Pub Date : 2010-06-04DOI: 10.2174/1876386301003010060
R. Monzani, L. Crozzoli, M. Ruvo
Traditional Chinese Medicine is a therapeutic system comparable to allopathic medicine. Its most known appli- cation concerns with pain control and that is why it is mostly performed by anesthesiologists, pain therapists or pure acu- puncturists. Acupuncture has great and wide potential: treatment of acute low back pain, intra-operative electro-analgesia and other therapeutic indications well recognized by WHO. Acupuncture points can be rubbed down, warmed up, electrically stimulated or simply hit. Their existence is scientifically proven. Acupuncture can be used in daily clinical practice: its efficacy as anti-emetic or preventive treatment for nausea and vom- iting associated with pregnancy, chemotherapy and individual sensitivity is well proven. Acupuncture can support medical therapy in the first approach to chronic pain and in the second step it can completely re- place pharmacological therapy. Although the number of treated patients is smaller, acupuncture seems to be similar to pharmacological therapy with re- gard to postoperative pain control.
{"title":"Acupuncture for Pain Treatment","authors":"R. Monzani, L. Crozzoli, M. Ruvo","doi":"10.2174/1876386301003010060","DOIUrl":"https://doi.org/10.2174/1876386301003010060","url":null,"abstract":"Traditional Chinese Medicine is a therapeutic system comparable to allopathic medicine. Its most known appli- cation concerns with pain control and that is why it is mostly performed by anesthesiologists, pain therapists or pure acu- puncturists. Acupuncture has great and wide potential: treatment of acute low back pain, intra-operative electro-analgesia and other therapeutic indications well recognized by WHO. Acupuncture points can be rubbed down, warmed up, electrically stimulated or simply hit. Their existence is scientifically proven. Acupuncture can be used in daily clinical practice: its efficacy as anti-emetic or preventive treatment for nausea and vom- iting associated with pregnancy, chemotherapy and individual sensitivity is well proven. Acupuncture can support medical therapy in the first approach to chronic pain and in the second step it can completely re- place pharmacological therapy. Although the number of treated patients is smaller, acupuncture seems to be similar to pharmacological therapy with re- gard to postoperative pain control.","PeriodicalId":53614,"journal":{"name":"Open Pain Journal","volume":"3 1","pages":"60-65"},"PeriodicalIF":0.0,"publicationDate":"2010-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68124389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-06-04DOI: 10.2174/1876386301003010052
J. Gagnier
Introduction - Natural health products (e.g., vitamins, minerals, herbal medicines) are frequently used for musculoskeletal pain and there is an increasing amount of high quality research being done to test the efficacy of these interventions. Low back pain is a very common condition and individuals suffering from these conditions are frequently seeking out these products. Objective - The objective of this paper is to review and summarize the evidence surrounding natural health products for chronic non-specific low back pain. Methods - We searched for systematic reviews and randomized controlled trials in PubMed and the Cochrane Library. We performed a best evidence synthesis of the resulting papers. Results - We included two systematic reviews and 2 additional randomized controlled trials published subsequently to these reviews. We found strong evidence for 50 mg harpagoside per dose of an aqueous extract of Harpagophytum procumbens per day reduces pain more than placebo. We found moderate evidence for 100 mg harpagoside per dose of an aqueous extract of Harpagophytum procumbens compared to placebo, for an extract of willow bark yielding 120 mg salicin per day compared with placebo, for 240 mg of salicin per day in reducing pain to a greater extent than placebo, for 240 mg of salicin per day as equivalent to 120 mg salicin, for no differences in pain and function between a 60 mg daily harpagoside dose of an aqueous extract of Harpagophytum procumbens and 12.5 mg rofecoxib per day, for no difference in pain and overall improvement between Spiroflor SRL homeopathic gel (SRL) and Cremor Capsici Compositus FNA, the capsici oleoresin gel, for intramuscular B12 when compared with placebo. We found limited evidence for topical Capsicum frutescens in the form of Rado-Salil cream or a Capsicum plaster for reducing pain more than placebo, for lavender oil in the treatment of chronic NSLBP, or vitamin C, zinc, and manganese in addition to prolotherapy. Adverse events for all interventions appeared to be mild and transient though we did not attempt to identify all relevant literature concerning adverse events. Conclusions - There is some evidence for several natural health products in the treatment of chronic non-specific low back pain. More research is needed for all of these interventions before they are incorporated into routine clinical practice and their reporting must be improved by referring to the recently published extensions of the CONSORT statement.
{"title":"Evidence based review of natural health products for non-specific low back pain","authors":"J. Gagnier","doi":"10.2174/1876386301003010052","DOIUrl":"https://doi.org/10.2174/1876386301003010052","url":null,"abstract":"Introduction - Natural health products (e.g., vitamins, minerals, herbal medicines) are frequently used for musculoskeletal pain and there is an increasing amount of high quality research being done to test the efficacy of these interventions. Low back pain is a very common condition and individuals suffering from these conditions are frequently seeking out these products. Objective - The objective of this paper is to review and summarize the evidence surrounding natural health products for chronic non-specific low back pain. Methods - We searched for systematic reviews and randomized controlled trials in PubMed and the Cochrane Library. We performed a best evidence synthesis of the resulting papers. Results - We included two systematic reviews and 2 additional randomized controlled trials published subsequently to these reviews. We found strong evidence for 50 mg harpagoside per dose of an aqueous extract of Harpagophytum procumbens per day reduces pain more than placebo. We found moderate evidence for 100 mg harpagoside per dose of an aqueous extract of Harpagophytum procumbens compared to placebo, for an extract of willow bark yielding 120 mg salicin per day compared with placebo, for 240 mg of salicin per day in reducing pain to a greater extent than placebo, for 240 mg of salicin per day as equivalent to 120 mg salicin, for no differences in pain and function between a 60 mg daily harpagoside dose of an aqueous extract of Harpagophytum procumbens and 12.5 mg rofecoxib per day, for no difference in pain and overall improvement between Spiroflor SRL homeopathic gel (SRL) and Cremor Capsici Compositus FNA, the capsici oleoresin gel, for intramuscular B12 when compared with placebo. We found limited evidence for topical Capsicum frutescens in the form of Rado-Salil cream or a Capsicum plaster for reducing pain more than placebo, for lavender oil in the treatment of chronic NSLBP, or vitamin C, zinc, and manganese in addition to prolotherapy. Adverse events for all interventions appeared to be mild and transient though we did not attempt to identify all relevant literature concerning adverse events. Conclusions - There is some evidence for several natural health products in the treatment of chronic non-specific low back pain. More research is needed for all of these interventions before they are incorporated into routine clinical practice and their reporting must be improved by referring to the recently published extensions of the CONSORT statement.","PeriodicalId":53614,"journal":{"name":"Open Pain Journal","volume":"3 1","pages":"52-59"},"PeriodicalIF":0.0,"publicationDate":"2010-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68123065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-05-20DOI: 10.2174/1876386301003020014
Alexander J Davies, Yong Ho Kim, S. Oh
{"title":"Painful Neuron-Microglia Interactions in the Trigeminal Sensory System~!2009-09-09~!2009-11-23~!2010-05-07~!","authors":"Alexander J Davies, Yong Ho Kim, S. Oh","doi":"10.2174/1876386301003020014","DOIUrl":"https://doi.org/10.2174/1876386301003020014","url":null,"abstract":"","PeriodicalId":53614,"journal":{"name":"Open Pain Journal","volume":"3 1","pages":"14-28"},"PeriodicalIF":0.0,"publicationDate":"2010-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68124438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-05-20DOI: 10.2174/1876386301003020029
L. Luongo, E. Palazzo, V. Novellis, S. Maione
{"title":"Role of Endocannabinoids in Neuron-Glial Crosstalk~!2009-10-27~!2009-12-10~!2010-05-07~!","authors":"L. Luongo, E. Palazzo, V. Novellis, S. Maione","doi":"10.2174/1876386301003020029","DOIUrl":"https://doi.org/10.2174/1876386301003020029","url":null,"abstract":"","PeriodicalId":53614,"journal":{"name":"Open Pain Journal","volume":"3 1","pages":"29-36"},"PeriodicalIF":0.0,"publicationDate":"2010-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68124466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-05-07DOI: 10.2174/1876386301003010003
P. Durham, Filip G. Garrett
Pain in the head and face, which can be very severe and debilitating, often involves activation of trigeminal ganglion nerves. The craniofacial symptoms can manifest as acute or transient conditions such as toothaches and headaches, or can transform into more chronic conditions such as migraine, rhinosinusitis, temporomandibular joint (TMJ) disorder, or trigeminal neuralgia. Traditionally, it is known that peripheral tissue injury or inflammation leads to excitation of trigeminal nerves that release inflammatory molecules in the periphery as well as facilitate transmission of nociceptive signals to the central nervous system. However, findings from recent studies have demonstrated that peripheral tissue injury or inflammation also leads to increased interactions between neuronal cell bodies and satellite glial cells within the trigeminal ganglion. These cell-to-cell interactions, which involve the transfer of key regulatory mediators via channels or gap junctions as well as paracrine signaling, are thought to play an important role in the induction and maintenance of peripheral sensitization of trigeminal nociceptors. The focus of this review will be on understanding the importance of the increased signaling between neuronal cell bodies and satellite glia cells in trigeminal ganglia to the development of persistent pain.
{"title":"Emerging Importance of Neuron-Satellite Glia Interactions within Trigeminal Ganglia in Craniofacial Pain","authors":"P. Durham, Filip G. Garrett","doi":"10.2174/1876386301003010003","DOIUrl":"https://doi.org/10.2174/1876386301003010003","url":null,"abstract":"Pain in the head and face, which can be very severe and debilitating, often involves activation of trigeminal ganglion nerves. The craniofacial symptoms can manifest as acute or transient conditions such as toothaches and headaches, or can transform into more chronic conditions such as migraine, rhinosinusitis, temporomandibular joint (TMJ) disorder, or trigeminal neuralgia. Traditionally, it is known that peripheral tissue injury or inflammation leads to excitation of trigeminal nerves that release inflammatory molecules in the periphery as well as facilitate transmission of nociceptive signals to the central nervous system. However, findings from recent studies have demonstrated that peripheral tissue injury or inflammation also leads to increased interactions between neuronal cell bodies and satellite glial cells within the trigeminal ganglion. These cell-to-cell interactions, which involve the transfer of key regulatory mediators via channels or gap junctions as well as paracrine signaling, are thought to play an important role in the induction and maintenance of peripheral sensitization of trigeminal nociceptors. The focus of this review will be on understanding the importance of the increased signaling between neuronal cell bodies and satellite glia cells in trigeminal ganglia to the development of persistent pain.","PeriodicalId":53614,"journal":{"name":"Open Pain Journal","volume":"3 1","pages":"3-13"},"PeriodicalIF":0.0,"publicationDate":"2010-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68123400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-05-07DOI: 10.2174/1876386301003010029
L. Luongo, E. Palazzo, V. Novellis, S. Maione
Evidence shows bidirectional crosstalk between neurons and glia, suggesting that glia play an active role in synaptic plasticity leading to chronic pain. Importantly, gliosis has been implicated in the development and maintenance of hyperalgesia or allodynia following chronic inflammation or nerve injury. Anandamide (AEA) and 2- arachidonoylglycerol (2-AG), or the lipoamino acid N-arachydonoyldopamine (NADA), are fatty acid derivative neuro- transmitters, named endocannabinoids (eCBs). These perform several biological actions, via the activation of cannabinoid type 1 and 2 (CB1/CB2) receptors belonging to the G-protein-coupled receptor family. The eCBs are produced on de- mand by neurons or glial cells and it has been suggested that they might be involved in the crosstalk between astrocytes, microglia, oligodendrocytes and neurons. In chronic pain, the modified glial or neural activity also seems to be associated with changes in eCB levels in pain processing areas either in the spinal cord or the brain. The activation of the eCB sys- tem in microglia or astrocytes could be crucial in modulating axonal growth and synaptogenesis at the base of neural phe- notypic changes. Furthermore, changes in eCBs levels have been suggested to affect the destiny of cells: death or survival may depend on a specific pain condition. Thus, although eCBs are emerging as neurotransmitters responsible for the regu- lation of glia-neuron crosstalk in chronic pain, the precise mechanisms leading to eCB production, the origin and the time- course of eCB release, the eCB release switch from one cell type to the other and their movement or catabolism across the glial or neural cell membrane nevertheless still remain unknown. These issues together with alternative eCB targets will be addressed in the current review.
{"title":"Role of Endocannabinoids in Neuron-Glial Crosstalk","authors":"L. Luongo, E. Palazzo, V. Novellis, S. Maione","doi":"10.2174/1876386301003010029","DOIUrl":"https://doi.org/10.2174/1876386301003010029","url":null,"abstract":"Evidence shows bidirectional crosstalk between neurons and glia, suggesting that glia play an active role in synaptic plasticity leading to chronic pain. Importantly, gliosis has been implicated in the development and maintenance of hyperalgesia or allodynia following chronic inflammation or nerve injury. Anandamide (AEA) and 2- arachidonoylglycerol (2-AG), or the lipoamino acid N-arachydonoyldopamine (NADA), are fatty acid derivative neuro- transmitters, named endocannabinoids (eCBs). These perform several biological actions, via the activation of cannabinoid type 1 and 2 (CB1/CB2) receptors belonging to the G-protein-coupled receptor family. The eCBs are produced on de- mand by neurons or glial cells and it has been suggested that they might be involved in the crosstalk between astrocytes, microglia, oligodendrocytes and neurons. In chronic pain, the modified glial or neural activity also seems to be associated with changes in eCB levels in pain processing areas either in the spinal cord or the brain. The activation of the eCB sys- tem in microglia or astrocytes could be crucial in modulating axonal growth and synaptogenesis at the base of neural phe- notypic changes. Furthermore, changes in eCBs levels have been suggested to affect the destiny of cells: death or survival may depend on a specific pain condition. Thus, although eCBs are emerging as neurotransmitters responsible for the regu- lation of glia-neuron crosstalk in chronic pain, the precise mechanisms leading to eCB production, the origin and the time- course of eCB release, the eCB release switch from one cell type to the other and their movement or catabolism across the glial or neural cell membrane nevertheless still remain unknown. These issues together with alternative eCB targets will be addressed in the current review.","PeriodicalId":53614,"journal":{"name":"Open Pain Journal","volume":"3 1","pages":"29-36"},"PeriodicalIF":0.0,"publicationDate":"2010-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68123048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-05-07DOI: 10.2174/1876386301003010014
Alexander J Davies, Yong Ho Kim, S. Oh
The trigeminal sensory system is unique in its innervation of structures specific to the orofacial area. Nocicep- tive trigeminal afferents are known to synapse with second-order neurons in the trigeminal subnucleus caudalis (Sp5C) in the brain stem. The activity of neurons within the Sp5C is responsible for the relay of nociceptive signals to higher brain centers. Recent evidence suggests that central sensitization may be fundamental to many trigeminal-specific painful neu- ropathies, including trigeminal neuralgia and migraine. Glia within the Sp5C are emerging as prime suspects in trigeminal central sensitization. In particular, microglial activation has been implicated in the development of neuropathic pain. It is possible that activated microglia release factors that alter the activity of second-order neurons or the synaptic activity of peripheral terminals within the Sp5C. Microglial activation has been characterized by changes in morphology, expression of membrane receptors and ion chan- nels, as well as alterations to cytokine and chemokine release. In addition, microglia have been studied in brain slice and dissociated culture where activation is characterized by changes to P2X receptor and potassium channel membrane cur- rents. However, little is known about resting and activated microglial membrane properties in the Sp5C and, furthermore, how these properties are affected following trigeminal nerve injury. This review summarizes the anatomical and patho- physiological importance of the Sp5C and focuses on recent studies on neurons and microglia in the trigeminal sensory system. The final part of the review aims to link important aspects of microglial membrane physiology with their potential role in chronic trigeminal pain conditions.
{"title":"Painful Neuron-Microglia Interactions in the Trigeminal Sensory System","authors":"Alexander J Davies, Yong Ho Kim, S. Oh","doi":"10.2174/1876386301003010014","DOIUrl":"https://doi.org/10.2174/1876386301003010014","url":null,"abstract":"The trigeminal sensory system is unique in its innervation of structures specific to the orofacial area. Nocicep- tive trigeminal afferents are known to synapse with second-order neurons in the trigeminal subnucleus caudalis (Sp5C) in the brain stem. The activity of neurons within the Sp5C is responsible for the relay of nociceptive signals to higher brain centers. Recent evidence suggests that central sensitization may be fundamental to many trigeminal-specific painful neu- ropathies, including trigeminal neuralgia and migraine. Glia within the Sp5C are emerging as prime suspects in trigeminal central sensitization. In particular, microglial activation has been implicated in the development of neuropathic pain. It is possible that activated microglia release factors that alter the activity of second-order neurons or the synaptic activity of peripheral terminals within the Sp5C. Microglial activation has been characterized by changes in morphology, expression of membrane receptors and ion chan- nels, as well as alterations to cytokine and chemokine release. In addition, microglia have been studied in brain slice and dissociated culture where activation is characterized by changes to P2X receptor and potassium channel membrane cur- rents. However, little is known about resting and activated microglial membrane properties in the Sp5C and, furthermore, how these properties are affected following trigeminal nerve injury. This review summarizes the anatomical and patho- physiological importance of the Sp5C and focuses on recent studies on neurons and microglia in the trigeminal sensory system. The final part of the review aims to link important aspects of microglial membrane physiology with their potential role in chronic trigeminal pain conditions.","PeriodicalId":53614,"journal":{"name":"Open Pain Journal","volume":"3 1","pages":"14-28"},"PeriodicalIF":0.0,"publicationDate":"2010-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68123409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-03-01DOI: 10.2174/1876386301003010144]
H Wang, W Guo, K Yang, F Wei, R Dubner, K Ren
We tested the hypothesis that primary afferent inputs play a role in astroglial hyperactivity after tissue injury. We first injected complete Freund's adjuvant (CFA, 0.05 ml, 1:1 oil/saline) into the masseter muscle, which upregulated glial fibrillary acidic protein (GFAP), a marker of astrocytes, interleukin (IL)-1β an inflammatory cytokine, and phosphorylation of serine896 of the NR1 subunit (P-NR1) of the NMDA receptor in the subnuclei interpolaris/caudalis (Vi/Vc) transition zone, an important structure for processing trigeminal nociceptive input. Local anesthetic block with lidocaine (2%) of the masseter muscle at 10 min prior to injection of CFA into the same site significantly reduced the CFA-induced increase in GFAP, IL-1β and P-NR1 (p<0.05, n=4/group). We then tested the effect of peripheral electrical stimulation (ES). The ES protocol was burst stimulation consisting of trains of 4 square pulses (10-100 Hz, 0.1-3 mA, 0.5 ms pulse width). Under pentobarbital anesthesia, an ES was delivered every 0.2 s for a total of 30 min. The Vi/Vc tissues were processed for immunohistochemistry or western blot analysis at 10-120 min after ES. Compared to naive and SHAM-treated rats, there was increased immunoreactivity against GFAP, IL-1β and P-NR1 in the Vi/Vc in rats receiving ES. Double staining showed that IL-1β was selectively localized in GFAP-positive astroglia, and P-NR1-immunoreactivity was localized to neurons. These findings indicate that primary afferent inputs are necessary and sufficient to induce astroglial hyperactivity and upregulation of IL-1β, as well as neuronal NMDA receptor phosphorylation.
{"title":"Contribution of Primary Afferent Input to Trigeminal Astroglial Hyperactivity, Cytokine Induction and NMDA Receptor Phosphorylation.","authors":"H Wang, W Guo, K Yang, F Wei, R Dubner, K Ren","doi":"10.2174/1876386301003010144]","DOIUrl":"https://doi.org/10.2174/1876386301003010144]","url":null,"abstract":"<p><p>We tested the hypothesis that primary afferent inputs play a role in astroglial hyperactivity after tissue injury. We first injected complete Freund's adjuvant (CFA, 0.05 ml, 1:1 oil/saline) into the masseter muscle, which upregulated glial fibrillary acidic protein (GFAP), a marker of astrocytes, interleukin (IL)-1β an inflammatory cytokine, and phosphorylation of serine896 of the NR1 subunit (P-NR1) of the NMDA receptor in the subnuclei interpolaris/caudalis (Vi/Vc) transition zone, an important structure for processing trigeminal nociceptive input. Local anesthetic block with lidocaine (2%) of the masseter muscle at 10 min prior to injection of CFA into the same site significantly reduced the CFA-induced increase in GFAP, IL-1β and P-NR1 (p<0.05, n=4/group). We then tested the effect of peripheral electrical stimulation (ES). The ES protocol was burst stimulation consisting of trains of 4 square pulses (10-100 Hz, 0.1-3 mA, 0.5 ms pulse width). Under pentobarbital anesthesia, an ES was delivered every 0.2 s for a total of 30 min. The Vi/Vc tissues were processed for immunohistochemistry or western blot analysis at 10-120 min after ES. Compared to naive and SHAM-treated rats, there was increased immunoreactivity against GFAP, IL-1β and P-NR1 in the Vi/Vc in rats receiving ES. Double staining showed that IL-1β was selectively localized in GFAP-positive astroglia, and P-NR1-immunoreactivity was localized to neurons. These findings indicate that primary afferent inputs are necessary and sufficient to induce astroglial hyperactivity and upregulation of IL-1β, as well as neuronal NMDA receptor phosphorylation.</p>","PeriodicalId":53614,"journal":{"name":"Open Pain Journal","volume":"2010 3","pages":"144-152"},"PeriodicalIF":0.0,"publicationDate":"2010-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3002905/pdf/nihms257583.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29546920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-01-01DOI: 10.2174/1876386301003010097
M. Kress
Cytokines are small proteins with a molecular mass lower than 30 kDa. They are produced and secreted on demand, have a short life span and only travel over short distances if not released into the blood circulation. In addition to the classical interleukins and the chemotactic chemokines, growth factors like VEGF or FGF and the colony stimulating factors are also considered cytokines since they have pleiotropic actions and regulatory function in the immune system. Despite the redundancy and pleiotropy of the cytokine network, specific actions of individual cytokines and endogenous control mechanisms have been identified. Particular local profiles of the classical proinflammatory cytokines are associated with inflammatory hypersensitivity and suggest an early involvement of TNFα, IL-1s and IL-6. An increasing number of novel cytokines and the more recently discovered chemokines are being associated with pathological pain states. Besides acting as pro- or anti-inflammatory mediators increasing evidence indicates that cytokines act on nociceptors. Neurons within the nociceptive system express neuronal receptors and specifically bind cytokines or chemokines which regulate neuronal excitability, sensitivity to external stimuli and synaptic plasticity. A first step to- wards a more mechanistic and individual pain therapeutic strategy could be avoidance of hypersensitive pain processing by either neutralization strategies for the proalgesic cytokines or by shifting the balance in favour of antialgesic members of the cytokine-chemokine network.
{"title":"Nociceptor Sensitization by Proinflammatory Cytokines And Chemokines","authors":"M. Kress","doi":"10.2174/1876386301003010097","DOIUrl":"https://doi.org/10.2174/1876386301003010097","url":null,"abstract":"Cytokines are small proteins with a molecular mass lower than 30 kDa. They are produced and secreted on demand, have a short life span and only travel over short distances if not released into the blood circulation. In addition to the classical interleukins and the chemotactic chemokines, growth factors like VEGF or FGF and the colony stimulating factors are also considered cytokines since they have pleiotropic actions and regulatory function in the immune system. Despite the redundancy and pleiotropy of the cytokine network, specific actions of individual cytokines and endogenous control mechanisms have been identified. Particular local profiles of the classical proinflammatory cytokines are associated with inflammatory hypersensitivity and suggest an early involvement of TNFα, IL-1s and IL-6. An increasing number of novel cytokines and the more recently discovered chemokines are being associated with pathological pain states. Besides acting as pro- or anti-inflammatory mediators increasing evidence indicates that cytokines act on nociceptors. Neurons within the nociceptive system express neuronal receptors and specifically bind cytokines or chemokines which regulate neuronal excitability, sensitivity to external stimuli and synaptic plasticity. A first step to- wards a more mechanistic and individual pain therapeutic strategy could be avoidance of hypersensitive pain processing by either neutralization strategies for the proalgesic cytokines or by shifting the balance in favour of antialgesic members of the cytokine-chemokine network.","PeriodicalId":53614,"journal":{"name":"Open Pain Journal","volume":"3 1","pages":"97-107"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68124218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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