Roles of Reactive Oxygen Species on Neuronal Excitability in Rat Substantia Gelatinosa Neurons

척수 아교질 신경세포의 흥분성에 대한 활성산소종의 역할

  • Choi, Jeong-Hee (Department of Oral Physiology, College of Dentistry) ;
  • Kim, Jae-Hyo (Department of Meridian and Acupoint, College of Oriental Medicine) ;
  • Lim, Sung-Jun (Department of Oral Physiology, College of Dentistry) ;
  • Park, Byung-Rim (Department of Physiology, College of Medicine) ;
  • Kwon, Kang-Beom (Department of Biochemistry, College of Oriental Medicine, Wonkwang University)
  • 최정희 (원광대학교 치과대학 구강생리학교실) ;
  • 김재효 (한의과대학 경혈학교실) ;
  • 임성준 (원광대학교 치과대학 구강생리학교실) ;
  • 박병림 (의과대학 생리학교실) ;
  • 권강범 (한의과대학 생화학교실)
  • Published : 2007.04.25

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. In the present study, whole cell patch clamp recordings were carried out on substantia gelatinosa (SG) neurons in spinal cord slice of neonatal rats to investigate the effects of ROS on neuronal excitability and excitatory synaptic transmission. In current clamp condition, tert-buthyl hydroperoxide (t-BuOOH), an ROS donor, induced a electrical hyperexcitability during t-BuOOH wash-out followed by a brief inhibition of excitability in SG neurons. Application of t-BuOOH depolarized membrane potential of SG neurons and increased the neuronal firing frequencies evoked by depolarizing current pulses. Phenyl-N-tert-buthylnitrone (PBN), an ROS scavenger, antagonized t-BuOOH induced hyperexcitability. IN voltage clamp conditions, t-BuOOH increased the frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs). In order to determine the site of action of t-BuOOH, miniature excitatory postsynaptic currents (mEPSCs) were recorded. t-BuOOH increased the frequency and amplitude of mEPSCs, indicating that it may modulate the excitability of the SG neurons via pre- and postsynaptic actions. These data suggest that ROS generated by peripheral nerve injury can induce central sensitization in spinal cord.

Keywords

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