The Experts below are selected from a list of 1179 Experts worldwide ranked by ideXlab platform
Ivan Garza - One of the best experts on this subject based on the ideXlab platform.
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the Trigeminal trophic syndrome an unusual cause of face pain dysaesthesias anaesthesia and skin soft tissue lesions
Cephalalgia, 2008Co-Authors: Ivan GarzaAbstract:The Trigeminal trophic syndrome is an unusual consequence of Trigeminal Nerve Injury that results in facial anaesthesia, dysaesthesia and skin ulceration. Limited knowledge is available. The aim of...
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the Trigeminal trophic syndrome an unusual cause of face pain dysaesthesias anaesthesia and skin soft tissue lesions
Cephalalgia, 2008Co-Authors: Ivan GarzaAbstract:The Trigeminal trophic syndrome is an unusual consequence of Trigeminal Nerve Injury that results in facial anaesthesia, dysaesthesia and skin ulceration. Limited knowledge is available. The aim of this study was to increase the knowledge of this syndrome by performing a retrospective medical record review and case series report. Fourteen cases were identified. The female:male ratio was 6:1. Mean age of onset was 45 years (range 6-82). The cause was iatrogenic in most. Latent period to onset ranged from days to almost one decade. The majority (n = 12) had bothersome dysaesthesias. Most (n = 9) self-manipulated the face; a third (n = 5) did not. Most ulcers affected the second Trigeminal division, mainly in the infraorbital Nerve distribution. Neuropathic and/or neuralgic facial pain occurred in 50% (n = 7). Pain intensity was severe in most (n = 6). Gabapentin gave relief in two. To conclude, Trigeminal trophic syndrome follows Injury to the Trigeminal Nerve or its nuclei. For unclear reasons, most ulcerations follow infraorbital Nerve distribution. Self-manipulation may contribute to ulcer development rather than being required. Gabapentin may help pain.
Barry J Sessle - One of the best experts on this subject based on the ideXlab platform.
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face sensorimotor cortex undergoes neuroplastic changes in a rat model of Trigeminal neuropathic pain
Experimental Brain Research, 2018Co-Authors: Dongyuan Yao, Barry J SessleAbstract:Trigeminal Nerve Injury can result in neuropathic pain behavior and alterations in motor function, but it is unclear if such Injury produces neuroplastic alterations in face sensorimotor cortex that could contribute to the alterations in motor function. Therefore, this study aimed to determine if Trigeminal Nerve Injury in a rat neuropathic pain model induces neuroplastic changes in jaw and tongue motor representations in face sensorimotor cortex in association with facial nociceptive behavior. Right infraorbital Nerve transection was performed in adult male Sprague-Dawley rats; sham-operated rats served as controls. Nociceptive behavior was assessed by testing facial mechanical sensitivity pre-operatively and post-operatively (1-28 days). Intracortical microstimulation was also applied post-operatively in a series of microelectrode penetrations to map jaw and tongue motor representations in the face sensorimotor cortex by analyzing anterior digastric and genioglossus electromyographic activities evoked by microstimulation at histologically verified sites in face primary somatosensory cortex (face-SI) as well as face primary motor cortex (face-MI). Compared to sham, infraorbital Nerve Injury induced a significant (2-way repeated-measures analysis of variance, P < 0.001) bilateral decrease in facial mechanical threshold that lasted up to 28 days post-operatively. Nerve Injury also induced a significant bilateral decrease compared to sham (P < 0.05) in the number of anterior digastric and/or genioglossus sites in face-MI and in face-SI. These findings indicate that Trigeminal Nerve Injury induces neuroplastic alterations in jaw and tongue motor representations in face sensorimotor cortex that are associated with facial nociceptive behavior and that may contribute to sensorimotor changes following Trigeminal Nerve Injury.
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involvement of medullary gabaergic system in extraterritorial neuropathic pain mechanisms associated with inferior alveolar Nerve transection
Experimental Neurology, 2015Co-Authors: Akiko Okadaogawa, Kozue Kita, Masamichi Shinoda, Yoshiki Imamura, Barry J Sessle, Yuka Nakaya, Masayuki Kobayashi, Koichi IwataAbstract:In order to determine if the functional changes in the GABAergic system in the Trigeminal spinal subnucleus caudalis (Vc) are involved in the mechanisms underlying extraterritorial neuropathic pain in the orofacial region following inferior alveolar Nerve transection (IANX), mechanical noxious behavior, phosphorylated extracellular signal-regulated kinase (pERK) immunohistochemistry and single neuronal activity were analyzed in vesicular GABA transporter (VGAT)-VenusA rats expressing fluorescent protein and the VGAT in Vc neurons. The number of VGAT-VenusA positive neurons was significantly reduced in IANX rats than naive and sham rats at 7days after Nerve transection. The number of VGAT-VenusA positive pERK-immunoreactive (IR) cells was significantly increased in IANX rats at 21days after IAN transection compared with naive and sham rats. The background activity and mechanical-evoked responses of Vc nociceptive neurons were significantly depressed after intrathecal application of the GABA receptor agonist muscimol in sham rats but not in IANX rats. Furthermore, the expression of potassium-chloride co-transporter 2 (KCC2) in the Vc was significantly reduced in IANX rats compared with sham rats. The head-withdrawal threshold (HWT) to mechanical stimulation of the whisker pad skin was significantly decreased in IANX rats compared with sham rats on days 7 and 21 after IANX. The significant reduction of the HWT and significant increase in the number of VGAT-VenusA negative pERK-IR cells were observed in KCC2 blocker R-DIOA-injected rats compared with vehicle-injected rats on day 21 after sham treatment. These findings revealed that GABAergic Vc neurons might be reduced in their number at the early period after IANX and the functional changes might occur in GABAergic neurons from inhibitory to excitatory at the late period after IANX, suggesting that the neuroplastic changes occur in the GABAergic neuronal network in the Vc due to morphological and functional changes at different time periods following IANX and resulting in the extraterritorial neuropathic pain in the orofacial region following Trigeminal Nerve Injury.
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involvement of erk phosphorylation of Trigeminal spinal subnucleus caudalis neurons in thermal hypersensitivity in rats with infraorbital Nerve Injury
PLOS ONE, 2013Co-Authors: Ikuko Suzuki, Kuniya Honda, Masamichi Shinoda, Yoshiyuki Tsuboi, Kazuo Shibuta, Ayano Katagiri, Masaaki Kiyomoto, Barry J Sessle, Shingo Matsuura, Kinuyo OharaAbstract:To evaluate the involvement of the mitogen-activated protein kinase (MAPK) cascade in orofacial neuropathic pain mechanisms, this study assessed nocifensive behavior evoked by mechanical or thermal stimulation of the whisker pad skin, phosphorylation of extracellular signal-regulated kinase (ERK) in Trigeminal spinal subnucleus caudalis (Vc) neurons, and Vc neuronal responses to mechanical or thermal stimulation of the whisker pad skin in rats with the chronic constriction Nerve Injury of the infraorbital Nerve (ION-CCI). The mechanical and thermal nocifensive behavior was significantly enhanced on the side ipsilateral to the ION-CCI compared to the contralateral whisker pad or sham rats. ION-CCI rats had an increased number of phosphorylated ERK immunoreactive (pERK-IR) cells which also manifested NeuN-IR but not GFAP-IR and Iba1-IR, and were significantly more in ION-CCI rats compared with sham rats following noxious but not non-noxious mechanical stimulation. After intrathecal administration of the MEK1 inhibitor PD98059 in ION-CCI rats, the number of pERK-IR cells after noxious stimulation and the enhanced thermal nocifensive behavior but not the mechanical nocifensive behavior were significantly reduced in ION-CCI rats. The enhanced background activities, afterdischarges and responses of wide dynamic range neurons to noxious mechanical and thermal stimulation in ION-CCI rats were significantly depressed following i.t. administration of PD98059, whereas responses to non-noxious mechanical and thermal stimulation were not altered. The present findings suggest that pERK-IR neurons in the Vc play a pivotal role in the development of thermal hypersensitivity in the face following Trigeminal Nerve Injury.
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pregabalin suppresses nociceptive behavior and central sensitization in a rat Trigeminal neuropathic pain model
The Journal of Pain, 2013Co-Authors: Hua Wang, Ye Cao, Chen Yu Chiang, Jonathan O Dostrovsky, Barry J SessleAbstract:Abstract The aim of this study was to determine whether pregabalin affects nociceptive behavior and central sensitization in a Trigeminal neuropathic pain model. A partial infraorbital Nerve transection (p-IONX) or sham operation was performed in adult male rats. Nociceptive withdrawal thresholds were tested with von Frey filaments applied to the bilateral vibrissal pads pre- and postoperatively. On postoperative day 7, the behavioral assessment was conducted before and at 30, 60, 120, and 180 minutes after and 24 hours after pregabalin (.1, 1, 10, 100 mg/kg intraperitoneally) or saline injection. The effects of pregabalin or saline were also examined on the mechanoreceptive field and response properties of nociceptive neurons recorded in the medullary dorsal horn at postoperative days 7 to 10. Reduced withdrawal thresholds reflecting bilateral mechanical allodynia were observed in p-IONX rats until postoperative day 28, but not in sham-operated rats. At postoperative day 7, pregabalin significantly and dose-dependently reversed the reduced mechanical withdrawal thresholds in p-IONX rats. Pregabalin also attenuated central sensitization of the neurons, as reflected in reversal of their reduced activation threshold, increased responses to pinch/pressure, and enhanced stimulus-response function. This study provides the first documentation that pregabalin attenuates the mechanical allodynia and central sensitization that characterize this Trigeminal neuropathic pain model, and supports its clinical use for treating craniofacial neuropathic pain. Perspective Trigeminal Nerve Injury in rats produced facial mechanical hypersensitivity and Trigeminal central sensitization of medullary dorsal horn neurons that were markedly attenuated by systemically administered pregabalin, suggesting its potential clinical utility for orofacial neuropathic pain.
Koichi Iwata - One of the best experts on this subject based on the ideXlab platform.
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Orofacial Neuropathic Pain-Basic Research and Their Clinical Relevancies
'Frontiers Media SA', 2021Co-Authors: Masamichi Shinoda, Noboru Noma, Yoshiki Imamura, Yoshinori Hayashi, Akiko Okada-ogawa, Suzuro Hitomi, Koichi IwataAbstract:Trigeminal Nerve Injury is known to cause severe persistent pain in the orofacial region. This pain is difficult to diagnose and treat. Recently, many animal studies have reported that rewiring of the peripheral and central nervous systems, non-neuronal cell activation, and up- and down-regulation of various molecules in non-neuronal cells are involved in the development of this pain following Trigeminal Nerve Injury. However, there are many unknown mechanisms underlying the persistent orofacial pain associated with Trigeminal Nerve Injury. In this review, we address recent animal data regarding the involvement of various molecules in the communication of neuronal and non-neuronal cells and examine the possible involvement of ascending pathways in processing pathological orofacial pain. We also address the clinical observations of persistent orofacial pain associated with Trigeminal Nerve Injury and clinical approaches to their diagnosis and treatment
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functional involvement of nucleus tractus solitarii neurons projecting to the parabrachial nucleus in Trigeminal neuropathic pain
Journal of Oral Science, 2019Co-Authors: Shinji Okada, Ayano Katagiri, Kinuyo Ohara, Hiroto Saito, Jun Lee, Toshimitsu Iinuma, Koichi IwataAbstract:Peripheral Nerve Injury can induce neuroplastic changes in the central nervous system and result in neuropathic pain. This study investigated functional involvement in dorsal paraTrigeminal nucleus (dPa5) and nucleus tractus solitarii (NTS) neurons projecting to the parabrachial nucleus (PBN) after Trigeminal Nerve Injury. Anatomical quantification was performed based on phosphorylated extracellular signal-regulated kinase (pERK) expression underlying orofacial neuropathic pain associated with infraorbital Nerve chronic constriction Injury (ION-CCI) in rats. ION-CCI rats exhibited heat and mechanical hypersensitivity in the ipsilateral upper lip. After injection of retrograde tracer fluorogold (FG) into the contralateral PBN, ION-CCI rats received capsaicin or noxious mechanical stimulation to the upper lip. The total number of FG-labeled neurons in dPa5 and NTS did not change after ION-CCI, and pERK expression in dPa5 did not differ between sham and ION-CCI rats. In the NTS contralateral to ION-CCI, the number of pERK-immunoreactive neurons and percentage of pERK-immunoreactive FG-labeled PBN projection neurons were increased after capsaicin stimulation in ION-CCI rats. The present findings suggest that enhanced noxious inputs from the NTS to the PBN after Trigeminal Nerve Injury modulates PBN neuron activity, which accompanies the affective components of orofacial neuropathic pain.
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involvement of medullary gabaergic system in extraterritorial neuropathic pain mechanisms associated with inferior alveolar Nerve transection
Experimental Neurology, 2015Co-Authors: Akiko Okadaogawa, Kozue Kita, Masamichi Shinoda, Yoshiki Imamura, Barry J Sessle, Yuka Nakaya, Masayuki Kobayashi, Koichi IwataAbstract:In order to determine if the functional changes in the GABAergic system in the Trigeminal spinal subnucleus caudalis (Vc) are involved in the mechanisms underlying extraterritorial neuropathic pain in the orofacial region following inferior alveolar Nerve transection (IANX), mechanical noxious behavior, phosphorylated extracellular signal-regulated kinase (pERK) immunohistochemistry and single neuronal activity were analyzed in vesicular GABA transporter (VGAT)-VenusA rats expressing fluorescent protein and the VGAT in Vc neurons. The number of VGAT-VenusA positive neurons was significantly reduced in IANX rats than naive and sham rats at 7days after Nerve transection. The number of VGAT-VenusA positive pERK-immunoreactive (IR) cells was significantly increased in IANX rats at 21days after IAN transection compared with naive and sham rats. The background activity and mechanical-evoked responses of Vc nociceptive neurons were significantly depressed after intrathecal application of the GABA receptor agonist muscimol in sham rats but not in IANX rats. Furthermore, the expression of potassium-chloride co-transporter 2 (KCC2) in the Vc was significantly reduced in IANX rats compared with sham rats. The head-withdrawal threshold (HWT) to mechanical stimulation of the whisker pad skin was significantly decreased in IANX rats compared with sham rats on days 7 and 21 after IANX. The significant reduction of the HWT and significant increase in the number of VGAT-VenusA negative pERK-IR cells were observed in KCC2 blocker R-DIOA-injected rats compared with vehicle-injected rats on day 21 after sham treatment. These findings revealed that GABAergic Vc neurons might be reduced in their number at the early period after IANX and the functional changes might occur in GABAergic neurons from inhibitory to excitatory at the late period after IANX, suggesting that the neuroplastic changes occur in the GABAergic neuronal network in the Vc due to morphological and functional changes at different time periods following IANX and resulting in the extraterritorial neuropathic pain in the orofacial region following Trigeminal Nerve Injury.
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trpa1 contributes to capsaicin induced facial cold hyperalgesia in rats
European Journal of Oral Sciences, 2014Co-Authors: Kuniya Honda, Akihiko Furukawa, Kozue Kita, Masamichi Shinoda, Noboru Noma, Koichi IwataAbstract:Honda K, Shinoda M, Furukawa A, Kita K, Noma N, Iwata K. TRPA1 contributesto capsaicin-induced facial cold hyperalgesia in rats.Eur J Oral Sci 2014; 122: 391–396. © 2014 Eur J Oral SciOrofacial cold hyperalgesia is known to cause severe persistent pain in the face fol-lowing Trigeminal Nerve Injury or inflammation, and transient receptor potential(TRP) vanilloid 1 (TRPV1) and TRP ankylin 1 (TRPA1) are thought to beinvolved in cold hyperalgesia. However, how these two receptors are involved incold hyperalgesia is not fully understood. To clarify the mechanisms underlyingfacial cold hyperalgesia, nocifensive behaviors to cold stimulation, the expression ofTRPV1 and TRPA1 in Trigeminal ganglion (TG) neurons, and TG neuronal excit-ability to cold stimulation following facial capsaicin injection were examined in rats.The head-withdrawal reflex threshold (HWRT) to cold stimulation of the lateralfacial skin was significantly decreased following facial capsaicin injection. Thisreduction of HWRT was significantly recovered following local injection of TRPV1antagonist as well as TRPA1 antagonist. Approximately 30% of TG neurons inner-vating the lateral facial skin expressed both TRPV1 and TRPA1, and about 64%of TRPA1-positive neurons also expressed TRPV1. The TG neuronal excitability tonoxious cold stimulation was significantly increased following facial capsaicin injec-tion and this increase was recovered by pretreatment with TRPA1 antagonist.These findings suggest that TRPA1 sensitization via TRPV1 signaling in TG neu-rons is involved in cold hyperalgesia following facial skin capsaicin injection.
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involvement of astroglial glutamate glutamine shuttle in modulation of the jaw opening reflex following infraorbital Nerve Injury
European Journal of Neuroscience, 2014Co-Authors: Rahman Md Mostafeezur, Masamichi Shinoda, Koichi Iwata, Syunpei Unno, Hossain Md Zakir, Hanako Takatsuji, Kojiro Takahashi, Yoshiaki Yamada, Kensuke Yamamura, Junichi KitagawaAbstract:To evaluate the mechanisms underlying orofacial motor dysfunction associated with Trigeminal Nerve Injury, we studied the astroglial cell activation following chronic constriction Injury (CCI) of the infraorbital Nerve (ION) immunohistochemically, nocifensive behavior in ION-CCI rats, and the effect of the glutamine synthase (GS) blocker methionine sulfoximine (MSO) on the jaw-opening reflex (JOR), and also studied whether glutamate-glutamine shuttle mechanism is involved in orofacial motor dysfunction. GFAP-immunoreactive (IR) cells were observed in the Trigeminal motor nucleus (motV) 3 and 14 days after ION-CCI, and the nocifensive behavior and JOR amplitude were also strongly enhanced at these times. The number of GS- and GFAP-IR cells was also significantly higher in ION-CCI rats on day 7. The amplitude and duration of the JOR were strongly suppressed after MSO microinjection (m.i.) into the motV compared with that before MSO administration in ION-CCI rats. After MSO administration, the JOR amplitude was strongly suppressed, and the duration of the JOR was shortened. Forty minutes after m.i. of glutamine, the JOR amplitude was gradually returned to the control level and the strongest attenuation of the suppressive effect of MSO was observed at 180 min after glutamine m.i. In addition, glutamine also attenuated the MSO effect on the JOR duration, and the JOR duration was extended and returned to the control level thereafter. The present findings suggest that astroglial glutamate-glutamine shuttle in the motV is involved in the modulation of excitability of the Trigeminal motoneurons affecting the enhancement of various jaw reflexes associated with Trigeminal Nerve Injury.
Masamichi Shinoda - One of the best experts on this subject based on the ideXlab platform.
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Orofacial Neuropathic Pain-Basic Research and Their Clinical Relevancies
'Frontiers Media SA', 2021Co-Authors: Masamichi Shinoda, Noboru Noma, Yoshiki Imamura, Yoshinori Hayashi, Akiko Okada-ogawa, Suzuro Hitomi, Koichi IwataAbstract:Trigeminal Nerve Injury is known to cause severe persistent pain in the orofacial region. This pain is difficult to diagnose and treat. Recently, many animal studies have reported that rewiring of the peripheral and central nervous systems, non-neuronal cell activation, and up- and down-regulation of various molecules in non-neuronal cells are involved in the development of this pain following Trigeminal Nerve Injury. However, there are many unknown mechanisms underlying the persistent orofacial pain associated with Trigeminal Nerve Injury. In this review, we address recent animal data regarding the involvement of various molecules in the communication of neuronal and non-neuronal cells and examine the possible involvement of ascending pathways in processing pathological orofacial pain. We also address the clinical observations of persistent orofacial pain associated with Trigeminal Nerve Injury and clinical approaches to their diagnosis and treatment
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involvement of medullary gabaergic system in extraterritorial neuropathic pain mechanisms associated with inferior alveolar Nerve transection
Experimental Neurology, 2015Co-Authors: Akiko Okadaogawa, Kozue Kita, Masamichi Shinoda, Yoshiki Imamura, Barry J Sessle, Yuka Nakaya, Masayuki Kobayashi, Koichi IwataAbstract:In order to determine if the functional changes in the GABAergic system in the Trigeminal spinal subnucleus caudalis (Vc) are involved in the mechanisms underlying extraterritorial neuropathic pain in the orofacial region following inferior alveolar Nerve transection (IANX), mechanical noxious behavior, phosphorylated extracellular signal-regulated kinase (pERK) immunohistochemistry and single neuronal activity were analyzed in vesicular GABA transporter (VGAT)-VenusA rats expressing fluorescent protein and the VGAT in Vc neurons. The number of VGAT-VenusA positive neurons was significantly reduced in IANX rats than naive and sham rats at 7days after Nerve transection. The number of VGAT-VenusA positive pERK-immunoreactive (IR) cells was significantly increased in IANX rats at 21days after IAN transection compared with naive and sham rats. The background activity and mechanical-evoked responses of Vc nociceptive neurons were significantly depressed after intrathecal application of the GABA receptor agonist muscimol in sham rats but not in IANX rats. Furthermore, the expression of potassium-chloride co-transporter 2 (KCC2) in the Vc was significantly reduced in IANX rats compared with sham rats. The head-withdrawal threshold (HWT) to mechanical stimulation of the whisker pad skin was significantly decreased in IANX rats compared with sham rats on days 7 and 21 after IANX. The significant reduction of the HWT and significant increase in the number of VGAT-VenusA negative pERK-IR cells were observed in KCC2 blocker R-DIOA-injected rats compared with vehicle-injected rats on day 21 after sham treatment. These findings revealed that GABAergic Vc neurons might be reduced in their number at the early period after IANX and the functional changes might occur in GABAergic neurons from inhibitory to excitatory at the late period after IANX, suggesting that the neuroplastic changes occur in the GABAergic neuronal network in the Vc due to morphological and functional changes at different time periods following IANX and resulting in the extraterritorial neuropathic pain in the orofacial region following Trigeminal Nerve Injury.
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trpa1 contributes to capsaicin induced facial cold hyperalgesia in rats
European Journal of Oral Sciences, 2014Co-Authors: Kuniya Honda, Akihiko Furukawa, Kozue Kita, Masamichi Shinoda, Noboru Noma, Koichi IwataAbstract:Honda K, Shinoda M, Furukawa A, Kita K, Noma N, Iwata K. TRPA1 contributesto capsaicin-induced facial cold hyperalgesia in rats.Eur J Oral Sci 2014; 122: 391–396. © 2014 Eur J Oral SciOrofacial cold hyperalgesia is known to cause severe persistent pain in the face fol-lowing Trigeminal Nerve Injury or inflammation, and transient receptor potential(TRP) vanilloid 1 (TRPV1) and TRP ankylin 1 (TRPA1) are thought to beinvolved in cold hyperalgesia. However, how these two receptors are involved incold hyperalgesia is not fully understood. To clarify the mechanisms underlyingfacial cold hyperalgesia, nocifensive behaviors to cold stimulation, the expression ofTRPV1 and TRPA1 in Trigeminal ganglion (TG) neurons, and TG neuronal excit-ability to cold stimulation following facial capsaicin injection were examined in rats.The head-withdrawal reflex threshold (HWRT) to cold stimulation of the lateralfacial skin was significantly decreased following facial capsaicin injection. Thisreduction of HWRT was significantly recovered following local injection of TRPV1antagonist as well as TRPA1 antagonist. Approximately 30% of TG neurons inner-vating the lateral facial skin expressed both TRPV1 and TRPA1, and about 64%of TRPA1-positive neurons also expressed TRPV1. The TG neuronal excitability tonoxious cold stimulation was significantly increased following facial capsaicin injec-tion and this increase was recovered by pretreatment with TRPA1 antagonist.These findings suggest that TRPA1 sensitization via TRPV1 signaling in TG neu-rons is involved in cold hyperalgesia following facial skin capsaicin injection.
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involvement of astroglial glutamate glutamine shuttle in modulation of the jaw opening reflex following infraorbital Nerve Injury
European Journal of Neuroscience, 2014Co-Authors: Rahman Md Mostafeezur, Masamichi Shinoda, Koichi Iwata, Syunpei Unno, Hossain Md Zakir, Hanako Takatsuji, Kojiro Takahashi, Yoshiaki Yamada, Kensuke Yamamura, Junichi KitagawaAbstract:To evaluate the mechanisms underlying orofacial motor dysfunction associated with Trigeminal Nerve Injury, we studied the astroglial cell activation following chronic constriction Injury (CCI) of the infraorbital Nerve (ION) immunohistochemically, nocifensive behavior in ION-CCI rats, and the effect of the glutamine synthase (GS) blocker methionine sulfoximine (MSO) on the jaw-opening reflex (JOR), and also studied whether glutamate-glutamine shuttle mechanism is involved in orofacial motor dysfunction. GFAP-immunoreactive (IR) cells were observed in the Trigeminal motor nucleus (motV) 3 and 14 days after ION-CCI, and the nocifensive behavior and JOR amplitude were also strongly enhanced at these times. The number of GS- and GFAP-IR cells was also significantly higher in ION-CCI rats on day 7. The amplitude and duration of the JOR were strongly suppressed after MSO microinjection (m.i.) into the motV compared with that before MSO administration in ION-CCI rats. After MSO administration, the JOR amplitude was strongly suppressed, and the duration of the JOR was shortened. Forty minutes after m.i. of glutamine, the JOR amplitude was gradually returned to the control level and the strongest attenuation of the suppressive effect of MSO was observed at 180 min after glutamine m.i. In addition, glutamine also attenuated the MSO effect on the JOR duration, and the JOR duration was extended and returned to the control level thereafter. The present findings suggest that astroglial glutamate-glutamine shuttle in the motV is involved in the modulation of excitability of the Trigeminal motoneurons affecting the enhancement of various jaw reflexes associated with Trigeminal Nerve Injury.
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involvement of erk phosphorylation of Trigeminal spinal subnucleus caudalis neurons in thermal hypersensitivity in rats with infraorbital Nerve Injury
PLOS ONE, 2013Co-Authors: Ikuko Suzuki, Kuniya Honda, Masamichi Shinoda, Yoshiyuki Tsuboi, Kazuo Shibuta, Ayano Katagiri, Masaaki Kiyomoto, Barry J Sessle, Shingo Matsuura, Kinuyo OharaAbstract:To evaluate the involvement of the mitogen-activated protein kinase (MAPK) cascade in orofacial neuropathic pain mechanisms, this study assessed nocifensive behavior evoked by mechanical or thermal stimulation of the whisker pad skin, phosphorylation of extracellular signal-regulated kinase (ERK) in Trigeminal spinal subnucleus caudalis (Vc) neurons, and Vc neuronal responses to mechanical or thermal stimulation of the whisker pad skin in rats with the chronic constriction Nerve Injury of the infraorbital Nerve (ION-CCI). The mechanical and thermal nocifensive behavior was significantly enhanced on the side ipsilateral to the ION-CCI compared to the contralateral whisker pad or sham rats. ION-CCI rats had an increased number of phosphorylated ERK immunoreactive (pERK-IR) cells which also manifested NeuN-IR but not GFAP-IR and Iba1-IR, and were significantly more in ION-CCI rats compared with sham rats following noxious but not non-noxious mechanical stimulation. After intrathecal administration of the MEK1 inhibitor PD98059 in ION-CCI rats, the number of pERK-IR cells after noxious stimulation and the enhanced thermal nocifensive behavior but not the mechanical nocifensive behavior were significantly reduced in ION-CCI rats. The enhanced background activities, afterdischarges and responses of wide dynamic range neurons to noxious mechanical and thermal stimulation in ION-CCI rats were significantly depressed following i.t. administration of PD98059, whereas responses to non-noxious mechanical and thermal stimulation were not altered. The present findings suggest that pERK-IR neurons in the Vc play a pivotal role in the development of thermal hypersensitivity in the face following Trigeminal Nerve Injury.
Kazuo Tanne - One of the best experts on this subject based on the ideXlab platform.
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p2x7 receptor in the Trigeminal sensory nuclear complex contributes to tactile allodynia hyperalgesia following Trigeminal Nerve Injury
European Journal of Pain, 2013Co-Authors: Goshi Ito, Yohei Suekawa, Mineo Watanabe, Koji Takahashi, Toshihiro Inubushi, K. Murasaki, Naoto Hirose, S. Hiyama, Takashi Uchida, Kazuo TanneAbstract:Background The present study directly addresses the roles of the P2X7 receptor (P2X7R), an ionotropic adenosine triphosphate (ATP) receptor, and cytokines in the induction of orofacial pain following chronic constriction Injury (CCI) of the infraorbital Nerve (IoN). Methods Rats were anesthetized, and ligatures of 4-0 chromic gut were tied around the IoN. A438079, a P2X7R antagonist or SB203580, a phosphorylated (p)-p38 mitogen-activated protein kinase (MAPK) inhibitor, was infused intrathecally into CCI-treated rats. In another group of rats, 3′-O-(4-benzoylbenzoyl) adenosine 5′-triphosphate (BzATP), a P2X7R agonist, was infused intrathecally with A438079, SB203580 or etanercept, a tumor necrosis factor (TNF)-α receptor-binding recombinant drug. Results CCI of the IoN induced tactile allodynia/hyperalgesia and up-regulation of P2X7R, membrane-bound TNF-α (mTNF-α) and soluble TNF-α (sTNF-α) in the Trigeminal sensory nuclear complex (TNC). Tactile allodynia/hyperalgesia or up-regulation of mTNF-α and sTNF-α in the TNC following CCI of the IoN was inhibited by A438079. SB203580 also attenuated tactile allodynia/hyperalgesia or up-regulation of mTNF-α, but not the up-regulation of sTNF-α in the TNC. Treatment of rats with BzATP induced tactile allodynia/hyperalgesia and up-regulation of sTNF-α and p-p38 in the TNC. Tactile allodynia/hyperalgesia or up-regulation of sTNF-α following BzATP treatment was inhibited by SB203580 and etanercept. Conclusions Based on these findings, phosphorylation of p38 MAPK via P2X7R may induce tactile allodynia/hyperalgesia, which is most likely mediated by sTNF-α released by microglia.
