Levels of mitochondrial reactive oxygen species increase in rat neuropathic spinal dorsal horn neurons

Eun Sung Park, Xiu Gao, Jin Chung, Kyungsoon Chung

Research output: Contribution to journalArticle

98 Citations (Scopus)

Abstract

Reactive oxygen species (ROS) are toxic agents that may be involved in various neurodegenerative diseases. Recent studies indicate that ROS are also involved in persistent pain through a spinal mechanism. Since the major source of ROS in neurons is mitochondria, mitochondrial ROS generation was examined in dorsal horn neurons of neuropathic rats. Neuropathic rats were produced by L5 spinal nerve ligation and mitochondrial ROS was detected by the mitochondrial marker, Mitotracker Red® CM-H2XRos (MT-Red). Neurons were identified immunohistochemically for the neuronal marker NeuN. The number of MT-Red positive cells was increased 60-100% in the neuropathic dorsal horn. Approximately 75-85% of MT-Red positive cells were neurons. These data suggest that increased mitochondrial ROS in dorsal horn neurons may contribute to central sensitization in neuropathic rats.

Original languageEnglish (US)
Pages (from-to)108-111
Number of pages4
JournalNeuroscience Letters
Volume391
Issue number3
DOIs
StatePublished - Jan 2 2006

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Posterior Horn Cells
Reactive Oxygen Species
Neurons
Central Nervous System Sensitization
Spinal Nerves
Poisons
Neurodegenerative Diseases
Ligation
Mitochondria
Pain

Keywords

  • Central sensitisation
  • Free radicals
  • Mitotracker
  • Persistent pain
  • ROS

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Levels of mitochondrial reactive oxygen species increase in rat neuropathic spinal dorsal horn neurons. / Park, Eun Sung; Gao, Xiu; Chung, Jin; Chung, Kyungsoon.

In: Neuroscience Letters, Vol. 391, No. 3, 02.01.2006, p. 108-111.

Research output: Contribution to journalArticle

Park, Eun Sung ; Gao, Xiu ; Chung, Jin ; Chung, Kyungsoon. / Levels of mitochondrial reactive oxygen species increase in rat neuropathic spinal dorsal horn neurons. In: Neuroscience Letters. 2006 ; Vol. 391, No. 3. pp. 108-111.
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