title: Cutaneous magnetic stimulation reduces rat chronic pain via activation of the supra-spinal descending pathway.
abstract: Recent studies have demonstrated that magnetic stimulation (MS) can induce cellular responses such as Ca(2+) influx into the cultured neurons and glia, leading to increased intracellular phosphorylation. We have demonstrated previously that MS reduces rat neuropathic pain associated with the prevention of neuronal degeneration. Thus, we aimed to elucidate the actions of MS in relation to modulation of spinal neuron-glia and the descending inhibitory system in chronic pain. The male SD rats intrathecally implanted with catheters were subjected to sciatic nerve ligation (CCI). MS is a low power apparatus characterized by two different frequencies, 2 KHz and 83 MHz. Rats were given MS to the skin (injured sciatic nerve) for 10 min from the seventh day after CCI. The paw withdrawal latency (PWL) evoked by thermal stimuli was measured for 14 days after CCI. Immunohistochemistry for Iba-1 or GFAP was performed after 4% paraformaldehyde fixation (microscopic analysis). We employed microdialysis for measuring CSF 5-HIAA as a reflection of 5-HT release by MS stimulation. Following CCI, rats showed a decrease in PWL after CCI, and the decrease continued until the 14th day. With MS treatment, the decrease in PWL was reduced during the 10-14 day after CCI. Injection of JNK-1 inhibitors on the 14th day antagonized the analgesic effect of MS. MS also eliminated the CCI-induced decrease in GFAP immunoreactivity. Moreover, MS evoked spinal 5-HT release reflected by increase in spinal 5-HIAA level. Thus, we demonstrate that a novel magnetic stimulator used cutaneously can ameliorate chronic pain by not only preventing abnormal spinal neuron-glia interaction, but also through the activation of the supra-spinal descending inhibitory system.
authors.affiliation: Division of Neurosciences, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan.
authors.forename: Shun-ji
authors.initials: SJ
authors.lastname: Shiiba
authors.forename: Satoru
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Hironori
authors.initials: H
authors.lastname: Sasaki
authors.forename: Mitsuharu
authors.initials: M
authors.lastname: Nishi
authors.forename: Kozo
authors.initials: K
authors.lastname: Ishikawa
authors.forename: Seiko
authors.initials: S
authors.lastname: Yasuda
authors.forename: Nobuko
authors.initials: N
authors.lastname: Tokuda
authors.forename: Osamu
authors.initials: O
authors.lastname: Nakanishi
authors.forename: Toshizo
authors.initials: T
authors.lastname: Ishikawa
mesh_terms: D000698:Analgesia; D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D059350:Chronic Pain / Q000503:physiopathology / Q000628:therapy*; D003251:Constriction, Pathologic; D004525:Efferent Pathways / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006897:Hydroxyindoleacetic Acid / Q000378:metabolism; D007837:Latency Period, Psychological; D055909:Magnetic Field Therapy / Q000379:methods*; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012867:Skin / Q000187:drug effects / Q000503:physiopathology*; D013116:Spinal Cord / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology; D013997:Time Factors
chemical_list: D005904:Glial Fibrillary Acidic Protein; D009270:Naloxone; D006897:Hydroxyindoleacetic Acid