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James W Grau - One of the best experts on this subject based on the ideXlab platform.
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Brain-Dependent Processes Fuel Pain-Induced Hemorrhage After Spinal Cord Injury.
Frontiers in Systems Neuroscience, 2019Co-Authors: Joshua A. Reynolds, Melissa K. Henwood, Joel D. Turtle, Rachel E. Baine, David T. Johnston, James W GrauAbstract:Pain (Nociceptive) input caudal to a spinal contusion injury can undermine long-term recovery and increase tissue loss (secondary injury). Prior work suggests that Nociceptive Stimulation has this effect because it fosters the breakdown of the blood-spinal cord barrier at the site of injury, allowing blood to infiltrate the tissue. The present study examined whether these effects impact tissue rostral and caudal to the site of injury. In addition, the study evaluated whether cutting communication with the brain, by means of a rostral transection, affects the development of hemorrhage. Eighteen hrs after rats received a lower thoracic (T11-12) contusion injury, half underwent a spinal transection at T2. Noxious electrical Stimulation (shock) was applied 6 hrs later. Cellular assays showed that, in non-transected rats, Nociceptive Stimulation increased hemoglobin content, activated pro-inflammatory cytokines and engaged signals related to cell death at the site of injury. These effects were not observed in transected animals. In the next experiment, the spinal transection was performed at the time of contusion injury. Nociceptive Stimulation was applied 24 hrs later and tissue was sectioned for microscopy. In non-transected rats Nociceptive Stimulation increased the area of hemorrhage and this effect was blocked by spinal transection. These findings imply that the adverse effect of noxious Stimulation depends upon spared ascending fibers and the activation of rostral (brain) systems. If true, Stimulation should induce less hemorrhage after a severe contusion injury that blocks transmission to the brain. To test this, rats were given a mild, moderate, or severe, injury and electrical Stimulation was applied 24 hrs later. Histological analyses of longitudinal sections showed that Nociceptive Stimulation triggered less hemorrhage after a severe contusion injury. The results suggest that brain-dependent processes drive pain-induced hemorrhage after spinal cord injury.
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peripheral noxious Stimulation reduces withdrawal threshold to mechanical stimuli after spinal cord injury role of tumor necrosis factor alpha and apoptosis
Pain, 2014Co-Authors: Sandra M Garraway, Adam R Ferguson, Sarah A Woller, Russell J Huie, John J Hartman, Michelle A Hook, Rajesh C Miranda, Yungjen Huang, James W GrauAbstract:Abstract We previously showed that peripheral noxious input after spinal cord injury (SCI) inhibits beneficial spinal plasticity and impairs recovery of locomotor and bladder functions. These observations suggest that noxious input may similarly affect the development and maintenance of chronic neuropathic pain, an important consequence of SCI. In adult rats with a moderate contusion SCI, we investigated the effect of noxious tail Stimulation, administered 1 day after SCI on mechanical withdrawal responses to von Frey stimuli from 1 to 28 days after treatment. In addition, because the proinflammatory cytokine tumor necrosis factor alpha (TNFα) is implicated in numerous injury-induced processes including pain hypersensitivity, we assessed the temporal and spatial expression of TNFα, TNF receptors, and several downstream signaling targets after Stimulation. Our results showed that unlike sham surgery or SCI only, Nociceptive Stimulation after SCI induced mechanical sensitivity by 24 h. These behavioral changes were accompanied by increased expression of TNFα. Cellular assessments of downstream targets of TNFα revealed that Nociceptive Stimulation increased the expression of caspase 8 and the active subunit (12 kDa) of caspase 3, indicative of active apoptosis at a time point consistent with the onset of mechanical allodynia. In addition, immunohistochemical analysis revealed distinct morphological signs of apoptosis in neurons and microglia at 24 h after Stimulation. Interestingly, expression of the inflammatory mediator NFκB was unaltered by Nociceptive Stimulation. These results suggest that noxious input caudal to the level of SCI can increase the onset and expression of behavioral responses indicative of pain, potentially involving TNFα signaling.
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impact of behavioral control on the processing of Nociceptive Stimulation
Frontiers in Physiology, 2012Co-Authors: James W Grau, Eric D Crown, Sandra M Garraway, Russell J Huie, Michelle A Hook, Kyle M Baumbauer, Adam R FergusonAbstract:How Nociceptive signals are processed within the spinal cord, and whether these signals lead to behavioral signs of neuropathic pain, depends upon their relation to other events and behavior. Our work shows that these relations can have a lasting effect on spinal plasticity, inducing a form of learning that alters the effect of subsequent Nociceptive stimuli. The capacity of lower spinal systems to adapt, in the absence of brain input, is examined in spinally transected rats that receive a Nociceptive shock to the tibialis anterior muscle of one hind leg. If shock is delivered whenever the leg is extended (controllable Stimulation), it induces an increase in flexion duration that minimizes net shock exposure. This learning is not observed in subjects that receive the same amount of shock independent of leg position (uncontrollable Stimulation). These two forms of Stimulation have a lasting, and divergent, effect on subsequent learning: Controllable Stimulation enables learning whereas uncontrollable Stimulation disables it (learning deficit). Uncontrollable Stimulation also enhances mechanical reactivity (allodynia). We review evidence that training with controllable Stimulation engages a BDNF-dependent process that can both prevent and reverse the consequences of uncontrollable shock. We relate these effects to changes in BDNF protein and TrkB signaling. Controllable Stimulation is also shown to counter the effects of peripheral inflammation (from intradermal capsaicin). A model is proposed that assumes Nociceptive input is gated at an early stage, within the dorsal horn. his gate is sensitive to current environmental relations (between proprioceptive and Nociceptive input), allowing Stimulation to be classified as controllable or uncontrollable. We further propose that the status of this gate is affected by past experience and that a history of uncontrollable Stimulation will promote the development of neuropathic pain.
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instrumental learning within the spinal cord v evidence the behavioral deficit observed after noncontingent Nociceptive Stimulation reflects an intraspinal modification
Behavioural Brain Research, 2003Co-Authors: Robin L Joynes, Adam R Ferguson, Eric D Crown, Brianne C Patton, James W GrauAbstract:Spinally transected rats given leg shock whenever one hindlimb is extended learn to maintain the leg in a flexed position, which minimizes net shock exposure. Yoked rats, that receive an equal amount of shock independent of leg position (noncontingent shock), do not exhibit an increase in flexion duration. Yoked rats also fail to learn when response contingent shock is applied to the previously shocked leg, a behavioral deficit that resembles learned helplessness. This deficit could reflect either a peripheral (e.g. muscle fatigue) or central effect. Experiment 1 showed that spinalized rats given noncontingent shock to one hind limb fail to learn when response-contingent shock is applied to the contralateral leg. Experiment 2 demonstrated that blocking the afferent input to the spinal cord, by cutting the sciatic nerve, blocked the development of the deficit. Experiment 3 found that intrathecal lidocaine has a protective effect and prevents the deficit. These findings suggest that noncontingent Nociceptive Stimulation induces an intraspinal modification that undermines behavioral potential.
In Koo Hwang - One of the best experts on this subject based on the ideXlab platform.
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valeriana officinalis root extract suppresses physical stress by electric shock and psychological stress by Nociceptive Stimulation evoked responses by decreasing the ratio of monoamine neurotransmitters to their metabolites
BMC Complementary and Alternative Medicine, 2014Co-Authors: Hyo Young Jung, Jung Hoon Choi, Youngil Kwak, Yeo Sung Yoon, In Koo HwangAbstract:In this study, we investigate the effects of valerian root extracts (VE) on physical and psychological stress responses by utilizing a communication box. Eight-week-old ICR mice received oral administration of VE (100 mg/kg/0.5 ml) or equal volume of distilled water in every day for 3 weeks prior to being subjected to physical or psychological stress for 3 days, which are induced by communication box developed for physical electric shock and psychological stress by Nociceptive Stimulation-evoked responses. The stress condition was assessed by forced swimming test and serum corticosterone levels. In addition, norepinephrine (NE), serotonin (5-HT), and their metabolites such as 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) and 5-hydroxyindoleacetic acid (5-HIAA) were measured in the hippocampus and amygdala at 1 h after final stress condition, respectively. Immobility time and corticosterone levels were significantly increased in both the physical and psychological stress groups compared to the control group. The administration of VE significantly reduced these parameters in both the physical and psychological stress groups. In addition, compared to the control group, physical and psychological stress groups showed significantly increased levels of MHPG-SO4 and 5-HIAA in the hippocampus and amygdala, respectively. The administration of VE significantly suppressed the increase of MHPG-SO4 and 5-HIAA in the two stress groups. These results suggest that VE can suppress physical and psychological stress responses by modulating the changes in 5-HT and NE turnover in the hippocampus and amygdala.
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Valeriana officinalis root extract suppresses physical stress by electric shock and psychological stress by Nociceptive Stimulation-evoked responses by decreasing the ratio of monoamine neurotransmitters to their metabolites
BMC Complementary and Alternative Medicine, 2014Co-Authors: Hyo Young Jung, Jung Hoon Choi, Youngil Kwak, Yeo Sung Yoon, In Koo HwangAbstract:Background In this study, we investigate the effects of valerian root extracts (VE) on physical and psychological stress responses by utilizing a communication box. Methods Eight-week-old ICR mice received oral administration of VE (100 mg/kg/0.5 ml) or equal volume of distilled water in every day for 3 weeks prior to being subjected to physical or psychological stress for 3 days, which are induced by communication box developed for physical electric shock and psychological stress by Nociceptive Stimulation-evoked responses. The stress condition was assessed by forced swimming test and serum corticosterone levels. In addition, norepinephrine (NE), serotonin (5-HT), and their metabolites such as 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO_4) and 5-hydroxyindoleacetic acid (5-HIAA) were measured in the hippocampus and amygdala at 1 h after final stress condition, respectively. Results Immobility time and corticosterone levels were significantly increased in both the physical and psychological stress groups compared to the control group. The administration of VE significantly reduced these parameters in both the physical and psychological stress groups. In addition, compared to the control group, physical and psychological stress groups showed significantly increased levels of MHPG-SO_4 and 5-HIAA in the hippocampus and amygdala, respectively. The administration of VE significantly suppressed the increase of MHPG-SO_4 and 5-HIAA in the two stress groups. Conclusion These results suggest that VE can suppress physical and psychological stress responses by modulating the changes in 5-HT and NE turnover in the hippocampus and amygdala.
Lars Arendtnielsen - One of the best experts on this subject based on the ideXlab platform.
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evaluation of sympathetic vasoconstrictor response following Nociceptive Stimulation of latent myofascial trigger points in humans
Acta Physiologica, 2009Co-Authors: Yoshiyuki Kimura, Hong You Ge, Yang Zhang, M Kimura, Hiroyuki Sumikura, Lars ArendtnielsenAbstract:Aim: Myofascial trigger points (MTrPs) are a major cause of musculoskeletal pain. It has been reported that Stimulation of a latent MTrP increases motor activity and facilitates muscle pain via activation of the sympathetic nervous system. However, the magnitude of the sympathetic vasoconstrictor response following Stimulation of MTrP has not been studied in healthy volunteers. The aims of this study were to (1) evaluate the magnitude of the vasoconstrictor response following a Nociceptive Stimulation (intramuscular glutamate) of MTrPs and a breath-hold manoeuvre (activation of sympathetic outflow) and (2) assess whether the vasoconstrictor response can be further modulated by combining a Nociceptive Stimulation of MTrPs and breath-hold. Methods: Fourteen healthy subjects were recruited in this study. This study consisted of four sessions (normal breath group as control, breath-hold group, glutamate MTrP injection group and glutamate MTrP injection + breath-hold group). Skin blood flow and skin temperature in both forearms were measured with laser Doppler flowmetry and infrared thermography, respectively, in each session (before the treatment, during the treatment and after the treatment). Results: Glutamate injection into MTrPs decreased skin temperature and blood flow in the peripheral area. The magnitudes of the reduction were comparable to those induced by the breath-hold manoeuvre, which has been used to induce sympathetic vasoconstrictor response. Conclusion: The combination of glutamate injection into latent MTrPs together with the breath-hold manoeuvre did not result in further decrease in skin temperature and blood flow, indicating that sympathetic vasoconstrictor activity is fully activated by Nociceptive Stimulation of MTrPs.
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attenuated skin blood flow response to Nociceptive Stimulation of latent myofascial trigger points
Archives of Physical Medicine and Rehabilitation, 2009Co-Authors: Yoshiyuki Kimura, Hong You Ge, Yang Zhang, Lars ArendtnielsenAbstract:Abstract Zhang Y, Ge H-Y, Yue S-W, Kimura Y, Arendt-Nielsen L. Attenuated skin blood flow response to Nociceptive Stimulation of latent myofascial trigger points. Objectives To investigate the effect of painful Stimulation of latent myofascial trigger points (MTrPs) on skin blood flow and to evaluate the relative sensitivity of laser Doppler flowmetry (LDF) and thermography in the measurement of skin blood flow. Design Painful Stimulation was obtained by a bolus injection of glutamate (0.1mL, 0.5M) into a latent MTrP located in the right or left brachioradialis muscles. A bolus of glutamate injection into a non-MTrP served as control. Pain intensity (visual analog scale [VAS]) was assessed after glutamate injection. Pressure pain threshold (PPT) was recorded bilaterally in the brachioradialis muscle before and after glutamate-induced pain. Skin blood flow and surface skin temperature were measured bilaterally in the forearms before, during, and after glutamate-induced pain with LDF and thermography. Setting A biomedical research facility. Participants Fifteen healthy volunteer subjects. Interventions Not applicable. Main Outcome Measures VAS, PPT, skin blood flow, and surface skin temperature. Results Glutamate injection into latent MTrPs induced higher pain intensity (F=7.16; P P P P >.05). Conclusions The present study demonstrated an attenuated skin blood flow response after painful Stimulation of latent MTrPs compared with non-MTrPs, suggesting increased sympathetic vasoconstriction activity at latent MTrPs. Additionally, LDF was more sensitive than thermography in the detection of the changes in skin blood flow after intramuscular Nociceptive Stimulation.
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induction of muscle cramps by Nociceptive Stimulation of latent myofascial trigger points
Experimental Brain Research, 2008Co-Authors: Hong You Ge, Yuqing Zhang, Shellie Boudreau, Lars ArendtnielsenAbstract:The aim of this present study is to test the hypothesis that Nociceptive Stimulation of latent myofascial trigger points (MTrPs) increases the occurrence of local muscle cramps. Nociceptive muscle Stimulation was obtained by a bolus injection of glutamate (0.1 ml, 0.5 M) into a latent MTrP and a control point (a non-MTrP) located in the right or left gastrocnemius medialis muscles in 14 healthy subjects. A bolus of isotonic saline (0.9%, 0.1 ml) injection served as a control. The injections were guided by intramuscular electromyography (EMG) showing resting spontaneous electrical activity at a latent MTrP and no such activity at a non-MTrP. Intramuscular and surface EMG activities in the gastrocnemius medialis muscle were recorded pre-, during-, and post-injection for a period of 8 min to monitor the occurrence of muscle cramps, which are characterized by a brief episodic burst of high levels of EMG activity. The results showed that glutamate and isotonic saline injections into the latent MTrPs induced higher peak pain intensity than into the non-MTrPs (both P < 0.05). Glutamate injection induced higher peak pain intensity than isotonic saline injection into either latent MTrPs or non-MTrPs (both P < 0.05). Muscle camps were observed in 92.86% of the subjects following glutamate injection into the latent MTrPs, but not into the non-MTrPs (P < 0.001). No muscle cramps were recorded following isotonic saline injection into either the latent MTrPs or the non-MTrPs. These results suggest that latent MTrPs could be involved in the genesis of muscle cramps. Focal increase in Nociceptive sensitivity at MTrPs constitutes one of the mechanisms underlying muscle cramps.
Hyo Young Jung - One of the best experts on this subject based on the ideXlab platform.
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valeriana officinalis root extract suppresses physical stress by electric shock and psychological stress by Nociceptive Stimulation evoked responses by decreasing the ratio of monoamine neurotransmitters to their metabolites
BMC Complementary and Alternative Medicine, 2014Co-Authors: Hyo Young Jung, Jung Hoon Choi, Youngil Kwak, Yeo Sung Yoon, In Koo HwangAbstract:In this study, we investigate the effects of valerian root extracts (VE) on physical and psychological stress responses by utilizing a communication box. Eight-week-old ICR mice received oral administration of VE (100 mg/kg/0.5 ml) or equal volume of distilled water in every day for 3 weeks prior to being subjected to physical or psychological stress for 3 days, which are induced by communication box developed for physical electric shock and psychological stress by Nociceptive Stimulation-evoked responses. The stress condition was assessed by forced swimming test and serum corticosterone levels. In addition, norepinephrine (NE), serotonin (5-HT), and their metabolites such as 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) and 5-hydroxyindoleacetic acid (5-HIAA) were measured in the hippocampus and amygdala at 1 h after final stress condition, respectively. Immobility time and corticosterone levels were significantly increased in both the physical and psychological stress groups compared to the control group. The administration of VE significantly reduced these parameters in both the physical and psychological stress groups. In addition, compared to the control group, physical and psychological stress groups showed significantly increased levels of MHPG-SO4 and 5-HIAA in the hippocampus and amygdala, respectively. The administration of VE significantly suppressed the increase of MHPG-SO4 and 5-HIAA in the two stress groups. These results suggest that VE can suppress physical and psychological stress responses by modulating the changes in 5-HT and NE turnover in the hippocampus and amygdala.
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Valeriana officinalis root extract suppresses physical stress by electric shock and psychological stress by Nociceptive Stimulation-evoked responses by decreasing the ratio of monoamine neurotransmitters to their metabolites
BMC Complementary and Alternative Medicine, 2014Co-Authors: Hyo Young Jung, Jung Hoon Choi, Youngil Kwak, Yeo Sung Yoon, In Koo HwangAbstract:Background In this study, we investigate the effects of valerian root extracts (VE) on physical and psychological stress responses by utilizing a communication box. Methods Eight-week-old ICR mice received oral administration of VE (100 mg/kg/0.5 ml) or equal volume of distilled water in every day for 3 weeks prior to being subjected to physical or psychological stress for 3 days, which are induced by communication box developed for physical electric shock and psychological stress by Nociceptive Stimulation-evoked responses. The stress condition was assessed by forced swimming test and serum corticosterone levels. In addition, norepinephrine (NE), serotonin (5-HT), and their metabolites such as 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO_4) and 5-hydroxyindoleacetic acid (5-HIAA) were measured in the hippocampus and amygdala at 1 h after final stress condition, respectively. Results Immobility time and corticosterone levels were significantly increased in both the physical and psychological stress groups compared to the control group. The administration of VE significantly reduced these parameters in both the physical and psychological stress groups. In addition, compared to the control group, physical and psychological stress groups showed significantly increased levels of MHPG-SO_4 and 5-HIAA in the hippocampus and amygdala, respectively. The administration of VE significantly suppressed the increase of MHPG-SO_4 and 5-HIAA in the two stress groups. Conclusion These results suggest that VE can suppress physical and psychological stress responses by modulating the changes in 5-HT and NE turnover in the hippocampus and amygdala.
Anne Stankewitz - One of the best experts on this subject based on the ideXlab platform.
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neuronal mechanisms during repetitive trigemino Nociceptive Stimulation in migraine patients
Pain, 2010Co-Authors: David Aderjan, Anne StankewitzAbstract:Habituation deficits in various sensory modalities have been observed in migraine patients in several experimental designs. The underlying neuronal mechanisms are, however, still unknown. Past studies have used electrophysiological measures and focussed on habituation behaviour during one single session. We were interested in how repeated painful Stimulation over several days is processed, perceived and modulated in migraineurs. Fifteen migraine patients and 15 healthy controls were stimulated daily with a 20 min trigeminal pain paradigm for eight consecutive days, using functional MRI performed on days one and eight and one follow-up measurement three months later. The results demonstrate that migraine patients did not differ in behavioural pain ratings compared to the controls at any time. However, functional imaging data revealed a significant difference in several brain areas over time. The activity level in the prefrontal cortex (PFC) and the rostral anterior cingulate cortex (rACC) increased in healthy control subjects from day one to day eight, whereas it decreased in migraine patients. These data suggest that several brain areas known to be involved in endogenous pain control show a completely opposite behaviour in migraine patients compared to healthy controls. These brain networks seem not to be disrupted per se in migraine patients but changed activity over time responding to repetitive Nociceptive input. The alteration of pain inhibitory circuits may be the underlying mechanism responsible for the dys-functional neuronal filters of sensory input.
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a new trigemino Nociceptive Stimulation model for event related fmri
Cephalalgia, 2010Co-Authors: Anne Stankewitz, H L Voit, U Bingel, C PeschkeAbstract:Functional imaging of human trigemino-Nociceptive processing provides meaningful insights into altered pain processing in head and face pain diseases. Although functional magnetic resonance imaging...