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<p>Methylmercury is a neurotoxic substance that is ubiquitously present in the environment and is known to cause a variety of neurological symptoms, including sensory impairment. Although methylmercury exposure causes conflicting symptoms of hyperalgesia and hypoalgesia, the relationship between methylmercury toxicity and these symptoms has not been clarified. In this study, C57BL/6 male mice exposed to methylmercury chloride (final concentration 30&#xa0;ppm) in drinking water ad libitum were temporally evaluated for changes in pain sensitivity. The results show that hyperalgesia (increased mechanosensitivity and thermosensitivity) was induced from 3 to 7&#xa0;weeks after methylmercury exposure, followed by hypoalgesia (decreased mechanosensitivity and thermosensitivity) from 13 to 15&#xa0;weeks after exposure. Furthermore, immunohistochemical staining of neuronal activity in spinal cord dorsal horn neurons reveals a dramatic increase in c-Fos-positive neurons (activated neurons) after 4&#xa0;weeks of methylmercury exposure and a decrease in the number of activated neurons after 14&#xa0;weeks of exposure. In addition, the amount of mercury accumulated in the spinal cord dorsal horn increased depending on the duration of exposure. These results suggest that gradual dysfunction of spinal dorsal horn neurons, dependent on the amount of methylmercury accumulated, is involved in the observed biphasic change in pain sensitivity. This study is the first to examine dynamic changes in pain sensitivity due to methylmercury exposure in a mouse model and provides important information for investigating the molecular mechanisms involved in methylmercury-induced sensory impairment.</p>

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Methylmercury causes pain disorders by disrupting the neuronal function of spinal dorsal horn neurons in mice

  • 期刊论文

  • 发表日期：

    2025年12月14日

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  • Ryota Yamagata,
  • Miyu Fujishima,
  • Yuna Shoji,
  • Naoya Yamashita,
  • Wataru Nemoto,
  • Gi-Wook Hwang

摘要

Methylmercury is a neurotoxic substance that is ubiquitously present in the environment and is known to cause a variety of neurological symptoms, including sensory impairment. Although methylmercury exposure causes conflicting symptoms of hyperalgesia and hypoalgesia, the relationship between methylmercury toxicity and these symptoms has not been clarified. In this study, C57BL/6 male mice exposed to methylmercury chloride (final concentration 30 ppm) in drinking water ad libitum were temporally evaluated for changes in pain sensitivity. The results show that hyperalgesia (increased mechanosensitivity and thermosensitivity) was induced from 3 to 7 weeks after methylmercury exposure, followed by hypoalgesia (decreased mechanosensitivity and thermosensitivity) from 13 to 15 weeks after exposure. Furthermore, immunohistochemical staining of neuronal activity in spinal cord dorsal horn neurons reveals a dramatic increase in c-Fos-positive neurons (activated neurons) after 4 weeks of methylmercury exposure and a decrease in the number of activated neurons after 14 weeks of exposure. In addition, the amount of mercury accumulated in the spinal cord dorsal horn increased depending on the duration of exposure. These results suggest that gradual dysfunction of spinal dorsal horn neurons, dependent on the amount of methylmercury accumulated, is involved in the observed biphasic change in pain sensitivity. This study is the first to examine dynamic changes in pain sensitivity due to methylmercury exposure in a mouse model and provides important information for investigating the molecular mechanisms involved in methylmercury-induced sensory impairment.