Database : MEDLINE
Search on : Nociceptive and Pain [Words]
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[PMID]: 29499192
[Au] Autor:Sandes SMS; Heimfarth L; Brito RG; Santos PL; Gouveia DN; Carvalho AMS; Quintans JSS; da Silva-Júnior EF; de Aquino TM; França PHB; de Araújo-Júnior JX; Albuquerque-Júnior RLC; Zengin G; Schmitt M; Bourguignon JJ; Quintans-Júnior LJ
[Ad] Address:Laboratory of Neuroscience and Pharmacological Assay (LANEF), Graduate Program in Health Sciences, Federal University of Sergipe, São Cristóvão, Sergipe, Brazil.
[Ti] Title:Evidence for the involvement of TNF-α, IL-1ß and IL-10 in the antinociceptive and anti-inflammatory effects of indole-3-guanylhydrazone hydrochloride, an aromatic aminoguanidine, in rodents.
[So] Source:Chem Biol Interact;286:1-10, 2018 Feb 27.
[Is] ISSN:1872-7786
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:BACKGROUND: Indole-3-guanylhydrazone hydrochloride (LQM01) is a new derivative of aminoguanidine hydrochloride, an aromatic aminoguanidine. METHODS: Mice were treated with LQM01 (5, 10, 25 or 50 mg/kg, i.p.), vehicle (0.9% saline i.p.) or a standard drug. The mice were subjected to carrageenan-induced pleurisy, abdominal writhing induced by acetic acid, the formalin test and the hot-plate test. The model of non-inflammatory chronic muscle pain induced by saline acid was also used. Mice from the chronic protocol were assessed for withdrawal threshold, muscle strength and motor coordination. LQM01 or vehicle treated mice were evaluated for Fos protein. RESULTS: LQM01 inhibits TNF-α and IL-1ß production, as well as leukocyte recruitment during inflammation process. The level of IL-10 in LQM01-treated mice increased in pleural fluid. In addition, LQM01 decreased the nociceptive behavior in the acetic acid induced writhing test, the formalin test (both phases) and increased latency time on the hot-plate. LQM01 treatment also decreased mechanical hyperalgesia in mice with chronic muscle pain, with no changes in muscle strength and motor coordination. LQM01 reduced the number of Fos positive cells in the superficial dorsal horn. This compound exhibited antioxidant properties in in vitro assays. CONCLUSIONS: LQM01 has an outstanding anti-inflammatory and analgesic profile, probably mediated through a reduction in proinflammatory cytokines release, increase in IL-10 production and reduction in neuron activity in the dorsal horn of the spinal cord in mice. GENERAL SIGNIFICANCE: Beneficial effects of LQM01 suggest that it has some important clinical features and can play a role in the management of 'dysfunctional pain' and inflammatory diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 23332 MEDLINE  
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[PMID]: 29477359
[Au] Autor:Sadeghi M; Erickson A; Castro J; Deiteren A; Harrington AM; Grundy L; Adams DJ; Brierley SM
[Ad] Address:Illawarra Health & Medical Research Institute (IHMRI), University of Wollongong, Wollongong, NSW, 2522, Australia.
[Ti] Title:Contribution of membrane receptor signalling to chronic visceral pain.
[So] Source:Int J Biochem Cell Biol;98:10-23, 2018 Mar 05.
[Is] ISSN:1878-5875
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Irritable bowel syndrome and inflammatory bowel disease are major forms of chronic visceral pain, which affect over 15% of the global population. In order to identify new therapies, it is important to understand the underlying causes of chronic visceral pain. This review provides recent evidence demonstrating that inflammation or infection of the gastrointestinal tract triggers specific changes in the neuronal excitability of sensory pathways responsible for the transmission of nociceptive information from the periphery to the central nervous system. Specific changes in the expression and function of a variety of ion channels and receptors have been documented in inflammatory and chronic visceral pain conditions relevant to irritable bowel syndrome and inflammatory bowel disease. An increase in pro-nociceptive mechanisms enhances peripheral drive from the viscera and provides an underlying basis for enhanced nociceptive signalling during chronic visceral pain states. Recent evidence also highlights increases in anti-nociceptive mechanisms in models of chronic visceral pain, which present novel targets for pharmacological treatment of this condition.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 23332 MEDLINE  
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[PMID]: 29424769
[Au] Autor:Hellman N; Kuhn BL; Lannon EW; Payne MF; Sturycz CA; Palit S; Shadlow JO; Rhudy JL
[Ad] Address:Department of Psychology, The University of Tulsa, Tulsa OK.
[Ti] Title:Emotional Modulation of Pain and Spinal Nociception in Sexual Assault Survivors.
[So] Source:Psychosom Med;, 2018 Feb 09.
[Is] ISSN:1534-7796
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Sexual assault (SA) is associated with an increased risk for chronic pain and affective distress. Given that emotional processes modulate pain (e.g., negative emotions enhance pain, positive emotions inhibit pain), increased pain risk in SA survivors could stem from a disruption of emotional modulation processes. METHODS: A well-validated affective picture-viewing paradigm was used to study emotional modulation of pain in 33 healthy, pain-free SA survivors and a control group of 33 healthy, pain-free individuals with no reported history of SA (matched on age, sex, race, and number of non-SA traumas). Unpleasant (mutilation), neutral, and pleasant (erotica) pictures were presented while painful electrocutaneous stimulations were delivered at the ankle. Pain intensity ratings and nociceptive flexion reflex magnitudes (NFR; a physiologic measure of spinal nociception) were recorded in response to electric stimuli. Multilevel models were used to analyze the data with Group (SA vs. no-SA) and Content (mutilation, neutral, erotica) as IVs. RESULTS: Both groups demonstrated similar emotional modulation of pain [FGroupXContent(F(2,646.52)=0.44, p=.65], but a main effect of group [FGroup(1,65.42)=4.24, p=.043] indicated the SA group experienced more overall pain from electric stimuli (hyperalgesia). A significant Group X Content interaction for NFR (p=.035) indicated that emotional modulation of NFR was present for the no-SA group [FContentSimpleEffect(2,684.55)=12.43, p<.001], but not the SA group [FContentSimpleEffect(2,683.38)=1.71, p=.18]. CONCLUSIONS: These findings suggest SA survivors have difficulty emotionally engaging brain-to-spinal cord mechanisms to modulate spinal nociception. A disruption of descending inhibition plus hyperalgesia could contribute to comorbidity between sexual trauma and chronic pain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1097/PSY.0000000000000567

  4 / 23332 MEDLINE  
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[PMID]: 29421433
[Au] Autor:Touchette JC; Little JW; Wilken GH; Salvemini D; Macarthur H
[Ad] Address:Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO, USA.
[Ti] Title:The Neurotoxin DSP-4 Induces Hyperalgesia in Rats that is Accompanied by Spinal Oxidative Stress and Cytokine Production.
[So] Source:Neuroscience;376:13-23, 2018 Feb 05.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Central neuropathic pain (CNP) a significant problem for many people, is not well-understood and difficult to manage. Dysfunction of the central noradrenergic system originating in the locus coeruleus (LC) may be a causative factor in the development of CNP. The LC is the major noradrenergic nucleus of the brain and plays a significant role in central modulation of nociceptive neurotransmission. Here, we examined CNS pathophysiological changes induced by intraperitoneal administration of the neurotoxin DSP-4 (N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride). Administration of DSP-4 decreased levels of norepinephrine in spinal tissue and cerebrospinal fluid (CSF) and led to the development of thermal and mechanical hyperalgesia over 21 days, that was reversible with morphine. Hyperalgesia was accompanied by significant increases in noradrenochrome (oxidized norepinephrine) and expression of 4-hydroxynonenal in CSF and spinal cord tissue respectively at day 21, indicative of oxidative stress. In addition, spinal levels of pro-inflammatory cytokines (interleukins 6 and 17A, tumor necrosis factor-α), as well as the anti-inflammatory cytokine interleukin10 were also significantly elevated at day 21, indicating that an inflammatory response occurred. The inflammatory effect of DSP-4 presented in this study that includes oxidative stress may be particularly useful in elucidating mechanisms of CNP in inflammatory disease states.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 23332 MEDLINE  
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[PMID]: 28741447
[Au] Autor:Ho KWD; Wallace MR; Sibille KT; Bartley EJ; Cruz-Almeida Y; Glover TL; King CD; Goodin BR; Addison A; Edberg JC; Staud R; Bradley LA; Fillingim RB
[Ti] Title:Single Nucleotide Polymorphism in the COL11A2 Gene Associated with Heat Pain Sensitivity in Knee Osteoarthritis.
[So] Source:Mol Pain;13:1744806917724259, 2017 Jan-Dec.
[Is] ISSN:1744-8069
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Abstract: Pain is one of the most prominent symptoms of osteoarthritis. However, there is often discordance between the pain experienced by individuals with osteoarthritis and the degree of articular pathology. This suggests that individual differences, including genetic variability in the central processing of nociceptive stimuli, may impact the presentation of osteoarthritis. Here, we show that the single nucleotide polymorphism rs16868943 in the collagen gene COL11A2 is significantly associated with lowered heat pain tolerance on the arm in participants with knee osteoarthritis (P = 1.21 × 10−6, P = 0.0053 after Bonferroni correction, beta = −3.42). A total of 161 knee osteoarthritis participants were included and evaluated for heat, punctate and pressure pain sensitivity of the affected knee and the ipsilateral arm. Each participant was genotyped for 4392 single nucleotide polymorphisms in genes implicated in pain perception, inflammation and mood and tested for association with pain sensitivity. The minor A allele of single nucleotide polymorphism rs16868943 was significantly associated with lower arm heat pain tolerance after correction for age, gender, race, and study site. This single nucleotide polymorphism was also nominally associated with other measures of heat pain sensitivity, including lowered knee heat pain tolerance (P = 1.14 × 10−5, P = 0.05 after Bonferroni correction), lowered arm heat pain threshold (P = 0.0039, uncorrected) and lowered knee heat pain threshold (P = 0.003, uncorrected). Addition of genotypes from 91 participants without knee pain produced a significant interaction between knee osteoarthritis status and the rs16868943 single nucleotide polymorphism in heat pain tolerance (P = 1.71 × 10−5), such that rs16868943 was not associated with heat pain tolerance in participants without knee pain (P = 0.12, beta = 1.3). This is the first study to show genetic association with heat pain tolerance in individuals with osteoarthritis. The association is specific to participants who have already developed knee osteoarthritis, suggesting that the COL11A2 gene, which has previously been associated with familial osteoarthritis, may play a role in pain sensitization after the development of osteoarthritis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1707
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1177/1744806917724259

  6 / 23332 MEDLINE  
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[PMID]: 29522721
[Au] Autor:Hawkins JL; Moore NJ; Miley D; Durham PL
[Ad] Address:Missouri State University, JVIC-CBLS, 524 North Boonville Avenue, Springfield, MO 65806, United States.
[Ti] Title:Secondary Traumatic Stress Increases Expression of Proteins Implicated in Peripheral and Central Sensitization of Trigeminal Neurons.
[So] Source:Brain Res;, 2018 Mar 06.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The pathology of migraine, a common neurological disease, involves sensitization and activation of trigeminal nociceptive neurons to promote hyperalgesia and allodynia during an attack. Migraineurs often exhibit characteristics of a hyperexcitable or hypervigilant nervous system. One of the primary reported risk factors for development of a hyperexcitable trigeminal system is chronic, unmanaged stress and anxiety. While primary traumatic stress is a commonly cited risk factor for many pain conditions, exposure to secondary traumatic stress early in life is also thought to be a contributing risk factor. The goal of this study was to investigate cellular changes within the spinal trigeminal nucleus and trigeminal ganglion mediated by secondary traumatic stress. Male Sprague Dawley rats (sender) were subjected to forced swim testing (primary traumatic stress) and were then housed in close visual, olfactory, and auditory proximity to the breeding male and female rats, pregnant female rats, or female rats and their nursing offspring (all receivers). In response to secondary stress, levels of calcitonin gene-related peptide, active forms of the mitogen activated protein kinases ERK, JNK, and p38, and astrocyte expression of glial fibrillary acidic protein were significantly elevated in the spinal trigeminal nucleus in day 45 offspring when compared to naïve offspring. In addition, increased nuclear expression of ERK and p38 was observed in trigeminal ganglion neurons. Our results demonstrate that secondary traumatic stress promotes cellular events associated with prolonged trigeminal sensitization in the offspring, and provides a mechanism of how early life stress may function as a risk factor for migraine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  7 / 23332 MEDLINE  
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[PMID]: 29477655
[Au] Autor:Sanna MD; Galeotti N
[Ad] Address:Department of Neurosciences, Psychology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, Viale G. Pieraccini 6, 50139 Florence, Italy. Electronic address: maria.sanna@unifi.it.
[Ti] Title:The HDAC1/c-JUN complex is essential in the promotion of nerve injury-induced neuropathic pain through JNK signaling.
[So] Source:Eur J Pharmacol;825:99-106, 2018 Feb 27.
[Is] ISSN:1879-0712
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract: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. Administration of a selective HDAC1 inhibitor (LG325) in SNI-subjected mice significantly attenuated behavior related to injury-induced pain. Understanding the HDAC1 pathway in epigenetic regulation of pathological pain is of great medical relevance. Spared nerve injury (SNI) mice showed a significant increase in the HDAC1 protein levels within spinal cord in coincidence with the nociceptive phenotype at 1 and 3 weeks after nerve injury. No variation in HDAC3, DNMT3a, AcH3, MBD3 and MeCP2 levels was detected. Increased expression of HDAC1 is accompanied by activation of the JNK-c-Jun signaling pathway. A robust spinal JNK-1 overphosphorylation was observed post nerve-injury along with a selective JNK-dependent increase in p-c-Jun and HDAC1 protein levels. Co-immunoprecipitation experiments showed the presence of a heterodimeric complex between HDAC1 and c-Jun in SNI mice indicating that these transcription factors can act together to regulate transcription through heterodimerization. Stimulation of c-Jun phosphorylation was prevented by the selective HDAC1 inhibitor LG325. We found that HDAC1 was associated with c-Jun in nuclei of spinal dorsal horn astrocytes expressing JNK. On the other hand, the presence of HDAC1 and c-Jun interaction was not detected in control mice. These findings provide new insights into the mechanisms underlying the anti-nociceptive activity of HDAC inhibitors. Taken together, these data support a role for histone deacetylase in the emergence of neuropathic pain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  8 / 23332 MEDLINE  
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[PMID]: 29427595
[Au] Autor:Shen Y; Guan S; Ge H; Xiong W; He L; Liu L; Yin C; Liu H; Li G; Xu C; Xu H; Liu S; Li G; Liang S; Gao Y
[Ad] Address:Department of Physiology, Basic Medical College, Nanchang University, Nanchang, Jiangxi 330006, PR China.
[Ti] Title:Effects of palmatine on rats with comorbidity of diabetic neuropathic pain and depression.
[So] Source:Brain Res Bull;139:56-66, 2018 Feb 07.
[Is] ISSN:1873-2747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Diabetic neuropathic pain (DNP) is one of the common complications of diabetes. Depression (DP) is also one of the common complications of diabetes. P2X receptors play an important role in the transmission of nociceptive signal and are associated with depressive illness. In the study, the hyperalgesia, allodynia and depressive behaviours of rats with comorbidity of DNP and DP were confirmed by the thermal withdrawal latency (TWL) test, mechanical withdrawal threshold (MWT) test, sucrose preference test (SPT), immobility time of forced swimming test (IMFST) and open-field test (OFT). The change in expression of the P2X receptor of the hippocampus was observed through RT-PCR, qPCR, Western blotting and immunohistochemical staining methods The results showed that palmatine treatment can alleviate the hyperalgesia, allodynia and depressive behaviours of rats with comorbidity of DNP and DP. Meanwhile, the expression of P2X receptors, GFAP, TNF-α and IL-1ß in the hippocampus of the rats with comorbidity of DNP and DP was significantly increased compared with the control rats, and palmatine treatment could decrease the expression. Furthermore, the enhanced phosphorylation of ERK1/2 in the hippocampus of rats with DNP and DP was decreased noticeably by palmatine treatment. The results of this study suggest that palmatine can alleviate the comorbidity of DNP and DP by inhibiting the expression of P2X receptors in the hippocampus, and its action may be related to suppression of the phosphorylation of ERK1/2 and the release of TNF-α and IL-1ß in the hippocampus.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  9 / 23332 MEDLINE  
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[PMID]: 29421324
[Au] Autor:Lichtner G; Auksztulewicz R; Kirilina E; Velten H; Mavrodis D; Scheel M; Blankenburg F; von Dincklage F
[Ad] Address:Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Klinik für Anästhesiologie mit Schwerpunkt operative Intensivmedizin (CCM, CVK), Berlin, Germany.
[Ti] Title:Effects of propofol anesthesia on the processing of noxious stimuli in the spinal cord and the brain.
[So] Source:Neuroimage;172:642-653, 2018 Feb 05.
[Is] ISSN:1095-9572
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Drug-induced unconsciousness is an essential component of general anesthesia, commonly attributed to attenuation of higher-order processing of external stimuli and a resulting loss of information integration capabilities of the brain. In this study, we investigated how the hypnotic drug propofol at doses comparable to those in clinical practice influences the processing of somatosensory stimuli in the spinal cord and in primary and higher-order cortices. Using nociceptive reflexes, somatosensory evoked potentials and functional magnet resonance imaging (fMRI), we found that propofol abolishes the processing of innocuous and moderate noxious stimuli at low to medium concentration levels, but that intense noxious stimuli evoked spinal and cerebral responses even during deep propofol anesthesia that caused profound electroencephalogram (EEG) burst suppression. While nociceptive reflexes and somatosensory potentials were affected only in a minor way by further increasing doses of propofol after the loss of consciousness, fMRI showed that increasing propofol concentration abolished processing of intense noxious stimuli in the insula and secondary somatosensory cortex and vastly increased processing in the frontal cortex. As the fMRI functional connectivity showed congruent changes with increasing doses of propofol - namely the temporal brain areas decreasing their connectivity with the bilateral pre-/postcentral gyri and the supplementary motor area, while connectivity of the latter with frontal areas is increased - we conclude that the changes in processing of noxious stimuli during propofol anesthesia might be related to changes in functional connectivity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  10 / 23332 MEDLINE  
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[PMID]: 29521811
[Au] Autor:Falk S
[Ad] Address:Department of Neuroscience, Blegdamsvej 3B, 2200 Copenhagen N, Denmark.
[Ti] Title:Carbenoxolone as a novel therapy for attenuation of cancer-induced bone pain.
[So] Source:Pain;, 2018 Mar 06.
[Is] ISSN:1872-6623
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pain is a major complication for cancer patients significantly compromising their quality of life. Current treatment is far from optimal and particularly bone-related cancer pain poses an increasing clinical and socio-economical problem. Connexins, key proteins in cell-cell communication, have the potential to affect cancer-induced bone pain at multiple levels, including nociceptive signaling and bone degradation. This study tested the analgesic potential of carbenoxolone, a broad-acting connexin blocker, in a mouse model of cancer-induced bone pain. In addition, a pharmacological approach was used to elucidate the underlying mechanisms using the two specific blockers 37,43Gap27 and 43Gap26. Compared with vehicle treatment, chronic systemic administration of 20 mg/kg or 40 mg/kg carbenoxolone caused a significantly later onset and attenuation of movement-evoked and on-going pain, assessed with limb use and weight-bearing respectively. In addition, the carbenoxolone-treated groups demonstrated a significant delay in time to reach the humane endpoint. Acute intrathecal administration of 37,43Gap27 significantly attenuated both limb use and weight-bearing, whereas 43Gap26 had a less pronounced effect. Carbenoxolone treatment had a minor effect on the bone degradation in the early phase of disease progression, whereas no effect was observed in the late phase. Surprisingly, connexin43 was down-regulated in the cancer-bearing animals compared with shams. The results suggest that connexins are involved in cancer-induced bone pain, and that carbenoxolone could be a novel analgesic treatment for the pain state.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1097/j.pain.0000000000001197


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