The Experts below are selected from a list of 2790 Experts worldwide ranked by ideXlab platform
Lars Arendtnielsen - One of the best experts on this subject based on the ideXlab platform.
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a review of topical high concentration l menthol as a translational model of Cold Allodynia and hyperalgesia
European Journal of Pain, 2014Co-Authors: Hjalte Holm Andersen, Rasmus Vinther Olsen, Heidi Guldborg Moller, Peter Winther Eskelund, Parisa Gazerani, Lars ArendtnielsenAbstract:Background Cold Allodynia and Cold hyperalgesia are both elusive features of neuropathic pain, particularly in patients with various polyneuropathies. Numerous studies have suggested that topical application of L-menthol causes temporary Cold hypersensitivity and thus acts as a proxy for associated symptoms. This review summarizes studies on L-menthol-induced nociception, Cold Allodynia and Cold hyperalgesia in vitro, in animals and in humans. Methods A comprehensive literature search was performed using the PubMed and Google Scholar databases until February 2013. Obtained manuscripts were reviewed for relevancy and reference lists of the retrieved articles were cross-checked for additional important studies. Solely the literature regarding topical application of L-menthol in humans was attained systematically. Of the total identified studies (96), 10 met the inclusion criteria being controlled studies applying L-menthol at a concentration of ≥30%. Results The extracted data are meticulously compared and presented with emphasis on clarity and transparency. In seven animal studies, Cold Allodynia or hyperalgesia was successfully established utilizing various methods. Eight studies in healthy volunteers unanimously reported a significant increase in Cold pain threshold, representing Cold Allodynia and increased supra-threshold Cold pain sensitivity, thus demonstrating Cold hyperalgesia. Conclusions Topical high-concentration L-menthol consistently induces Cold hypersensitivity in animals and humans, thus constituting a predictable surrogate model of Cold Allodynia and hyperalgesia. Understanding translational features of this model and its underlying mechanisms could be valuable in preclinical and human phases of drug development and in improving current treatment of patients with polyneuropathy.
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a review of topical high concentration l menthol as a translational model of Cold Allodynia and hyperalgesia
European Journal of Pain, 2014Co-Authors: Hjalte Holm Andersen, Rasmus Vinther Olsen, Heidi Guldborg Moller, Peter Winther Eskelund, Parisa Gazerani, Lars ArendtnielsenAbstract:Background Cold Allodynia and Cold hyperalgesia are both elusive features of neuropathic pain, particularly in patients with various polyneuropathies. Numerous studies have suggested that topical application of L-menthol causes temporary Cold hypersensitivity and thus acts as a proxy for associated symptoms. This review summarizes studies on L-menthol-induced nociception, Cold Allodynia and Cold hyperalgesia in vitro, in animals and in humans. Methods A comprehensive literature search was performed using the PubMed and Google Scholar databases until February 2013. Obtained manuscripts were reviewed for relevancy and reference lists of the retrieved articles were cross-checked for additional important studies. Solely the literature regarding topical application of L-menthol in humans was attained systematically. Of the total identified studies (96), 10 met the inclusion criteria being controlled studies applying L-menthol at a concentration of ≥30%. Results The extracted data are meticulously compared and presented with emphasis on clarity and transparency. In seven animal studies, Cold Allodynia or hyperalgesia was successfully established utilizing various methods. Eight studies in healthy volunteers unanimously reported a significant increase in Cold pain threshold, representing Cold Allodynia and increased supra-threshold Cold pain sensitivity, thus demonstrating Cold hyperalgesia. Conclusions Topical high-concentration L-menthol consistently induces Cold hypersensitivity in animals and humans, thus constituting a predictable surrogate model of Cold Allodynia and hyperalgesia. Understanding translational features of this model and its underlying mechanisms could be valuable in preclinical and human phases of drug development and in improving current treatment of patients with polyneuropathy.
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the effects of menthol on Cold Allodynia and wind up like pain in upper limb amputees with different levels of phantom limb pain
Neuroscience Letters, 2013Co-Authors: Lars Arendtnielsen, Lene Vase, Peter Svensson, Lone Nikolajsen, Troels S JensenAbstract:Abstract The mechanisms underlying phantom limb pain are not fully known, but hypersensitivity appears to be a central element. Menthol has previously been suggested as a model for hypersensitivity, but it has not yet been investigated if different levels of neuropathic pain may influence the effects of menthol or if topical application of menthol may act as a model for hypersensitivity in patients with phantom limb pain. In the present study, menthol ( l -menthol 40%) was applied to the affected and non-affected sides in 24 upper-limb amputees with different levels of phantom limb pain to test if menthol could induce Cold Allodynia and exacerbate wind-up-like pain. The average level of phantom limb pain was significantly related to Cold Allodynia ( P = 0.044). Prior to application of menthol, the level of phantom limb pain was significantly related to the level of wind-up-like pain following both brush ( P = 0.040) and pinprick ( P = 0.033) stimulation. After application of menthol, the level of phantom limb pain was only related to wind-up-like pain following brush ( P = 0.011) but not pinprick stimulation ( P = 0.233). This study indicates that menthol does influence hypersensitivity in phantom limb pain patients, and it is the first study to show that menthol may exacerbate wind-up-like pain in this group of neuropathic pain patients. The findings suggest that menthol may act as a model for studying sensitization in phantom limb patients.
Sun Kwang Kim - One of the best experts on this subject based on the ideXlab platform.
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The Suppressive Effects of Cinnamomi Cortex and Its Phytocompound Coumarin on Oxaliplatin-Induced Neuropathic Cold Allodynia in Rats
Molecules (Basel Switzerland), 2016Co-Authors: Changmin Kim, Ji Hwan Lee, Woojin Kim, Yangseok Kim, Kyungjin Lee, Sun Kwang KimAbstract:Oxaliplatin, a chemotherapy drug, induces acute peripheral neuropathy characterized by Cold Allodynia, spinal glial activation and increased levels of pro-inflammatory cytokines. Herein, we determined whether Cinnamomi Cortex (C. Cortex), a widely used medicinal herb in East Asia for Cold-related diseases, could attenuate oxaliplatin-induced Cold Allodynia in rats and the mechanisms involved. A single oxaliplatin injection (6 mg/kg, i.p.) induced significant Cold Allodynia signs based on tail immersion tests using Cold water (4 °C). Daily oral administration of water extract of C. Cortex (WECC) (100, 200, and 400 mg/kg) for five consecutive days following an oxaliplatin injection dose-dependently alleviated Cold Allodynia with only a slight difference in efficacies between the middle dose at 200 mg/kg and the highest dose at 400 mg/kg. WECC at 200 mg/kg significantly suppressed the activation of astrocytes and microglia and decreased the expression levels of IL-1β and TNF in the spinal cord after injection with oxaliplatin. Furthermore, oral administration of coumarin (10 mg/kg), a major phytocompound of C. Cortex, markedly reduced Cold Allodynia. These results indicate that C. Cortex has a potent anti-allodynic effect in oxaliplatin-injected rats through inhibiting spinal glial cells and pro-inflammatory cytokines. We also suggest that coumarin might play a role in the anti-allodynic effect of C. Cortex.
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Nicotinic Acetylcholine Receptors Mediate the Suppressive Effect of an Injection of Diluted Bee Venom into the GV3 Acupoint on Oxaliplatin-Induced Neuropathic Cold Allodynia in Rats.
Biological & pharmaceutical bulletin, 2015Co-Authors: Heera Yoon, Hyunsu Bae, Min Joon Kim, Insoo Yoon, Sun Kwang KimAbstract:Oxaliplatin, a platinum-based chemotherapy drug, often induces acute neuropathic pain, especially Cold Allodynia, even after a single administration. Subcutaneous injection of diluted bee venom (BV) into acupoints has been used to treat various pain symptoms in traditional oriental medicine. Although we previously demonstrated the suppressive effect of BV injection on oxaliplatin-induced Cold Allodynia in rats, its neurochemical mechanism remained unclear. This study investigates whether and how the cholinergic system mediates the relieving effect of BV injection on Cold Allodynia in oxaliplatin-administered rats. The behavioral signs of Cold Allodynia induced by an oxaliplatin administration (6 mg/kg, intraperitoneally (i.p.)) were evaluated by a tail immersion test in Cold water (4°C). BV (0.25 mg/kg, subcutaneously (s.c.)) injection into the Yaoyangguan acupoint, located between the spinous processes of the fourth and fifth lumbar vertebrae, significantly alleviated the Cold Allodynia. This relieving effect of BV injection on oxaliplatin-induced Cold Allodynia was blocked by a pretreatment with mecamylamine (a non-selective nicotinic receptor antagonist, 2 mg/kg, i.p.), but not by atropine (a non-selective muscarinic receptor antagonist, 1 mg/kg, i.p.). Further, dihydro-β-erythroidinehydrobromide (DHβE, an α4β2 nicotinic antagonist, 5 mg/kg, i.p.) prevented the anti-allodynic effect of BV, whereas methyllycaconitine (an α7 nicotinic antagonist, 6 mg/kg, i.p.) did not. Finally, intrathecal administration of DHβE (10 nM) blocked the BV-induced anti-allodynic effect. These results suggest that nicotinic acetylcholine receptors, especially spinal α4β2 receptors, but not muscarinic receptors, mediate the suppressive effect of BV injection on oxaliplatin-induced acute Cold Allodynia in rats.
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Serotonergic mechanism of the relieving effect of bee venom acupuncture on oxaliplatin-induced neuropathic Cold Allodynia in rats
BMC complementary and alternative medicine, 2014Co-Authors: Ji-hye Lee, Byung-il Min, Heera Yoon, Fu-shi Quan, Sun Kwang KimAbstract:Background Oxaliplatin, an important chemotherapy drug for advanced colorectal cancer, often induces peripheral neuropathy, especially Cold Allodynia. Our previous study showed that bee venom acupuncture (BVA), which has been traditionally used in Korea to treat various pain symptoms, potently relieves oxaliplatin-induced Cold Allodynia in rats. However, the mechanism for this anti-allodynic effect of BVA remains poorly understood. We investigated whether and how the central serotonergic system, a well-known pathway for acupuncture analgesia, mediates the relieving effect of BVA on Cold Allodynia in oxaliplatin-injected rats.
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effect of bee venom acupuncture on oxaliplatin induced Cold Allodynia in rats
Evidence-based Complementary and Alternative Medicine, 2013Co-Authors: Bongsoo Lim, Sun Kwang Kim, Hak Jin Moon, Munsoo Gil, Joon Ki Min, Giseog Lee, Hyunsu Bae, Byung-il MinAbstract:Oxaliplatin, a chemotherapy drug, often leads to neuropathic Cold Allodynia after a single administration. Bee venom acupuncture (BVA) has been used in Korea to relieve various pain symptoms and is shown to have a potent antiallodynic effect in nerve-injured rats. We examined whether BVA relieves oxaliplatin-induced Cold Allodynia and which endogenous analgesic system is implicated. The Cold Allodynia induced by an oxaliplatin injection (6 mg/kg, i.p.) was evaluated by immersing the rat’s tail into Cold water (4°C) and measuring the withdrawal latency. BVA (1.0 mg/kg, s.c.) at Yaoyangguan (GV3), Quchi (LI11), or Zusanli (ST36) acupoints significantly reduced Cold Allodynia with the longest effect being shown in the GV3 group. Conversely, a high dose of BVA (2.5 mg/kg) at GV3 did not show a significant antiallodynic effect. Phentolamine (α-adrenergic antagonist, 2 mg/kg, i.p.) partially blocked the relieving effect of BVA on Allodynia, whereas naloxone (opioid antagonist, 2 mg/kg, i.p.) did not. We further confirmed that an intrathecal administration of idazoxan (α2-adrenergic antagonist, 50 μg) blocked the BVA-induced anti-allodynic effect. These results indicate that BVA alleviates oxaliplatin-induced Cold Allodynia in rats, at least partly, through activation of the noradrenergic system. Thus, BVA might be a potential therapeutic option in oxaliplatin-induced neuropathy.
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Spinal GABA receptors mediate the suppressive effect of electroacupuncture on Cold Allodynia in rats.
Brain research, 2010Co-Authors: Jung-hyun Park, Jae-bok Han, Sun Kwang Kim, Jung-hyuk Park, Boram Sun, Byung-il MinAbstract:Abstract This study was performed to determine whether spinal GABAergic systems mediate the relieving effects of low frequency electroacupuncture (EA) on Cold Allodynia in a rat tail model of neuropathic pain. For neuropathic surgery, the right superior caudal trunk was resected at the level between the S1 and S2 spinal nerves innervating the tail. Two weeks after the nerve injury, the intrathecal catheter was implanted. Five days after the catheterization, rats were intrathecally injected with gabazine (GABAA receptor antagonist, 0.0003, 0.001 or 0.003 μg), or saclofen (GABAB receptor antagonist, 3, 10 or 30 μg). Ten minutes after the injection, EA (2 Hz) was applied to the ST36 acupoint for 30 min. The Cold Allodynia was assessed by the tail immersion test (i.e. immersing the tail in Cold (4 °C) water and measuring the latency of an abrupt tail movement) before and after the EA treatment. EA stimulation at ST36 significantly inhibited the Cold Allodynia sign, whereas EA at non-acupoint and plain acupuncture at ST36 (without electrical stimulation) did not show antiallodynic effects. Intrathecal administration of gabazine or saclofen blocked the relieving effects of ST36 EA stimulation on Cold Allodynia. These results suggest that spinal GABAA and GABAB receptors mediate the suppressive effect of low frequency EA on Cold Allodynia in the tail neuropathic rats.
Hjalte Holm Andersen - One of the best experts on this subject based on the ideXlab platform.
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a review of topical high concentration l menthol as a translational model of Cold Allodynia and hyperalgesia
European Journal of Pain, 2014Co-Authors: Hjalte Holm Andersen, Rasmus Vinther Olsen, Heidi Guldborg Moller, Peter Winther Eskelund, Parisa Gazerani, Lars ArendtnielsenAbstract:Background Cold Allodynia and Cold hyperalgesia are both elusive features of neuropathic pain, particularly in patients with various polyneuropathies. Numerous studies have suggested that topical application of L-menthol causes temporary Cold hypersensitivity and thus acts as a proxy for associated symptoms. This review summarizes studies on L-menthol-induced nociception, Cold Allodynia and Cold hyperalgesia in vitro, in animals and in humans. Methods A comprehensive literature search was performed using the PubMed and Google Scholar databases until February 2013. Obtained manuscripts were reviewed for relevancy and reference lists of the retrieved articles were cross-checked for additional important studies. Solely the literature regarding topical application of L-menthol in humans was attained systematically. Of the total identified studies (96), 10 met the inclusion criteria being controlled studies applying L-menthol at a concentration of ≥30%. Results The extracted data are meticulously compared and presented with emphasis on clarity and transparency. In seven animal studies, Cold Allodynia or hyperalgesia was successfully established utilizing various methods. Eight studies in healthy volunteers unanimously reported a significant increase in Cold pain threshold, representing Cold Allodynia and increased supra-threshold Cold pain sensitivity, thus demonstrating Cold hyperalgesia. Conclusions Topical high-concentration L-menthol consistently induces Cold hypersensitivity in animals and humans, thus constituting a predictable surrogate model of Cold Allodynia and hyperalgesia. Understanding translational features of this model and its underlying mechanisms could be valuable in preclinical and human phases of drug development and in improving current treatment of patients with polyneuropathy.
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a review of topical high concentration l menthol as a translational model of Cold Allodynia and hyperalgesia
European Journal of Pain, 2014Co-Authors: Hjalte Holm Andersen, Rasmus Vinther Olsen, Heidi Guldborg Moller, Peter Winther Eskelund, Parisa Gazerani, Lars ArendtnielsenAbstract:Background Cold Allodynia and Cold hyperalgesia are both elusive features of neuropathic pain, particularly in patients with various polyneuropathies. Numerous studies have suggested that topical application of L-menthol causes temporary Cold hypersensitivity and thus acts as a proxy for associated symptoms. This review summarizes studies on L-menthol-induced nociception, Cold Allodynia and Cold hyperalgesia in vitro, in animals and in humans. Methods A comprehensive literature search was performed using the PubMed and Google Scholar databases until February 2013. Obtained manuscripts were reviewed for relevancy and reference lists of the retrieved articles were cross-checked for additional important studies. Solely the literature regarding topical application of L-menthol in humans was attained systematically. Of the total identified studies (96), 10 met the inclusion criteria being controlled studies applying L-menthol at a concentration of ≥30%. Results The extracted data are meticulously compared and presented with emphasis on clarity and transparency. In seven animal studies, Cold Allodynia or hyperalgesia was successfully established utilizing various methods. Eight studies in healthy volunteers unanimously reported a significant increase in Cold pain threshold, representing Cold Allodynia and increased supra-threshold Cold pain sensitivity, thus demonstrating Cold hyperalgesia. Conclusions Topical high-concentration L-menthol consistently induces Cold hypersensitivity in animals and humans, thus constituting a predictable surrogate model of Cold Allodynia and hyperalgesia. Understanding translational features of this model and its underlying mechanisms could be valuable in preclinical and human phases of drug development and in improving current treatment of patients with polyneuropathy.
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A review of topical high‐concentration L‐menthol as a translational model of Cold Allodynia and hyperalgesia
European Journal of Pain, 2013Co-Authors: Hjalte Holm Andersen, Rasmus Vinther Olsen, Heidi Guldborg Moller, Peter Winther Eskelund, Parisa Gazerani, Lars Arendt-nielsenAbstract:Background Cold Allodynia and Cold hyperalgesia are both elusive features of neuropathic pain, particularly in patients with various polyneuropathies. Numerous studies have suggested that topical application of L-menthol causes temporary Cold hypersensitivity and thus acts as a proxy for associated symptoms. This review summarizes studies on L-menthol-induced nociception, Cold Allodynia and Cold hyperalgesia in vitro, in animals and in humans. Methods A comprehensive literature search was performed using the PubMed and Google Scholar databases until February 2013. Obtained manuscripts were reviewed for relevancy and reference lists of the retrieved articles were cross-checked for additional important studies. Solely the literature regarding topical application of L-menthol in humans was attained systematically. Of the total identified studies (96), 10 met the inclusion criteria being controlled studies applying L-menthol at a concentration of ≥30%. Results The extracted data are meticulously compared and presented with emphasis on clarity and transparency. In seven animal studies, Cold Allodynia or hyperalgesia was successfully established utilizing various methods. Eight studies in healthy volunteers unanimously reported a significant increase in Cold pain threshold, representing Cold Allodynia and increased supra-threshold Cold pain sensitivity, thus demonstrating Cold hyperalgesia. Conclusions Topical high-concentration L-menthol consistently induces Cold hypersensitivity in animals and humans, thus constituting a predictable surrogate model of Cold Allodynia and hyperalgesia. Understanding translational features of this model and its underlying mechanisms could be valuable in preclinical and human phases of drug development and in improving current treatment of patients with polyneuropathy.
Byung-il Min - One of the best experts on this subject based on the ideXlab platform.
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Serotonergic mechanism of the relieving effect of bee venom acupuncture on oxaliplatin-induced neuropathic Cold Allodynia in rats
BMC complementary and alternative medicine, 2014Co-Authors: Ji-hye Lee, Byung-il Min, Heera Yoon, Fu-shi Quan, Sun Kwang KimAbstract:Background Oxaliplatin, an important chemotherapy drug for advanced colorectal cancer, often induces peripheral neuropathy, especially Cold Allodynia. Our previous study showed that bee venom acupuncture (BVA), which has been traditionally used in Korea to treat various pain symptoms, potently relieves oxaliplatin-induced Cold Allodynia in rats. However, the mechanism for this anti-allodynic effect of BVA remains poorly understood. We investigated whether and how the central serotonergic system, a well-known pathway for acupuncture analgesia, mediates the relieving effect of BVA on Cold Allodynia in oxaliplatin-injected rats.
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effect of bee venom acupuncture on oxaliplatin induced Cold Allodynia in rats
Evidence-based Complementary and Alternative Medicine, 2013Co-Authors: Bongsoo Lim, Sun Kwang Kim, Hak Jin Moon, Munsoo Gil, Joon Ki Min, Giseog Lee, Hyunsu Bae, Byung-il MinAbstract:Oxaliplatin, a chemotherapy drug, often leads to neuropathic Cold Allodynia after a single administration. Bee venom acupuncture (BVA) has been used in Korea to relieve various pain symptoms and is shown to have a potent antiallodynic effect in nerve-injured rats. We examined whether BVA relieves oxaliplatin-induced Cold Allodynia and which endogenous analgesic system is implicated. The Cold Allodynia induced by an oxaliplatin injection (6 mg/kg, i.p.) was evaluated by immersing the rat’s tail into Cold water (4°C) and measuring the withdrawal latency. BVA (1.0 mg/kg, s.c.) at Yaoyangguan (GV3), Quchi (LI11), or Zusanli (ST36) acupoints significantly reduced Cold Allodynia with the longest effect being shown in the GV3 group. Conversely, a high dose of BVA (2.5 mg/kg) at GV3 did not show a significant antiallodynic effect. Phentolamine (α-adrenergic antagonist, 2 mg/kg, i.p.) partially blocked the relieving effect of BVA on Allodynia, whereas naloxone (opioid antagonist, 2 mg/kg, i.p.) did not. We further confirmed that an intrathecal administration of idazoxan (α2-adrenergic antagonist, 50 μg) blocked the BVA-induced anti-allodynic effect. These results indicate that BVA alleviates oxaliplatin-induced Cold Allodynia in rats, at least partly, through activation of the noradrenergic system. Thus, BVA might be a potential therapeutic option in oxaliplatin-induced neuropathy.
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Spinal GABA receptors mediate the suppressive effect of electroacupuncture on Cold Allodynia in rats.
Brain research, 2010Co-Authors: Jung-hyun Park, Jae-bok Han, Sun Kwang Kim, Jung-hyuk Park, Boram Sun, Byung-il MinAbstract:Abstract This study was performed to determine whether spinal GABAergic systems mediate the relieving effects of low frequency electroacupuncture (EA) on Cold Allodynia in a rat tail model of neuropathic pain. For neuropathic surgery, the right superior caudal trunk was resected at the level between the S1 and S2 spinal nerves innervating the tail. Two weeks after the nerve injury, the intrathecal catheter was implanted. Five days after the catheterization, rats were intrathecally injected with gabazine (GABAA receptor antagonist, 0.0003, 0.001 or 0.003 μg), or saclofen (GABAB receptor antagonist, 3, 10 or 30 μg). Ten minutes after the injection, EA (2 Hz) was applied to the ST36 acupoint for 30 min. The Cold Allodynia was assessed by the tail immersion test (i.e. immersing the tail in Cold (4 °C) water and measuring the latency of an abrupt tail movement) before and after the EA treatment. EA stimulation at ST36 significantly inhibited the Cold Allodynia sign, whereas EA at non-acupoint and plain acupuncture at ST36 (without electrical stimulation) did not show antiallodynic effects. Intrathecal administration of gabazine or saclofen blocked the relieving effects of ST36 EA stimulation on Cold Allodynia. These results suggest that spinal GABAA and GABAB receptors mediate the suppressive effect of low frequency EA on Cold Allodynia in the tail neuropathic rats.
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effects of electroacupuncture on Cold Allodynia in a rat model of neuropathic pain mediation by spinal adrenergic and serotonergic receptors
Experimental Neurology, 2005Co-Authors: Sun Kwang Kim, Byung Gil Hwang, Jung-hyuk Park, Byung-il Min, Sang Jin Bae, Ji Hoon Kim, Dong Suk ParkAbstract:The present study was performed to examine the effects of electroacupuncture (EA) on Cold Allodynia and its mechanisms related to the spinal adrenergic and serotonergic systems in a rat model of neuropathic pain. For the neuropathic surgery, the right superior caudal trunk was resected at the level between S1 and S2 spinal nerves innervating the tail. Two weeks after the nerve injury, EA stimulation (2 or 100 Hz) was delivered to Zusanli (ST36) for 30 min. The behavioral signs of Cold Allodynia were evaluated by the tail immersion test [i.e., immersing the tail in Cold water (4 degrees C) and measuring the latency to an abrupt tail movement] before and after the stimulation. And then, we examined the effects of intrathecal injection of prazosin (alpha1-adrenoceptor antagonist, 30 microg), yohimbine (alpha2-adrenoceptor antagonist, 30 microg), NAN-190 (5-HT1A antagonist, 15 microg), ketanserin (5-HT2A antagonist, 30 microg), and MDL-72222 (5-HT3 antagonist, 12 microg) on the action of EA stimulation. Although both 2 Hz and 100 Hz EA significantly relieved the Cold Allodynia signs, 2 Hz EA induced more robust effects than 100 Hz EA. In addition, intrathecal injection of yohimbine, NAN-190, and MDL-72222, but not prazosin and ketanserin, significantly blocked the relieving effects of 2 Hz EA on Cold Allodynia. These results suggest that low-frequency (2 Hz) EA is more suitable for the treatment of Cold Allodynia than high-frequency (100 Hz) EA, and spinal alpha2-adrenergic, 5-HT1A and 5-HT3, but not alpha1-adrenergic and 5-HT2A, receptors play important roles in mediating the relieving effects of 2 Hz EA on Cold Allodynia in neuropathic rats.
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Effects of alpha1- and alpha2-adrenoreceptor antagonists on Cold Allodynia in a rat tail model of neuropathic pain.
Brain research, 2005Co-Authors: Sun Kwang Kim, Byung Gil Hwang, Byung-il Min, Ji Hoon Kim, Gi Yong Yoo, Dong Suk ParkAbstract:Systemic administrations (0.1, 0.5, and 2 mg/kg) of alpha1-adrenoreceptor (AR) antagonist prazosin dose-dependently attenuated Cold Allodynia in a rat tail model of neuropathic pain, whereas alpha2-AR antagonist yohimbine exacerbated it. These results suggest that the functions of alpha1- and alpha2-AR in this model are excitatory and inhibitory, respectively, consistent with their general properties. It is also proposed that Cold Allodynia can be reversed by alpha1-AR antagonist and exacerbated by alpha2-AR antagonist.
Munekazu Naito - One of the best experts on this subject based on the ideXlab platform.
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physical disuse contributes to widespread chronic mechanical hyperalgesia tactile Allodynia and Cold Allodynia through neurogenic inflammation and spino parabrachio amygdaloid pathway activation
Pain, 2020Co-Authors: Yusuke Ohmichi, Makoto Tsuda, Mika Ohmichi, Ryoichi Tashima, Koji Osuka, Kaori Fukushige, Dominika Kanikowska, Yugo Fukazawa, Hiromu Yawo, Munekazu NaitoAbstract:Physical disuse could lead to a state of chronic pain typified by complex regional pain syndrome type I due to fear of pain through movement (kinesiophobia) or inappropriate resting procedures. However, the mechanisms by which physical disuse is associated with acute/chronic pain and other pathological signs remain unresolved. We have previously reported that inflammatory signs, contractures, disuse muscle atrophy, spontaneous pain-like behaviors, and chronic widespread mechanical hyperalgesia based on central plasticity occurred after 2-weeks of cast immobilization in chronic post-cast pain (CPCP) rat model. In the present study, we also demonstrated dystrophy-like changes, both peripheral nociceptive signals and activation of the central pain pathway in CPCP rats. This was done by the following methods: (1) vascular permeability (Evans blue dye) and inflammatory- and oxidative stress-related messenger RNA (mRNA) changes (real-time quantitative polymerase chain reaction); (2) immunofluorescence of pERK and/or c-Fos expression in the spino-parabrachio-amygdaloid pathway; and (3) blockade of nociceptive-related signals using sciatic nerve block (SNB). Furthermore, we demonstrated tactile Allodynia using an optogenetic method in a transgenic rat line (W-TChR2V4), Cold Allodynia using the acetone test, and activation of dorsal horn neurons in the chronic phase associated with chronic mechanical hyperalgesia using c-Fos immunofluorescence. In addition, we showed that nociceptive signals in the acute phase are involved in chronic pathological pain-like behaviors by studying the effects of SNB. Thus, we conclude that physical disuse contributes to dystrophy-like changes, spontaneous pain-like behavior, and chronic widespread pathological pain-like behaviors in CPCP rats after 2 weeks of cast immobilization.
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physical disuse contributes to widespread chronic mechanical hyperalgesia tactile Allodynia and Cold Allodynia through neurogenic inflammation and spino parabrachio amygdaloid pathway activation
Pain, 2020Co-Authors: Yusuke Ohmichi, Makoto Tsuda, Mika Ohmichi, Ryoichi Tashima, Koji Osuka, Kaori Fukushige, Dominika Kanikowska, Yugo Fukazawa, Hiromu Yawo, Munekazu NaitoAbstract:Physical disuse could lead to a state of chronic pain typified by complex regional pain syndrome type I due to fear of pain through movement (kinesiophobia) or inappropriate resting procedures. However, the mechanisms by which physical disuse is associated with acute/chronic pain and other pathological signs remain unresolved. We have previously reported that inflammatory signs, contractures, disuse muscle atrophy, spontaneous pain-like behaviors, and chronic widespread mechanical hyperalgesia based on central plasticity occurred after 2-weeks of cast immobilization in chronic post-cast pain (CPCP) rat model. In the present study, we also demonstrated dystrophy-like changes, both peripheral nociceptive signals and activation of the central pain pathway in CPCP rats. This was done by the following methods: (1) vascular permeability (Evans blue dye) and inflammatory- and oxidative stress-related messenger RNA (mRNA) changes (real-time quantitative polymerase chain reaction); (2) immunofluorescence of pERK and/or c-Fos expression in the spino-parabrachio-amygdaloid pathway; and (3) blockade of nociceptive-related signals using sciatic nerve block (SNB). Furthermore, we demonstrated tactile Allodynia using an optogenetic method in a transgenic rat line (W-TChR2V4), Cold Allodynia using the acetone test, and activation of dorsal horn neurons in the chronic phase associated with chronic mechanical hyperalgesia using c-Fos immunofluorescence. In addition, we showed that nociceptive signals in the acute phase are involved in chronic pathological pain-like behaviors by studying the effects of SNB. Thus, we conclude that physical disuse contributes to dystrophy-like changes, spontaneous pain-like behavior, and chronic widespread pathological pain-like behaviors in CPCP rats after 2 weeks of cast immobilization.