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Repetitive transcranial magnetic stimulation (rTMS) induced-changes of excitabilities of anterior cingulate cortex in the neuropathic pain model mice
| Content Provider | Semantic Scholar |
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| Author | Yuhi, Tomoaki Fueta, Yukiko Ueno, Susumu Tsuji, Sadatoshi |
| Copyright Year | 2011 |
| Abstract | s / Neuroscience Research 71S (2011) e108–e415 e359 the vomeronasal organ and activate the select vomeronasal neural pathway in sexually-naïve male mice but not in father mice. doi:10.1016/j.neures.2011.07.1572 P4-j18 Repetitive transcranial magnetic stimulation (rTMS) induced-changes of excitabilities of anterior cingulate cortex in the neuropathic pain model mice Tomoaki Yuhi 1 , Yukiko Fueta 2, Susumu Ueno 3, Sadatoshi Tsuji 1 1 Dep. of Neurol., Sch. of Med., Univ. Occupation. Environ. Hlth., Kitakyushu, Japan 2 Dept. of Hlth. Manage., School of Hlth. Sci., Univ. of Occupation. Environ. Hlth 3 Dept. of Environ. Toxiol., Institute of Indust. Ecolog. Sci., Univ. of Occupation. Environ. Hlth. We tried to clarify whether rTMS will change the excitabilities of anterior cingulate cortex in the neuropathic pain model mice. Partial sciatic nerve injury model (Seltzer model) was used as neuropathic pain model. Left side sciatic nerve of 5 weeks old ddY mice (n = 10) were ligated with 9-0 silk suture around approximately 1/3 to 1/2 the diameter. In sham-operated mice (n = 5) the nerve was exposed, but not ligated. From 7 to 10 weeks old, nerve-ligated mice were divided into two groups with or without rTMS. Repetitive TMS(+) group (n = 5) have received rTMS (1 Hz, 120% of motor threshold, 1000 stimuli/day) with a round coil (diameter = 8 cm) using magnetic stimulator (Nihon Koden, Japan) for 5 days/week and rTMS(−) group (n = 5) were exposed the audible artifact of rTMS. At 11 weeks, all mice of each group were decapitated and slices of anterior cingulate cortex were prepared. Stimulus–response curve of field excitatory postsynaptic potentials (fEPSP) and paired-pulse ratio (PPR) of fEPSP were recorded in these slices. Stimulus–response curves of fEPSP in rTMS(−) group (ligated) was significantly shifted to the left, comparing with that in sham-operated group (p < 0.01). This excitatory changes of S–R curves of fEPSP was diminished in rTMS(+) (ligated) group. PPR of fEPSP were no significant difference between rTMS(−) and rTMS(+) group. Our results suggest rTMS decreases the excitabilities of anterior cingulated cortex and suppress the neuropathic pain in mouse neuropathic pain model. Research fund: KAKENHI (20602018). doi:10.1016/j.neures.2011.07.1573 P4-j19 Analysis of sleep disturbance associated with the change in nerve function in the cingulate cortex under neuropathic pain Akira Yamashita 1 , Satoshi Imai 1, Hiroshi Horiuchi 1, Michiko Narita 1, Tsutomu Suzuki 2, Minoru Narita 1 1 Dept. Pharmacol., Sch. Pharm. Pharmaceut. Sci. Hoshi Univ., Tokyo, Japan 2 Dept. Toxicol., Sch. Pharm. Pharmaceut. Sci. Hoshi Univ., Tokyo, Japan Insomnia is a common problem for people with chronic pain. Cortical GABAergic neurons are part of the neurobiological substrate that underlies homeostatic sleep regulation. In the present study, we confirmed that sciatic nerve ligation caused thermal hyperalgesia and tactile allodynia in mice. Mild noxious heat stimuli caused a significant increase in the release of glutamate in the cingulate cortex of nerve-ligated mice compared to that of shamoperated mice. In this experimental model for neuropathic pain, we found an increase in wakefulness and a decrease in non-rapid eye movement (NREM) sleep under a neuropathic pain-like state. The membrane-bound GABA transporters (GATs) on activated glial fibrillary acidic protein (GFAP)-positive astrocytes were significantly increased in the cingulate cortex of mice with sciatic nerve ligation. In an experiment with primary cultured glial cells from the mouse cortex, treatment with glutamate led to the translocation of GATs from intracellular vesicles to the plasma membrane. Furthermore, extracellular GABA levels in the cingulate cortex after depolarization were rapidly decreased by nerve injury. Under this condition, sleep disturbance induced by sciatic nerve ligation was improved by the intra-cingulate cortex injection of a GATs inhibitor. These findings provide novel evidence that sciatic nerve ligation decreases extracellular-released GABA along with an increase in membrane-bound GATs on activated astrocytes in the cingulate cortex of mice. These phenomena may, at least in part, explain the insomnia in patients with neuropathic pain. doi:10.1016/j.neures.2011.07.1574 P4-j20 Differential activation of mitogen-activated protein kinases and glial cells in the trigeminal sensory nuclear complex following lingual nerve injury Ryuji Terayama 1 , Naoko Fujisawa 1,2, Daisuke Yamaguchi 1,4, Shinji Omura 1,4, Hiroyuki Ichikawa 3, Tomosada Sugimoto 1 1 Dept of Oral Function and Anatomy, Grad Sch of Med, Dent and Pharm Sci, Okayama Univ, Okayama, Japan 2 Dept of Orthodontics and Dentofacial Orthopedics, Grad Sch of Med, Dent and Pharm Sci, Okayama Univ, Okayama, Japan 3 Dept of Oral and Craniofacial Anatomy, Tohoku Univ Grad Sch of Dent, Sendai, Japan 4 ASAHI College of Medical Art and Sciences Mitogen-activated protein kinases (MAPKs) play a pivotal role in the mediation of cellular responses to a variety of signaling molecules. The current study demonstrates phosphorylation of extracellular signal-regulated kinase (ERK) and p38 MAPK in each subdivision of the trigeminal sensory nuclear complex (TSNC) following lingual nerve injury. Immunohistochemical labeling for phosphorylated ERK (p-ERK) or phosphorylated p38 (p-p38) MAPK was performed in histological sections of the brainstem. A transient increase in the immunoreactivity for p-ERK was found in each subdivision of the TSNC followed by a prolonged increase in the immunoreactivity for p-p38 MAPK after nerve injury. Double immunofluorescence labeling with cell-specific markers revealed that ERK and p38 MAPK were phosphorylated predominantly by OX-42-positive microglia or GFAP-positive astrocytes. Increased immunofluorescence labeling for OX-42 and GFAP indicated that microglia and astrocytes were activated by nerve injury in the TSNC. Activation of MAPKs and glial cells in the rostral subdivisions of the TSNC was comparable with that in the subnucleus caudalis of the trigeminal spinal tract nucleus (Vc). We conclude that differential activation of MAPKs and glial cells in the rostral subdivisions of the TSNC as well as the Vc may have a substantial role in the pathogenesis of neuropathic pain following trigeminal nerve injury. Research fund: KAKENHI (20592324, 22592035). doi:10.1016/j.neures.2011.07.1575 P4-j21 Contribution of spinal galectin-3 to acute herpetic allodynia in mice Ichiro Takasaki 1 , Atsushi Sasaki 2, Tsugunobu Andoh 2, Yasushi Kuraishi 2 1 Life Sci Res Ctr, Univ. of Toyama 2 Univ. of Toyama, Toyama, Japan To identify endogenous factors involved in herpetic pain, we performed genome-wide microarray analysis of the spinal cord of mice which suffered from herpetic pain induced by inoculation with herpes simplex virus type-1, which revealed marked induction of galectin-3, a -galactosidebinding lectin. Herpes zoster-like skin lesions and pain-related responses to tactile stimuli (allodynia) became apparent on day 5 after inoculation and increased until day 7. Galectin-3 mRNA was slightly induced on day 5 and markedly increased until day 7 in the lumbar dorsal horn on the inoculated side. Galectin-3 was also markedly increased on day 6 in that location. Galectin-3-expressing cells were mainly localized in the superficial dorsal horn, round in shape, and positive for the monocyte/microglia marker Iba-1. In the deep dorsal horn, there were Iba-1-positive cells with ramified and stout processes, which were negative for galectin-3. There were many infiltrated CD3-positive T cell, but the most cells were negative for galectin-3. Galectin-3-expressing cells were negative for the neuronal marker NeuN and the astrocyte marker glial fibrillary acidic protein. Deficiency in galectin-3 markedly reduced herpetic allodynia, without showing an effect on herpes zoster-like skin lesions. C-Fos was induced in the lumbar dorsal horn of mice with herpetic allodynia, which was markedly suppressed by galectin-3 deficiency. Intrathecal injection of galectin-3 produced mechanical allodynia and increased c-Fos expression in the dorsal horn of the spinal cord in naive mice. The present results suggest that galectin-3 in macrophages infiltrating in the spinal dorsal horn contributes to herpetic allodynia. Galectin-3 may be a new therapeutic target for the treatment of acute herpetic pain. Research fund: KAKENHI (17700346) and KAKENHI (19700337). doi:10.1016/j.neures.2011.07.1576 |
| File Format | PDF HTM / HTML |
| DOI | 10.1016/j.neures.2011.07.1573 |
| Volume Number | 71 |
| Alternate Webpage(s) | https://api.elsevier.com/content/article/pii/S0168010211017561 |
| Alternate Webpage(s) | https://www.sciencedirect.com/science/article/pii/S0168010211017561?dgcid=api_sd_search-api-endpoint |
| Alternate Webpage(s) | https://doi.org/10.1016/j.neures.2011.07.1573 |
| Journal | Neuroscience Research |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
