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Janet L Taylor - One of the best experts on this subject based on the ideXlab platform.
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signals of motor command bias joint position sense in the presence of feedback from proprioceptors
Journal of Applied Physiology, 2009Co-Authors: Janette L Smith, Matthew Crawford, Uwe Proske, Janet L TaylorAbstract:Joint position sense is believed to be mediated by Muscle Afferent signals. Because a “phantom” hand produced by a sensory and motor nerve block appears to move in the direction of voluntary effort, signals of “motor command” or “effort” can influence perceived joint position. To determine whether this occurs when sensory signals are available, three studies assessed position sense when motor command and Afferent signals were available, but joint movement was prevented. First, the hand was positioned to stop movement at the proximal joint of the middle finger, and movement at the distal joint was impossible because the Muscles had been “disengaged”. Voluntary efforts produced illusory position changes in the direction of the effort (12.6 ± 2.0° distal joint; 12.3 ± 2.3° proximal joint for efforts at 30% maximum; means ± SD). Second, when subjects attempted to move the index finger under isometric conditions, the index finger appeared to move 7.4 ± 1.2° in the direction of efforts. These illusions graded with the level of effort (10 or 30% maximum) and far exceeded any real joint movement. Finally, because changes in Muscle Afferent feedback might have accompanied the voluntary efforts, all forearm and hand Muscles were completely paralyzed by locally infused rocuronium. During paralysis, passive wrist position was signaled accurately, but, during attempted efforts (30% maximum), perceived wrist position changed by 9.7 ± 4.9°. Before paralysis, isometric efforts changed it by 6.7 ± 3.6°. Thus all studies concur: when joint movement is prevented, signals of motor command contribute to joint position sense.
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Signals of motor command bias joint position sense in the presence of feedback from proprioceptors.
Journal of Applied Physiology, 2008Co-Authors: Janette L Smith, Matthew Crawford, Uwe Proske, Janet L TaylorAbstract:Joint position sense is believed to be mediated by Muscle Afferent signals. Because a “phantom” hand produced by a sensory and motor nerve block appears to move in the direction of voluntary effort...
Markus Amann - One of the best experts on this subject based on the ideXlab platform.
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identifying the role of group iii iv Muscle Afferents in the carotid baroreflex control of mean arterial pressure and heart rate during exercise
The Journal of Physiology, 2018Co-Authors: Thomas J Hureau, Joshua C Weavil, Taylor S Thurston, Ryan M Broxterman, Ashley D Nelson, Amber D Bledsoe, Jacob E Jessop, Russell S Richardson, Walter D Wray, Markus AmannAbstract:KEY POINTS We investigated the contribution of group III/IV Muscle Afferents to carotid baroreflex resetting during electrically evoked (no central command) and voluntary (requiring central command) isometric knee extension exercise. Lumbar intrathecal fentanyl was used to attenuate the central projection of μ-opioid receptor-sensitive group III/IV leg Muscle Afferent feedback. Spontaneous carotid baroreflex control was assessed by loading and unloading the carotid baroreceptors with a variable pressure neck chamber. Group III/IV Muscle Afferents did not influence spontaneous carotid baroreflex responsiveness at rest or during exercise. Afferent feedback accounted for at least 50% of the exercise-induced increase in the carotid baroreflex blood pressure and heart rate operating points, adjustments that are critical for an appropriate cardiovascular response to exercise. These findings suggest that group III/IV Muscle Afferent feedback is, independent of central command, critical for the resetting of the carotid baroreflex blood pressure and heart rate operating points, but not for spontaneous baroreflex responsiveness. ABSTRACT This study sought to comprehensively investigate the role of metabolically and mechanically sensitive group III/IV Muscle Afferents in carotid baroreflex responsiveness and resetting during both electrically evoked (EVO, no central command) and voluntary (VOL, requiring central command) isometric single-leg knee-extension (15% of maximal voluntary contraction; MVC) exercise. Participants (n = 8) were studied under control conditions (CTRL) and following lumbar intrathecal fentanyl injection (FENT) to inhibit μ-opioid receptor-sensitive lower limb Muscle Afferents. Spontaneous carotid baroreflex control of mean arterial pressure (MAP) and heart rate (HR) were assessed following rapid 5 s pulses of neck pressure (NP, +40 mmHg) or suction (NS, -60 mmHg). Resting MAP (87 ± 10 mmHg) and HR (70 ± 8 bpm) were similar between CTRL and FENT conditions (P > 0.4). In terms of spontaneous carotid baroreflex responsiveness, FENT did not alter the change in MAP or HR responses to NP (+13 ± 5 mmHg, P = 0.85; +9 ± 3 bpm; P = 0.99) or NS (-13 ± 5 mmHg, P = 0.99; -24 ± 11 bpm; P = 0.49) at rest or during either exercise protocol, which were of a remarkably similar magnitude to rest. In contrast, FENT administration reduced the exercise-induced resetting of the operating point for MAP and HR during both EVO (116 ± 10 mmHg to 100 ± 15 mmHg and 93 ± 14 bpm to 82 ± 10 bpm) and VOL (107 ± 13 mmHg to 100 ± 17 mmHg and 89 ± 10 bpm to 72 ± 10 bpm) exercise bouts. Together, these findings document that group III/IV Muscle Afferent feedback is critical for the resetting of the carotid baroreflex MAP and HR operating points, independent of exercise-induced changes in central command, but not for spontaneous carotid baroreflex responsiveness.
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from petri dish to human new insights into the mechanisms mediating Muscle pain and fatigue with implications for health and disease
Experimental Physiology, 2015Co-Authors: Markus Amann, Alan R LightAbstract:With the onset of physical activity, contraction-induced mechanical and metabolic stimuli within working Muscle activate molecular receptors located on the terminals of both thinly myelinated (group III) and unmyelinated neurons (group IV). These thin-fibre Muscle Afferents project, via the dorsal horn of the spinal cord, to spinal and supraspinal sites within the CNS. Over the past 80 years, scientists have recognized the critical involvement of these Afferents in the cardiovascular and respiratory responses to exercise, fatigue mediated by the CNS, and musculoskeletal pain (Amann et al. 2015). However, despite a century of research, the exact metabolites and intramuscular receptors mediating group III/IV-activated physiological responses and noxious sensations have not been established. Furthermore, the effect of diseases such as heart failure, chronic fatigue syndrome (CFS) or fibromyalgia on the Muscle Afferent feedback system and the potential role of maladaptations of this system in debilitating symptoms of these diseases are largely unknown.
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autonomic responses to exercise group iii iv Muscle Afferents and fatigue
Autonomic Neuroscience: Basic and Clinical, 2015Co-Authors: Markus Amann, Joshua C Weavil, Simranjit K Sidhu, Tyler S Mangum, Massimo VenturelliAbstract:Group III and IV Muscle Afferents originating in exercising limb Muscle play a significant role in the development of fatigue during exercise in humans. Feedback from these sensory neurons to the central nervous system (CNS) reflexively increases ventilation and central (cardiac output) and peripheral (limb blood flow) hemodynamic responses during exercise and thereby assures adequate Muscle blood flow and O2 delivery. This response depicts a key factor in minimizing the rate of development of peripheral fatigue and in optimizing aerobic exercise capacity. On the other hand, the central projection of group III/IV Muscle Afferents impairs performance and limits the exercising human via its diminishing effect on the output from spinal motoneurons which decreases voluntary Muscle activation (i.e. facilitates central fatigue). Accumulating evidence from recent animal studies suggests the existence of two subtypes of group III/IV Muscle Afferents. While one subtype only responds to physiological and innocuous levels of endogenous intramuscular metabolites (lactate, ATP, protons) associated with 'normal', predominantly aerobic exercise, the other subtype only responds to higher and concurrently noxious levels of metabolites present in Muscle during ischemic contractions or following, for example, hypertonic saline infusions. This review discusses the mechanisms through which group III/IV Muscle Afferent feedback mediates both central and peripheral fatigue in exercising humans. We also briefly summarize the accumulating evidence from recent animal and human studies documenting the existence of two subtypes of group III/IV Muscle Afferents and the relevance of this discovery to the interpretation of previous work and the design of future studies.
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implications of group iii and iv Muscle Afferents for high intensity endurance exercise performance in humans
The Journal of Physiology, 2011Co-Authors: Markus Amann, Gregory M Blain, Lester T Proctor, Joshua J Sebranek, David F Pegelow, Jerome A DempseyAbstract:Non-technical summary We investigated the influence of group III/IV Muscle Afferents on central motor drive, the development of peripheral locomotor Muscle fatigue, and endurance performance time during high-intensity constant-load cycling exercise to exhaustion. Our findings suggest that, on the one hand, Afferent feedback ensures adequate circulatory and ventilatory responses to exercise which optimizes Muscle O2 transport and thereby facilitates exercise performance by preventing premature peripheral fatigue. On the other hand, Afferent feedback inhibits central motor drive, which is reflected in the restriction of the neural excitation of the locomotor musculature and the reduced tolerance for peripheral Muscle fatigue, and thereby limits exercise performance. Taken together, the current investigation revealed the net effects of sensory Afferent feedback on time to exhaustion during high-intensity constant-load cycling exercise and showed that intact group III/IV Muscle Afferent feedback is a vital component in achieving optimal endurance performance.
Brian E Cairns - One of the best experts on this subject based on the ideXlab platform.
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activation of rat masticatory Muscle Afferent fibres by acidic ph
Somatosensory and Motor Research, 2018Co-Authors: Parisa Gazerani, Brian E CairnsAbstract:Previous research findings have suggested an important role for acid sensing ion channels (ASICs) in Muscle pain mechanisms. This study was conducted to determine if masticatory Muscle Afferent fib...
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elevated fractalkine cx3cl1 levels in the trigeminal ganglion mechanically sensitize temporalis Muscle nociceptors
Molecular Neurobiology, 2017Co-Authors: Brian E Cairns, Melissa Obrien, Xudong Dong, Parisa GazeraniAbstract:It has been proposed that after nerve injury or tissue inflammation, fractalkine (CX3CL1) released from dorsal root ganglion neurons acts on satellite glial cells (SGCs) through CX3C receptor 1 (CX3CR1) to induce neuroplastic changes. The existence and importance of fractalkine/CX3CR1 signaling in the trigeminal ganglia has not yet been clarified. This study investigated (1) whether trigeminal ganglion neurons that innervate temporalis Muscle and their associated SGCs contain fractalkine and/or express CX3CR1, (2) if intraganglionic injection of fractalkine increases the mechanical sensitivity of temporalis Muscle Afferent fibers, (3) whether complete Freund’s adjuvant (CFA)-induced inflammation of the temporalis Muscle alters the expression of fractalkine or its receptor in the trigeminal ganglion, and (4) if intraganglionic administration of CX3CR1 antibodies alters Afferent mechanical sensitivity. Immunohistochemistry and in vivo electrophysiological recordings in male and female rats were used to address these questions. It was found that ∼50 % of temporalis ganglion neurons and ∼25 % of their associated SGCs express CX3CR1, while only neurons expressed fractalkine. Temporalis Muscle inflammation increased the expression of fractalkine, but only in male rats. Intraganglionic injection of fractalkine (25 g/ml; 3 μl) induced prolonged Afferent mechanical sensitization. Intraganglionic injection of CX3CR1 antibody increased Afferent mechanical threshold, but this effect was greater in controls than in rats with CFA-induced Muscle inflammation. These findings raise the possibility that basal fractalkine signalling within the trigeminal ganglion plays an important role in mechanical sensitivity of masticatory Muscle sensory Afferent fibers and that inhibition of CX3CR1 signaling within the trigeminal ganglia may induce analgesia through a peripheral mechanism.
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glutamate dysregulation in the trigeminal ganglion a novel mechanism for peripheral sensitization of the craniofacial region
Neuroscience, 2014Co-Authors: Jens Christian Laursen, Brian E Cairns, Xudong Dong, Lars Arendtnielsen, Ujendra Kumar, Rishi K Somvanshi, Parisa GazeraniAbstract:Abstract In the trigeminal ganglion (TG), satellite glial cells (SGCs) form a functional unit with neurons. It has been proposed that SGCs participate in regulating extracellular glutamate levels and that dysfunction of this SGC capacity can impact nociceptive transmission in craniofacial pain conditions. This study investigated whether SGCs release glutamate and whether elevation of TG glutamate concentration alters response properties of trigeminal Afferent fibers. Immunohistochemistry was used to assess glutamate content and the expression of excitatory amino acid transporter (EAAT)1 and EAAT2 in TG sections. SGCs contained glutamate and expressed EAAT1 and EAAT2. Potassium chloride (10 mM) was used to evoke glutamate release from cultured rat SGCs treated with the EAAT1/2 inhibitor (3S)-3-[[3-[[4-(trifluoromethyl)ben zoyl]amino]phenyl]methoxy]- l -aspartic acid (TFB-TBOA) or control. Treatment with TFB-TBOA (1 and 10 μM) significantly reduced the glutamate concentration from 10.6 ± 1.1 to 5.8 ± 1.4 μM and 3.0 ± 0.8 μM, respectively ( p N- methyl- d -aspartate receptor antagonist 2-amino-5-phosphonovalerate (APV) and increased by TFB-TBOA, whereas mechanical sensitization was only sensitive to APV. Antidromic invasion of Muscle Afferent fibers by electrical stimulation of the caudal brainstem (10 Hz) or local anesthesia of the brainstem with lidocaine did not alter glutamate-induced mechanical sensitization. These findings provide a novel mechanism whereby dysfunctional trigeminal SGCs could contribute to cranial Muscle tenderness in craniofacial pain conditions such as migraine headache.
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expression of nmda and oestrogen receptors by trigeminal ganglion neurons that innervate the rat temporalis Muscle
The Chinese journal of dental research : the official journal of the Scientific Section of the Chinese Stomatological Association, 2012Co-Authors: Mian Wei Wang, Ujendra Kumar, Xudong Dong, Brian E CairnsAbstract:OBJECTIVE: To assess whether N-methyl-D-aspartate (NMDA) receptor (NR) or oestrogen receptor (OR) expression plays a role in the differences that temporalis Muscle Afferent fibres are less sensitive to peripheral receptor activation than masseter Muscle Afferent fibres and do not exhibit sex-related differences in NMDA-evoked discharge. METHODS: Immunohistochemical techniques were used to examine the expression of NR1, 2A, and 2B subunits of the NMDA receptor in male and female rats and the co-expression of NR2B subunits with ORs in female rats by trigeminal ganglion neurons that innervate the temporalis Muscle. In vivo electrophysiological recording methods were employed to assess the response of Afferent fibres to injection of NMDA into the temporalis Muscle in female rats. RESULTS: Approximately 20% of temporalis ganglion neurons expressed NR1, NR2A and NR2B subunits, respectively, and there was no sex-related difference in the expression of these subunits. In female rats, both ORα and ORs receptors were identified in the trigeminal ganglion by Western blot. ORs were found on the majority (~80%) of temporalis ganglion neurons that expressed NR2B subunits. A significant positive correlation between blood oestrogen concentration and NMDA-evoked Afferent discharge was identified. CONCLUSION: The absence of sex-related differences in NMDA receptor expression may account for the lack of sex-related differences in NMDA-evoked temporalis Afferent discharge. The association of elevated oestrogen concentration with increased Afferent response to NMDA and the co-expression of NRs and ORs in temporalis ganglion neurons suggest that sensory input from the temporalis Muscle may be modulated by oestrogenic tone.
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serotonin 5 ht excites rat masticatory Muscle Afferent fibers through activation of peripheral 5 ht3 receptors
Pain, 2008Co-Authors: David Sung, Xudong Dong, Malin Ernberg, Ujendra Kumar, Brian E CairnsAbstract:Abstract In the present study, we combined immunohistochemical experiments with in vivo single unit recordings to examine whether 5-HT 3 receptors are expressed by masticatory (masseter and temporalis) sensory ganglion neurons and to investigate the effects of intramuscular injection of 5-HT on the excitability and mechanical threshold of rat masticatory Muscle Afferent fibers. The expression of 5-HT 3 receptors by masticatory ganglion neurons was examined using immunohistochemical techniques. In vivo extracellular single unit recording techniques were used to assess changes in the excitability of individual masticatory Muscle Afferent fibers. Immunohistochemical experiments detected a relatively high frequency (52%) of 5-HT 3 receptor expression by masticatory ganglion neurons. Injection of 5-HT (10 −4 , 10 −3 , 10 −2 M) evoked concentration-related increases in the magnitude of Afferent discharge, but did not significantly sensitize Muscle Afferent fibers to mechanical stimuli. No significant sex-related differences in 5-HT-evoked Afferent discharge were identified. Afferent discharge evoked by 5-HT was significantly attenuated by co-injection with the selective 5-HT 3 receptor antagonist tropisetron (10 −3 M). Afferent discharge was also evoked by the selective 5-HT 3 receptor agonist 2-methyl-5-HT. Unexpectedly, a significant concentration-related decrease in median blood pressure in response to 5-HT injection was found. This 5-HT-induced decrease in blood pressure was not antagonized by tropisetron or mimicked by 2-methyl-5-HT, indicating that the drop in blood pressure was not 5-HT 3 receptor-mediated. The present results indicate that 5-HT excites slowly conducting masticatory Muscle Afferent fibers through activation of peripheral 5-HT 3 receptors, and suggest that similar mechanisms may contribute to 5-HT-evoked Muscle pain in human subjects.
Janette L Smith - One of the best experts on this subject based on the ideXlab platform.
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signals of motor command bias joint position sense in the presence of feedback from proprioceptors
Journal of Applied Physiology, 2009Co-Authors: Janette L Smith, Matthew Crawford, Uwe Proske, Janet L TaylorAbstract:Joint position sense is believed to be mediated by Muscle Afferent signals. Because a “phantom” hand produced by a sensory and motor nerve block appears to move in the direction of voluntary effort, signals of “motor command” or “effort” can influence perceived joint position. To determine whether this occurs when sensory signals are available, three studies assessed position sense when motor command and Afferent signals were available, but joint movement was prevented. First, the hand was positioned to stop movement at the proximal joint of the middle finger, and movement at the distal joint was impossible because the Muscles had been “disengaged”. Voluntary efforts produced illusory position changes in the direction of the effort (12.6 ± 2.0° distal joint; 12.3 ± 2.3° proximal joint for efforts at 30% maximum; means ± SD). Second, when subjects attempted to move the index finger under isometric conditions, the index finger appeared to move 7.4 ± 1.2° in the direction of efforts. These illusions graded with the level of effort (10 or 30% maximum) and far exceeded any real joint movement. Finally, because changes in Muscle Afferent feedback might have accompanied the voluntary efforts, all forearm and hand Muscles were completely paralyzed by locally infused rocuronium. During paralysis, passive wrist position was signaled accurately, but, during attempted efforts (30% maximum), perceived wrist position changed by 9.7 ± 4.9°. Before paralysis, isometric efforts changed it by 6.7 ± 3.6°. Thus all studies concur: when joint movement is prevented, signals of motor command contribute to joint position sense.
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Signals of motor command bias joint position sense in the presence of feedback from proprioceptors.
Journal of Applied Physiology, 2008Co-Authors: Janette L Smith, Matthew Crawford, Uwe Proske, Janet L TaylorAbstract:Joint position sense is believed to be mediated by Muscle Afferent signals. Because a “phantom” hand produced by a sensory and motor nerve block appears to move in the direction of voluntary effort...
Matthew Crawford - One of the best experts on this subject based on the ideXlab platform.
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signals of motor command bias joint position sense in the presence of feedback from proprioceptors
Journal of Applied Physiology, 2009Co-Authors: Janette L Smith, Matthew Crawford, Uwe Proske, Janet L TaylorAbstract:Joint position sense is believed to be mediated by Muscle Afferent signals. Because a “phantom” hand produced by a sensory and motor nerve block appears to move in the direction of voluntary effort, signals of “motor command” or “effort” can influence perceived joint position. To determine whether this occurs when sensory signals are available, three studies assessed position sense when motor command and Afferent signals were available, but joint movement was prevented. First, the hand was positioned to stop movement at the proximal joint of the middle finger, and movement at the distal joint was impossible because the Muscles had been “disengaged”. Voluntary efforts produced illusory position changes in the direction of the effort (12.6 ± 2.0° distal joint; 12.3 ± 2.3° proximal joint for efforts at 30% maximum; means ± SD). Second, when subjects attempted to move the index finger under isometric conditions, the index finger appeared to move 7.4 ± 1.2° in the direction of efforts. These illusions graded with the level of effort (10 or 30% maximum) and far exceeded any real joint movement. Finally, because changes in Muscle Afferent feedback might have accompanied the voluntary efforts, all forearm and hand Muscles were completely paralyzed by locally infused rocuronium. During paralysis, passive wrist position was signaled accurately, but, during attempted efforts (30% maximum), perceived wrist position changed by 9.7 ± 4.9°. Before paralysis, isometric efforts changed it by 6.7 ± 3.6°. Thus all studies concur: when joint movement is prevented, signals of motor command contribute to joint position sense.
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Signals of motor command bias joint position sense in the presence of feedback from proprioceptors.
Journal of Applied Physiology, 2008Co-Authors: Janette L Smith, Matthew Crawford, Uwe Proske, Janet L TaylorAbstract:Joint position sense is believed to be mediated by Muscle Afferent signals. Because a “phantom” hand produced by a sensory and motor nerve block appears to move in the direction of voluntary effort...
