough-cancer-pain-is-associated-with-spinal-gap-junction-activation-via-regulation-of-connexin-43-in-a-mouse-model
#5
Xin Li, Siqing Jiang, Hui Yang, Qian Liao, Shousong Cao, Xuebin Yan, Dong Huang
Breakthrough cancer pain (BTcP) is a high-intensity, short-duration, unpredictable and uncontrollable pain. Recent studies have shown that activation of gap junction (GJ) in spinal cord plays an important role in the pathogenesis of BTcP. We examined the expressions of Glial fibrillary acidic protein (GFAP), connexin (Cx) 43 protein and phosphorylation of Cx43 (p-Cx43) in the spinal cord of mice. In addition, we investigated the effects of Gap26, a selective GJ blocker, on the expressions of GFAP, Cx43 and p-Cx43 in BTcP mice...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28747388/neuronal-p2x7-receptors-revisited-do-they-really-exist
#6
Peter Illes, Tahir Muhammad Khan, Patrizia Rubini
P2X7 receptors (Rs) constitute a subclass of ATP-sensitive ionotropic receptors (P2X1-P2X7). P2X7Rs have many distinguishing features, mostly based on their long intracellular C terminus regulating trafficking to the cell membrane, protein-protein interactions, and post-translational modification. Their C-terminal tail is especially important in enabling the transition from the nonselective ion channel mode to a membrane pore allowing the passage of large molecules. There is an ongoing dispute on the existence of neuronal P2X7Rs with consequences for our knowledge on their involvement in neuroinflammation, aggravating stroke, temporal lobe epilepsy, neuropathic pain, and various neurodegenerative diseases...
July 26, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28746076/safety-and-efficacy-of-neublastin-in-painful-lumbosacral-radiculopathy-a-randomized-double-blinded-placebo-controlled-phase-2-trial-using-bayesian-adaptive-design-the-sprint-trial
#7
Miroslav Backonja, Leslie Williams, Xiaopeng Miao, Nathaniel Katz, Crystal Chen
Neublastin (BG00010) is a first-in-class, glial cell-derived neurotrophic factor shown in preclinical studies and an early clinical trial to have potential for the treatment of neuropathic pain. SPRINT was a phase 2, multicenter, double-blinded, placebo-controlled study to evaluate efficacy/safety of 5 neublastin doses (50, 150, 400, 800, and 1200 μg/kg) administered as an intravenous injection 3 times/week for 1 week in patients with chronic painful lumbosacral radiculopathy, utilizing Bayesian response-adaptive study design...
June 21, 2017: Pain
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
#8
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
#9
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
#10
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
#11
REVIEW
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...
August 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
#12
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
#13
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
#14
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
#15
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...
September 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
#16
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
#17
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
#18
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
#19
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
#20
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
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