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척수 아교질 세포의 흥분성과 세포내 칼슘농도에 대한 활성산소의 영향에 대한 연구

Changes in Neuronal Excitability and Intracellular Calcium Concentration by Reactive Oxygen Species on Spinal Substantia Gelatinosa Neurons

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초록

Substantia gelatinosa (SG) neurons, lamina II of the spinal dorsal horn, receive sensory informations from peripheral neurons directly and send the informations to upper brain regions. In recent studies, it is reported that reactive oxygen species (ROS) takes part in generation and transmission of pain, but these are the results from behavioral test and immunohistochemical study. In the present study, we recorded neuronal excitability to investigate the effects of tert-buthyl hydroperoxide (t-BuOOH), a kind of ROS, on transmission of pain in SG using the patch clamp technique. We also used calcium imaging technique to measure the changes of intracellular calcium concentration. Depolarization and action potential were evoked by perfusion of t-BuOOH, and these are suppressed by PBN, an antioxidant. When we treated t-BuOOH, intracellular calcium concentration was increased, but it was rather decreased in extracellular calcium free solution and on the condition of pretreated APB, ruthenium red, and thapsigargin. We confirmed that t-BuOOH activates excitability of neurons in SG suggesting that ROS boosts nociception through central sensitization. This result is induced by increase of intracellular calcium, and the sources of calcium are from extracellular fluid and endoplasmic reticulum in neurons.

Abstract

Substantia gelatinosa (SG) neurons, lamina II of the spinal dorsal horn, receive sensory informations from peripheral neurons directly and send the informations to upper brain regions. In recent studies, it is reported that reactive oxygen species (ROS) takes part in generation and transmission of pain, but these are the results from behavioral test and immunohistochemical study. In the present study, we recorded neuronal excitability to investigate the effects of tert-buthyl hydroperoxide (t-BuOOH), a kind of ROS, on transmission of pain in SG using the patch clamp technique. We also used calcium imaging technique to measure the changes of intracellular calcium concentration. Depolarization and action potential were evoked by perfusion of t-BuOOH, and these are suppressed by PBN, an antioxidant. When we treated t-BuOOH, intracellular calcium concentration was increased, but it was rather decreased in extracellular calcium free solution and on the condition of pretreated APB, ruthenium red, and thapsigargin. We confirmed that t-BuOOH activates excitability of neurons in SG suggesting that ROS boosts nociception through central sensitization. This result is induced by increase of intracellular calcium, and the sources of calcium are from extracellular fluid and endoplasmic reticulum in neurons.

참고문헌 (28)

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