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Symposia

日本学術振興会先端研究拠点事業共催:痛み研究最前線
JSPS Core-to-Core Program:The front line of pain research

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開催日
2010年09月04日(土)
時 間
08:30 - 11:00
会 場
Room 1
Chairperson(s)
柿木 隆介 / Ryusuke Kakigi (自然科学研究機構 生理学研究所 統合生理研究系 / Department of Integrative Physiology, National Institute for Physiological Sciences)
水村 和枝 / Kazue Mizumura (名古屋大学環境医学研究所 神経系分野II / Dept. Neurosci. II, Res. Inst. Environ. Med., Nagoya Univ., Nagoya 464-8601, Japan)

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ストレスによる痛覚過敏のメカニズム---下行性疼痛調節系の関与
Involvement of descending facilitation in stress-induced hyperalgesia

演題番号 : S3-1-1-1

仙波 恵美子 / Emiko Senba:1 井辺 弘樹 / Hiroki Imbe:2 

1:和歌山県立医科大学医学部 第二解剖学 / Department of Anatomy & Neurobiology, Wakayama Medical University, Faculty of Medicine, Wakayama, Japan 2:和歌山県立医科大学医学部 第一生理学 / Department of Physiology, Wakayama Medical University, Faculty of Medicine, Wakayama, Japan 

 

Repeated exposure to non-noxious situation, such as chronic restraint stress, forced swim stress, cold environment, social defeat etc., can elicit hyperalgesia and allodynia in experimental animals. Clinically, stress markedly exacerbates pain in numerous painful pathologies, such as fibromyalgia, characterized by diffuse muscular pain and/or tenderness, low back pain and temporomandibular disorder. The mechanisms how stress exacerbates pain are still unknown, although supraspinal, spinal (reduced GABA release), and peripheral (sympathoadrenal catecholamine) mechanisms are implicated. We previously reported that chronic restrain stress induced thermal hyperalgesia in rats, in which phosphorylated ERK (p-ERK) and levels of tryptophan hydroxylase, a key enzyme of 5-HT production, were increased in the rostral ventromedial medulla (RVM). 5HT released from the bulbospinal neurons may exert facilitatory effects on spinal nociceptive processing probably through 5HT3 receptors. We also demonstrated that descending facilitation from the RVM is required for the enhancement of formalin-evoked nocifensive behavior following repeated forced swim stress, since the destruction of the RVM with ibotenic acid led to prevent the enhancement of formalin-evoked nocifensive behavior in the forced swim group. Therefore, we speculate that certain brain areas, which are involved in both stress response and central pain circuitry, could be sensitized by chronic stress condition and show exaggerated response to pain stimulation, leading to hyperalgesia via descending facilitation. Stress-induced sensitization based on the morphological changes has been reported in neurons in the anterior cingulate cortex and amygdala, which are implicated in the affective aspects of pain. In order to elucidate supraspinal mechanisms of stress-induced hyperalgesia, we compared formalin-induced c-fos and p-ERK expressions in the brains of chronically stressed and unstressed animals.

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