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Barry J. Sessle - One of the best experts on this subject based on the ideXlab platform.
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central α adrenoceptors contribute to Mustard Oil induced central sensitization in the rat medullary dorsal horn
Neuroscience, 2013Co-Authors: Hua Wang, Chen Yu Chiang, Yufeng Xie, Jonathan O Dostrovsky, Barry J. SessleAbstract:Our previous studies have demonstrated that application of the inflammatory irritant Mustard Oil (MO) to the tooth pulp produces trigeminal central sensitization that includes increases in mechanoreceptive field size and responses to noxious stimuli and decrease in activation threshold in brainstem nociceptive neurons of trigeminal subnucleus caudalis (the medullary dorsal horn, MDH). The aim of the present study was to test if central noradrenergic processes are involved in the central sensitization of MDH neurons and if α1-adrenoceptors or α2-adrenoceptors or both are involved. In urethane/α-chloralose-anesthetized rats, the activity of extracellularly recorded and functionally identified single nociceptive neurons in the MDH was studied. Continuous intrathecal (i.t.) superfusion of the adrenergic modulator guanethidine and α-adrenoceptor blocker phentolamine or selective α1-adrenoceptor antagonist prazosin over the medulla strongly attenuated all three MO-induced parameters of central sensitization in the MDH nociceptive neurons, compared to phosphate-buffered saline (as vehicle control). In contrast, i.t. superfusion of the selective α2-adrenoceptor antagonist yohimbine had little effect on the mechanoreceptive field expansion and the decreased mechanical activation threshold, and indeed facilitated responses to noxious stimuli of sensitized nociceptive neurons. Superfusion of each of the four chemicals alone did not affect baseline nociceptive neuronal properties. These findings provide the first documentation of the involvement of central noradrenergic processes in MDH in the development of the central sensitization, and that α1- and α2-adrenoceptors may be differentially involved.
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central sensitization in thalamic nociceptive neurons induced by Mustard Oil application to rat molar tooth pulp
Neuroscience, 2006Co-Authors: Sun Zhang, James W. Hu, Chen Yu Chiang, Soo Joung Park, Jonathan O Dostrovsky, Y Lu, Barry J. SessleAbstract:We have recently demonstrated that application of Mustard Oil (MO), a small-fiber excitant and inflammatory irritant, to the rat maxillary molar tooth pulp induces central sensitization that is reflected in changes in spontaneous activity, mechanoreceptive field (RF) size, mechanical activation threshold, and responses to graded mechanical stimuli applied to the neuronal RF in trigeminal brainstem subnucleus caudalis and subnucleus oralis. The aim of this study was to test whether central sensitization can be induced in nociceptive neurons of the posterior thalamus by MO application to the pulp. Single unit neuronal activity was recorded in the ventroposterior medial nucleus (VPM) or posterior nuclear group (PO) of the thalamus in anesthetized rats, and nociceptive neurons were classified as wide dynamic range (WDR) or nociceptive-specific (NS). MO application to the pulp was studied in 47 thalamic nociceptive neurons and found to excite over 50% of the 35 VPM neurons tested and to produce significant long-lasting (over 40 min) increases in spontaneous activity, cutaneous pinch RF size and responses to graded mechanical stimuli, and a decrease in threshold in the 29 NS neurons tested; a smaller but statistically significant increase in mean spontaneous firing rate and decrease in activation threshold occurred following MO in the six WDR neurons tested. Vehicle application to the pulp did not produce any significant changes in six VPM NS neurons tested. MO application to the pulp produced pronounced increases in spontaneous activity, pinch RF size, and responses to mechanical stimuli, and a decrease in threshold in three of the six PO neurons. In conclusion, application of the inflammatory irritant MO to the tooth pulp results in central sensitization of thalamic nociceptive neurons and this neuronal hyperexcitability likely contributes to the behavioral consequences of peripheral inflammation manifesting as pain referral, hyperalgesia and allodynia.
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neuroplasticity induced by tooth pulp stimulation in trigeminal subnucleus oralis involves nmda receptor mechanisms
Journal of Neurophysiology, 2001Co-Authors: Soo Joung Park, James W. Hu, Chen Yu Chiang, Barry J. SessleAbstract:We have recently demonstrated that application of the Mustard Oil (MO), a small-fiber excitant and inflammatory irritant, to the rat maxillary molar tooth pulp induces significant increases in jaw ...
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Administration of opiate antagonist naloxone induces recurrence of increased jaw muscle activities related to inflammatory irritant application to rat temporomandibular joint region
Journal of neurophysiology, 1994Co-Authors: Barry J. Sessle, H. VernonAbstract:1. Our recent studies in rats have demonstrated that the small-fiber excitant and inflammatory irritant Mustard Oil injected into the temporomandibular joint (TMJ) region can evoke a sustained and reversible increase of electromyographic (EMG) activity in jaw muscles and an acute inflammatory response. The aim of the present study was to test if opioid mechanisms are involved in modulating the EMG increase evoked by Mustard Oil. 2. Mustard Oil injected into the rat TMJ region evoked significant increases of jaw muscle EMG activity; the vehicle mineral Oil had no such effect. The increased EMG activity lasted up to 20 min, and by 30 min after the Mustard Oil injection had returned to control (preinjection) levels, at which time administration of the opiate antagonist naloxone (1.3 mg/kg i.v.) induced a significant recurrence of the increase in EMG activity. This "rekindling" of EMG activity appeared at 5 to 10 min after the naloxone administration and lasted for 10 to 20 min. In contrast, naloxone administration in the animals receiving mineral Oil injection into the TMJ region did not "rekindle" the EMG activity, nor did the administration of the peripherally acting opiate antagonist methylnaloxone or the vehicle of naloxone. 3. These findings reveal that the application of the opiate antagonist naloxone produces a recurrence of increased jaw muscle activity reflexively evoked by Mustard Oil injection into the rat TMJ region. They suggest that central opioid depressive mechanisms activated by the Mustard Oil-induced afferent barrage limit the duration of the evoked EMG changes.
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excitatory effects on neck and jaw muscle activity of inflammatory irritant applied to cervical paraspinal tissues
Pain, 1993Co-Authors: H. Vernon, Barry J. SessleAbstract:A study was carried out in 19 anaesthetized rats to determine if the electromyographic (EMG) activity of jaw and neck muscles could be influenced by injection of the inflammatory irritant Mustard Oil into deep paraspinal tissues surrounding the C1-3 vertebrae. The EMG activity was recorded ipsilaterally in the digastric, masseter and trapezius muscles and bilaterally in deep neck muscles (rectus capitis posterior). In comparison with control (vehicle) injections, Mustard Oil (20 microliters, 20%) injected into the deep paraspinal tissues induced significant increases in EMG activity in the neck muscles in all the animals and in the jaw muscles in the majority of the animals; the effects of Mustard Oil were more prominent in the former. The EMG response evoked by Mustard Oil injection was frequently reflected in two phases of enhanced activity. The early phase of the increase in EMG activity was usually initiated immediately following Mustard Oil injection (mean latency: 20.4 +/- 17.7 sec) and lasted 1.6 +/- 1.1 min. The second phase occurred 11.3 +/- 7.6 min later and lasted 11.0 +/- 8.1 min. Evans Blue extravasation was apparent in the deep paraspinal tissues surrounding the C1-3 vertebrae after Mustard Oil injection, and histological examination showed that Mustard Oil injection induced an inflammatory reaction in the rectus capitis posterior muscle. These results document that injection of the inflammatory irritant Mustard Oil into deep paraspinal tissues results in a sustained and reversible activation of both jaw and neck muscles. Such effects may be related to the reported clinical occurrence of increased muscle activity associated with trauma to deep tissues.
David A Bereiter - One of the best experts on this subject based on the ideXlab platform.
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effect of persistent monoarthritis of the temporomandibular joint region on acute Mustard Oil induced excitation of trigeminal subnucleus caudalis neurons in male and female rats
Pain, 2005Co-Authors: Keiichiro Okamoto, David A BereiterAbstract:The effect of persistent inflammation of the temporomandibular (TMJ) region on Fos-like immunoreactivity (Fos-LI) evoked by acute noxious stimulation of the same or opposite TMJ was assessed in male and cycling female rats. Two weeks after inflammation of the TMJ by complete Freund's adjuvant (CFA, 25 microg) the selective small fiber excitant, Mustard Oil (MO, 20%), was injected into the arthritic or opposite TMJ under barbiturate anesthesia. MO stimulation of the arthritic TMJ increased Fos-LI ipsilateral, but not contralateral, to MO compared to naive subjects in superficial laminae at the trigeminal subnucleus caudalis/upper cervical cord (Vc/C2) junction independent of sex hormone status. Unexpectedly, MO stimulation of the opposite TMJ in arthritic rats also produced a greater Fos-LI response ipsilateral to MO than naive animals. Fos-LI produced in the dorsal paratrigeminal region (dPa5) and Vc/C2 junction after MO stimulation of the normal TMJ was significantly greater in proestrous than diestrous females or male monoarthritic rats. In contrast to naive animals, Fos-LI was produced in deep laminae at the Vc/C2 junction ipsilateral to MO in CFA-treated animals independent of the site of prior CFA inflammation or sex hormone status. These results indicated that persistent monoarthritis of the TMJ region enhanced the excitability of trigeminal brainstem neurons to subsequent TMJ injury that occurred bilaterally in multiple regions of the lower trigeminal brainstem complex and depended on sex hormone status.
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excitatory amino release within spinal trigeminal nucleus after Mustard Oil injection into the temporomandibular joint region of the rat
Pain, 1996Co-Authors: David A Bereiter, Albert P BenettiAbstract:Inflammation of the temporomandibular joint (TMJ) region evokes pain and hyperalgesia as well as causing persistent changes in the response properties of central trigeminal neurons. To determine if excitatory amino acids have a role in TMJ-induced responses, extracellular concentrations were measured in microdialysate samples from probes positioned in the spinal trigeminal nucleus (Vsp) near the transition region between subnucleus interpolaris and subnucleus caudalis (Vi/Vc) in chloralose-anesthetized rats. Injection of the selective small fiber excitant, Mustard Oil (20 μl, 20% solution), into the ipsilateral TMJ region caused a transient (by 10 min) increase in glutamate (from 0.48 ± 0.16 to 1.94 ± 0.78 μM, P < 0.005) and aspartate (from 0.29 ± 0.11 to 1.78 ± 0.82 μM, P < 0.025) among sites located at the ventrolateral pole of the Vi/Vc transition region (n = 6). Samples from probes located within the ventral Vsp, but outside this Vi/Vc transition region (n = 9), did not show significant changes in amino acid concentrations. Glutamate and aspartate also increased after Mustard Oil injections into the contralateral TMJ region. Dialysate concentrations of serine and taurine did not change significantly after Mustard Oil injections. Addition of high potassium (150 mM) to the perfusate solution caused increases in glutamate and aspartate regardless of probe location. The transient and selective release of glutamate and aspartate within the Vi/Vc transition after acute irritation of the TMJ region is consistent with a proposed role for excitatory amino acids in mediating noxious sensory input from deep orofacial structures. Together with previous reports of c-fos expression, these results suggest that neurons within the ventrolateral portion of the Vi/Vc transition may serve as a relay site for the integration of sensory or reflex responses to acute inflammation of the TMJ region.
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distribution of fos like immunoreactivity in the caudal brainstem of the rat following noxious chemical stimulation of the temporomandibular joint
The Journal of Comparative Neurology, 1995Co-Authors: Charles B Hathaway, David A BereiterAbstract:Central expression of the protooncogene c-fos was used to examine areas receiving noxious sensory input from the rat temporomandibular joint (TMJ). Fos-like immunoreactivity (Fos-LI) in the caudal brainstem was visualized 2 hours after unilateral injection of the small-fiber-specific excitant /inflammatory irritant Mustard Oil into the TMJ region. Control animals received injection of either Mustard Oil into the subcutaneous fascia overlying the masseter muscle or mineral Oil vehicle into the TMJ region. In all groups, Fos-LI was consistently observed ipsilaterally in the spinal trigeminal nucleus and cervical dorsal horn and, bilaterally, in the nucleus of the solitary tract and. the ventrolateral medulla. The expression of Fos-LI ipsilaterally in the paratrigeminal nucleus was variable. Within the trigeminal sensory complex, Fos-LI was restricted to subnucleus caudalis and the caudal portions of subnucleus interpolaris near the level of the obex. Approximately 12% of Fos-LI cells in subnucleus caudalis and in the cervical dorsal horn were found in laminae III-VI. Compared to TMJ Mustard Oil injection, mineral Oil injection produced less Fos-LI at all rostrocaudal levels, whereas subcutaneous Mustard Oil injection produced less Fos-LI in caudal subnucleus caudalis but similar amounts in the cervical dorsal horn. Neither of these injections yielded significant ipsilateral responses in subnucleus caudalis, indicating that Fos-LI in this region following TMJ Mustard Oil injection could be ascribed solely to small-fiber stimulation in the deep TMJ region. The wide rostrocaudal distribution of Fos-LI within the caudal brainstem reflects the distribution of TMJ-responsive nociceptive neurons that may underlie the spread and referral of pain from the TMJ region. © 1995 Wiley-Liss, Inc.
Walter Vetter - One of the best experts on this subject based on the ideXlab platform.
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Various concentrations of erucic acid in Mustard Oil and Mustard
Food Chemistry, 2014Co-Authors: Christine Wendlinger, Simon Hammann, Walter VetterAbstract:Abstract Erucic acid is a typical constituent of Mustard or rape. Foodstuff with a high content of erucic acid is considered undesirable for human consumption because it has been linked to myocardial lipidosis and heart lesions in laboratory rats. As a result, several countries have restricted its presence in Oils and fats. In this study, the erucic acid content in several Mustard Oils and prepared Mustard samples from Germany and Australia was determined. Seven of nine Mustard Oil samples exceeded the permitted maximum levels established for erucic acid (range: 0.3–50.8%, limit: 5%). The erucic acid content in Mustard samples (n = 15) varied from 14% to 33% in the lipids. Two servings (i.e. 20 g) of the Mustards with the highest erucic acid content already surpassed the tolerable daily intake established by Food Standards Australia New Zealand. However, a careful selection of Mustard cultivars could lower the nutritional intake of erucic acid.
Hae Chul Park - One of the best experts on this subject based on the ideXlab platform.
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FAM19A5l Affects Mustard Oil-Induced Peripheral Nociception in Zebrafish
Molecular Neurobiology, 2021Co-Authors: Inyoung Jeong, Seongsik Yun, Anu Shahapal, Eun Bee Cho, Sun Wook Hwang, Jae Young Seong, Hae Chul ParkAbstract:Family with sequence similarity 19 (chemokine (C–C motif)-like) member A5 (FAM19A5) is a chemokine-like secretory protein recently identified as involved in the regulation of osteoclast formation, post-injury neointima formation, and depression. Although roles for FAM19A5 have been described in nervous system development and psychiatric disorders, its role in the nervous system remains poorly understood. Here, we analyzed the evolutionary history of FAM19A genes in vertebrates and identified FAM19A5l , a paralogous zebrafish gene originating from a common ancestral FAM19A5 gene. Further, zebrafish FAM19A5l is expressed in trigeminal and dorsal root ganglion neurons as well as distinct neuronal subsets of the central nervous system. Interestingly, FAM19A5l ^+ trigeminal neurons are nociceptive neurons that localized with TRPA1b and TRPV1 and respond to Mustard Oil treatment. Behavioral analysis further revealed that the nociceptive response to Mustard Oil decreases in FAM19A5l -knockout zebrafish larvae. In addition, TRPA1b and NGFa mRNA levels are down- and upregulated in FAM19A5l -knockout and -overexpressing transgenic zebrafish, respectively. Together, our data suggest that FAM19A5l plays a role in nociceptive responses to Mustard Oil by regulating TRPA1b and NGFa expression in zebrafish.
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fam19a5l affects Mustard Oil induced peripheral nociception in zebrafish
bioRxiv, 2020Co-Authors: Inyoung Jeong, Seongsik Yun, Anu Shahapal, Eun Bee Cho, Sun Wook Hwang, Jae Young Seong, Hae Chul ParkAbstract:SUMMARY Family with sequence similarity 19 (chemokine (C-C motif)-like), member A5 (FAM19A5) is a chemokine-like secretory protein recently identified to be involved in the regulation of osteoclast formation, post-injury neointima formation, and depression. Here, we identified FAM19A5l, an orthologous zebrafish gene that originated from a common ancestral FAM19A5 gene. FAM19A5l was expressed in trigeminal and dorsal root ganglion neurons as well as distinct neuronal subsets of the central nervous system of zebrafish. Interestingly, FAM19A5l+ trigeminal neurons were nociceptors that co-localized with TRPA1b and TRPV1, and responded to Mustard-Oil treatment. Behavioral analysis revealed that the nociceptive response to Mustard Oil decreased in FAM19A5l-knockout zebrafish larvae. In addition, TRPA1b and NGFa mRNA levels were down- and up-regulated in FAM19A5l-knockout and - overexpressing transgenic zebrafish, respectively. Together, our data suggested that FAM19A5l played a role in nociceptive responses to Mustard Oil by regulating TRPA1b and NGFa expression in zebrafish.
Mary M Heinricher - One of the best experts on this subject based on the ideXlab platform.
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nmda receptor mediated activation of medullary pro nociceptive neurons is required for secondary thermal hyperalgesia
Pain, 2007Co-Authors: Chang Jae Kim, Miranda J Neubert, Mary M HeinricherAbstract:There is now direct evidence that a class of neurons in the rostral ventromedial medulla (RVM) exerts a net facilitatory influence on spinal nociception. The present experiments were designed to test whether activation of these neurons, referred to as “on-cells”, is required as part of a positive feedback loop leading to secondary hyperalgesia in acute inflammation produced by topical application of Mustard Oil. Activity of a characterized RVM neuron and paw withdrawals to heat (plantar surface) were recorded in barbiturate-anesthetized rats. Following three baseline trials, Mustard Oil was applied to the skin above the knee. Cell activity and paw withdrawal latencies were monitored for an additional 45 min. Application of Mustard Oil produced an increase in on-cell discharge that was associated with a substantial decrease in withdrawal latency of the ipsilateral paw. Blocking on-cell activation using local infusion of the NMDA-receptor antagonist AP5 into the RVM prevented hyperalgesia. Secondary thermal hyperalgesia following Mustard Oil was also associated with a significant decrease in the firing of “off-cells”, a cell population thought to exert a net inhibitory influence on nociception. Depression of off-cell firing was unaffected by AP5 microinjection. The firing of “neutral cells”, which have no documented role in nociceptive modulation, was unchanged following Mustard Oil and also unaffected by AP5 infusion in the RVM. Brainstem descending controls are receiving increasing attention in efforts to understand hyperalgesia and persistent pain states. The present experiments demonstrate that a novel, NMDA-mediated activation of on-cells is required for secondary thermal hyperalgesia in acute inflammation.
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role for medullary pain facilitating neurons in secondary thermal hyperalgesia
Journal of Neurophysiology, 2006Co-Authors: Wendy Kincaid, Miranda J Neubert, Chang Jae Kim, Mary M HeinricherAbstract:The rostral ventromedial medulla (RVM) has recently received considerable attention in efforts to understand mechanisms of hyperalgesia and persistent pain states. Three classes of neurons can be identified in the RVM based on responses associated with nocifensive reflexes: on cells, off cells, and neutral cells. There is now direct evidence that on cells exert a net facilitating effect on spinal nociception and that off cells depress nociception. These experiments tested whether the secondary hyperalgesia produced by topical application of Mustard Oil involves an activation of on cells in RVM. Firing of a characterized RVM neuron and the latencies of withdrawal reflexes evoked by noxious heat were recorded in lightly anesthetized rats before and after application of Mustard Oil to the shaved skin of the leg above the knee. Mineral Oil was applied as a control. Mustard Oil produced a significant increase in ongoing and reflex-related discharge of on cells, as well as a decrease in the activity of off cells. neutral cell firing was uniformly unchanged after application of Mustard Oil. The alterations in on and off cell firing were associated with a significant decrease in the latency to withdraw the paw of the treated limb from the heat stimulus, and this hyperalgesia was blocked by microinjection of lidocaine within the RVM. Withdrawals evoked by heating the contralateral hindpaw, forepaw, and tail were unchanged after Mustard Oil application. These experiments support a pronociceptive role for on cells and suggest that these neurons contribute to secondary hyperalgesia in inflammation.
