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David Yarnitsky - One of the best experts on this subject based on the ideXlab platform.
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Paradoxical Heat Sensation in healthy subjects: peripherally conducted by A delta or C fibres?
Brain : a journal of neurology, 1999Co-Authors: Ezra Susser, David YarnitskyAbstract:Paradoxical Heat Sensation upon cooling of the skin has been reported in central as well as in peripheral neurological conditions. In our study, we examined this phenomenon in 35 naive healthy test subjects, of whom 23 experienced paradoxical Heat Sensation under test conditions. We measured the peripheral conduction velocities of cold Sensation, warm Sensation and of paradoxical Heat Sensation by using a quantitative sensory testing model of indirect peripheral conduction velocity measurement. This was based on comparison of measurements at a proximal and a distal site using two measurement methods, one inclusive and the other exclusive of reaction time. We found that the conduction velocity of paradoxical Heat Sensation (0.70 m/s) was similar to that of warm Sensation (0.68 m/s), and that the conduction velocity of cold Sensation (7.74-8.01 m/s) was considerably faster. Thus, we conclude that paradoxical Heat Sensation in healthy subjects is conducted peripherally via slow unmyelinated C fibres and not via the faster A delta fibres. Consequently, we propose that paradoxical Heat Sensation is encoded via the Heat sensing pathway, in accordance with the labelled-line code theory. The mechanisms proposed suggest a malfunctioning cold-sensing pathway disinhibiting the Heat-sensing pathway, at peripheral, central or both levels, thus facilitating a paradoxical Heat Sensation.
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Paradoxical Heat Sensation in healthy subjects: peripherally conducted by Aδ or C fibres?
Brain, 1999Co-Authors: Ezra Susser, David YarnitskyAbstract:Paradoxical Heat Sensation upon cooling of the skin has been reported in central as well as in peripheral neurological conditions. In our study, we examined this phenomenon in 35 naive healthy test subjects, of whom 23 experienced paradoxical Heat Sensation under test conditions. We measured the peripheral conduction velocities of cold Sensation, warm Sensation and of paradoxical Heat Sensation by using a quantitative sensory testing model of indirect peripheral conduction velocity measurement. This was based on comparison of measurements at a proximal and a distal site using two measurement methods, one inclusive and the other exclusive of reaction time. We found that the conduction velocity of paradoxical Heat Sensation (0.70 m/s) was similar to that of warm Sensation (0.68 m/s), and that the conduction velocity of cold Sensation (7.74–8.01 m/s) was considerably faster. Thus, we conclude that paradoxical Heat Sensation in healthy subjects is conducted peripherally via slow unmyelinated C fibres and not via the faster Aδ fibres. Consequently, we propose that paradoxical Heat Sensation is encoded via the Heat sensing pathway, in accordance with the labelled-line code theory. The mechanisms proposed suggest a malfunctioning cold-sensing pathway disinhibiting the Heat-sensing pathway, at peripheral, central or both levels, thus facilitating a paradoxical Heat Sensation.
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Paradoxical Heat Sensation in uremic polyneuropathy.
Muscle & nerve, 1995Co-Authors: Gil Yosipovitch, David Yarnitsky, Victor Mermelstein, Elliot Sprecher, Jonathan Reiss, Clara Witenberg, Jeshayachu A. Hemli, Geoffrey BonerAbstract:Sensory aspects of uremic neuropathy were studied in 36 patients using clinical assessment and quantitative sensory tests (QST). The outstanding abnormality in sensory quality was perception of Heat in response to low temperature stimuli. This paradoxical Heat Sensation was found in the foot in 42% (15) of patients, far beyond the normal prevalence of 10%. Paradoxical Sensation was positively related to cold hypoesthesia (P = 0.0004) suggesting disinhibition as a possible mechanism. Paradoxical Heat Sensation also positively related to creatinine level (P = 0.0012). Pruritus was present in 20 patients (56%), intensity not related to any biochemical or clinical parameter. Signs of sensory polyneuropathy (PNP), based on at least two abnormal parameters in the clinical assessment or QST, were found in 39% of patients (14), of whom 11 had paradoxical Heat Sensation. Thus, in 4 patients (11%), this sensory aberration preceded other signs for PNP. Paradoxical Heat Sensation seems to be a common and often early expression of the sensory neuropathy in uremia. © 1995 John Wiley & Sons, Inc.
Earl Carstens - One of the best experts on this subject based on the ideXlab platform.
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eugenol and carvacrol induce temporally desensitizing patterns of oral irritation and enhance innocuous warmth and noxious Heat Sensation on the tongue
Pain, 2013Co-Authors: Amanda H. Klein, Mirela Iodi Carstens, Earl CarstensAbstract:Eugenol and carvacrol, from the spices clove and oregano, respectively, are agonists of TRPV3, which is implicated in transduction of warmth and possibly Heat pain. We investigated the temporal dynamics of lingual irritation elicited by these agents, and their effects on innocuous warmth and Heat pain, using a half-tongue method in human subjects. The irritant Sensation elicited by both eugenol and carvacrol decreased across repeated applications at a 1-minute interstimulus interval (self-desensitization) which persisted for at least 10 minutes. Both agents also cross-desensitized capsaicin-evoked irritation. Eugenol and carvacrol significantly increased the magnitude of perceived innocuous warmth (44 °C) for >10 minutes, and briefly (<5 minutes) enhanced Heat pain elicited by a 49 °C stimulus. Similar albeit weaker effects were observed when thermal stimuli were applied after the tongue had been desensitized by repeated application of eugenol or carvacrol, indicating that the effect is not due solely to summation of chemoirritant and thermal Sensations. Neither chemical affected Sensations of innocuous cool or cold pain. A separate group of subjects was asked to subdivide eugenol and carvacrol irritancy into subqualities, the most frequently reported being numbing and warmth, with brief burning, stinging/pricking, and tingle, confirming an earlier study. Eugenol, but not carvacrol, reduced detection of low-threshold mechanical stimuli. Eugenol and carvacrol enhancement of innocuous warmth may involve sensitization of thermal gating of TRPV3 expressed in peripheral warm fibers. The brief Heat hyperalgesia following eugenol may involve a TRPV3-mediated enhancement of thermal gating of TRPV1 expressed in lingual polymodal nociceptors.
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Eugenol and carvacrol induce temporally desensitizing patterns of oral irritation and enhance innocuous warmth and noxious Heat Sensation on the tongue
Pain, 2013Co-Authors: Amanda H. Klein, Mirela Iodi Carstens, Earl CarstensAbstract:Eugenol and carvacrol, from the spices clove and oregano, respectively, are agonists of TRPV3, which is implicated in transduction of warmth and possibly Heat pain. We investigated the temporal dynamics of lingual irritation elicited by these agents, and their effects on innocuous warmth and Heat pain, using a half-tongue method in human subjects. The irritant Sensation elicited by both eugenol and carvacrol decreased across repeated applications at a 1-minute interstimulus interval (self-desensitization) which persisted for at least 10 minutes. Both agents also cross-desensitized capsaicin-evoked irritation. Eugenol and carvacrol significantly increased the magnitude of perceived innocuous warmth (44 °C) for >10 minutes, and briefly (
Jinsil Seong - One of the best experts on this subject based on the ideXlab platform.
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Neonatal capsaicin treatment in rats affects TRPV1-related noxious Heat Sensation and circadian body temperature rhythm.
Journal of the neurological sciences, 2014Co-Authors: Keun-yeong Jeong, Jinsil SeongAbstract:The transient receptor potential vanilloid 1 (TRPV1) is a cation channel that serves as a polymodal detector of noxious stimuli such as capsaicin. Therefore, capsaicin treatment has been used to investigate the physiological function of TRPV1. Here, we report physiological changes induced by treating neonatal rats with capsaicin. Capsaicin (50mg/kg) (cap-treated) or vehicle (vehicle-treated) was systemically administered to newborn SD rat pups within 48 h after birth. TRPV1 expression, intake volume of capsaicin water, and noxious Heat Sensation were measured 6 weeks after capsaicin treatment. Circadian body temperature and locomotion were recorded by biotelemetry. Expression of Per1, Per2, Bmal1 and Hsf1 (clock genes) was also investigated. Neonatal capsaicin treatment not only decreased TRPV1 expression but also induced desensitization to noxious Heat stimuli. Circadian body temperature of cap-treated rats increased significantly compared with that of vehicle-treated rats. Additionally, the amplitude of the circadian body temperature was reversed in cap-treated rats. Expression of the hypothalamic Hsf1 and liver Per2 clock genes followed a similar trend. Therefore, we suggest that these findings will be useful in studying various physiological mechanisms related to TRPV1.
Thomas Voets - One of the best experts on this subject based on the ideXlab platform.
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volatile anaesthetics inhibit the thermosensitive nociceptor ion channel transient receptor potential melastatin 3 trpm3
Biochemical Pharmacology, 2020Co-Authors: Balazs Kelemen, Erika Lisztes, Anita Vladar, Martin Hanyicska, Janos Almassy, Attila Olah, Attila Gabor Szollősi, Zsofia Penzes, Janos Posta, Thomas VoetsAbstract:Abstract Background Volatile anaesthetics (VAs) are the most widely used compounds to induce reversible loss of consciousness and maintain general anaesthesia during surgical interventions. Although the mechanism of their action is not yet fully understood, it is generally believed, that VAs depress central nervous system functions mainly through modulation of ion channels in the neuronal membrane, including 2-pore-domain K+ channels, GABA and NMDA receptors. Recent research also reported their action on nociceptive and thermosensitive TRP channels expressed in the peripheral nervous system, including TRPV1, TRPA1, and TRPM8. Here, we investigated the effect of VAs on TRPM3, a less characterized member of the thermosensitive TRP channels playing a central role in noxious Heat Sensation. Methods We investigated the effect of VAs on the activity of recombinant and native TRPM3, by monitoring changes in the intracellular Ca2+ concentration and measuring TRPM3-mediated transmembrane currents. Results All the investigated VAs (chloroform, halothane, isoflurane, sevoflurane) inhibited both the agonist-induced (pregnenolone sulfate, CIM0216) and Heat-activated Ca2+ signals and transmembrane currents in a concentration dependent way in HEK293T cells overexpressing recombinant TRPM3. Among the tested VAs, halothane was the most potent blocker (IC50 = 0.52 ± 0.05 mM). We also investigated the effect of VAs on native TRPM3 channels expressed in sensory neurons of the dorsal root ganglia. While VAs activated certain sensory neurons independently of TRPM3, they strongly and reversibly inhibited the agonist-induced TRPM3 activity. Conclusions These data provide a better insight into the molecular mechanism beyond the analgesic effect of VAs and propose novel strategies to attenuate TRPM3 dependent nociception.
Ezra Susser - One of the best experts on this subject based on the ideXlab platform.
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Paradoxical Heat Sensation in healthy subjects: peripherally conducted by A delta or C fibres?
Brain : a journal of neurology, 1999Co-Authors: Ezra Susser, David YarnitskyAbstract:Paradoxical Heat Sensation upon cooling of the skin has been reported in central as well as in peripheral neurological conditions. In our study, we examined this phenomenon in 35 naive healthy test subjects, of whom 23 experienced paradoxical Heat Sensation under test conditions. We measured the peripheral conduction velocities of cold Sensation, warm Sensation and of paradoxical Heat Sensation by using a quantitative sensory testing model of indirect peripheral conduction velocity measurement. This was based on comparison of measurements at a proximal and a distal site using two measurement methods, one inclusive and the other exclusive of reaction time. We found that the conduction velocity of paradoxical Heat Sensation (0.70 m/s) was similar to that of warm Sensation (0.68 m/s), and that the conduction velocity of cold Sensation (7.74-8.01 m/s) was considerably faster. Thus, we conclude that paradoxical Heat Sensation in healthy subjects is conducted peripherally via slow unmyelinated C fibres and not via the faster A delta fibres. Consequently, we propose that paradoxical Heat Sensation is encoded via the Heat sensing pathway, in accordance with the labelled-line code theory. The mechanisms proposed suggest a malfunctioning cold-sensing pathway disinhibiting the Heat-sensing pathway, at peripheral, central or both levels, thus facilitating a paradoxical Heat Sensation.
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Paradoxical Heat Sensation in healthy subjects: peripherally conducted by Aδ or C fibres?
Brain, 1999Co-Authors: Ezra Susser, David YarnitskyAbstract:Paradoxical Heat Sensation upon cooling of the skin has been reported in central as well as in peripheral neurological conditions. In our study, we examined this phenomenon in 35 naive healthy test subjects, of whom 23 experienced paradoxical Heat Sensation under test conditions. We measured the peripheral conduction velocities of cold Sensation, warm Sensation and of paradoxical Heat Sensation by using a quantitative sensory testing model of indirect peripheral conduction velocity measurement. This was based on comparison of measurements at a proximal and a distal site using two measurement methods, one inclusive and the other exclusive of reaction time. We found that the conduction velocity of paradoxical Heat Sensation (0.70 m/s) was similar to that of warm Sensation (0.68 m/s), and that the conduction velocity of cold Sensation (7.74–8.01 m/s) was considerably faster. Thus, we conclude that paradoxical Heat Sensation in healthy subjects is conducted peripherally via slow unmyelinated C fibres and not via the faster Aδ fibres. Consequently, we propose that paradoxical Heat Sensation is encoded via the Heat sensing pathway, in accordance with the labelled-line code theory. The mechanisms proposed suggest a malfunctioning cold-sensing pathway disinhibiting the Heat-sensing pathway, at peripheral, central or both levels, thus facilitating a paradoxical Heat Sensation.