Oxidative Stress-Induced Increase in Intracellular Ca2+ and Ca2+-Induced Increase in Oxidative Stress: An Experimental Model Using Dissociated Rat Brain Neurons

Oyama, Yasuo; Okazaki, Eisuke; Chikahisa, Lumi; Nagano, Tadayoshi; Sadakata, Chiharu

doi:10.1254/jjp.72.381

Cited by 25 publications

(10 citation statements)

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“…5B and C). It was previously reported that cellular oxidative stress induced an increase in intracellular Ca 2+ levels [47]. Although the molecular mechanism responsible for the elevation of Ormdl3 expression through FABP4 knockdown is currently unclear, it is possible that the ER stress observed in this study may be secondarily induced by oxidative stress and impaired Ca 2+ homeostasis as a result of FABP4 knockdown.…”

Section: Discussionmentioning

confidence: 58%

Cytoprotective role of the fatty acid binding protein 4 against oxidative and endoplasmic reticulum stress in 3T3‐L1 adipocytes

2014

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Section: Discussionmentioning

confidence: 58%

Cytoprotective role of the fatty acid binding protein 4 against oxidative and endoplasmic reticulum stress in 3T3‐L1 adipocytes

2014

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“…Various oxidants are known to increase the cytoplasmic free C a 2ϩ concentration, although the exact mechanism for the increase is yet to be established (Suzuki et al, 1997). H 2 O 2 has been shown to increase the intracellular C a 2ϩ level in rat neurons (Oyama et al, 1996). The results presented here indicate that the enhanced C a 2ϩ flux through the neuronal voltagedependent C a 2ϩ channels could contribute to the oxidantinduced increase in the cytosolic C a 2ϩ level.…”

Section: Discussionmentioning

confidence: 61%

Oxidation Regulates Cloned Neuronal Voltage-Dependent Ca²⁺Channels Expressed inXenopusOocytes

Ségui

Heinemann

et al. 1998

J. Neurosci.

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Functional modifications of neuronal P/Q-type voltagedependent Ca 2ϩ channels expressed in Xenopus oocytes by oxidation were examined electrophysiologically. Oxidation by external H 2 O 2 enhanced the whole-oocyte currents through the Ca 2ϩ channels composed of the ␣1A, ␣2/␦, and ␤3 subunits at negative voltages (Ͻ0 mV) without markedly affecting the currents at more positive voltages. Single-channel analysis showed that oxidation accelerates the overall channel opening process. The effect of H 2 O 2 to enhance the Ca 2ϩ channel activity did not require heterologous expression of the ␣2/␦ subunit, and it was not mimicked by a cysteine-specific oxidizing agent. The results suggest that oxidative stress may regulate the activity of neuronal Ca 2ϩ channels and that regulation by oxidation may be important in some clinical situations, such as in reperfusion injury after ischemic episodes.

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“…12,16) Oxidative stress is also induced by abnormally increasing [Ca 2ϩ ]i in neurons. 20,21) Therefore, if EGBL prevents increasing [Ca 2ϩ ]i of neurons by excessive activation of glutamate receptor, it would contribute to the neuroprotective action of EGBL. In this study, EGBL at concentrations of 3 mg/ml or more decreased the increase in [Ca 2ϩ ]i induced by kainate via an activation of non-NMDA receptor (Fig.…”

Section: Discussionmentioning

confidence: 99%

Extract of Ginkgo biloba Leaves Attenuates Kainate-Induced Increase in Intracellular Ca2+ Concentration of Rat Cerebellar Granule Neurons

Kanada

Nishimura

Yamaguchi

et al. 2005

Biological & Pharmaceutical Bulletin

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The idea that an excessive release of glutamate mediates neuronal cell death was proposed, as the excitotoxicity hypothesis, by Olney and de-Gubareff.1) Glutamate activates two types of its receptor, N-methyl-D-aspartate (NMDA) type and non-NMDA one.2) Excessive activation of glutamate receptors, resulting in increase in intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i) and generation of reactive oxygen species (ROS), is involved in neuronal disorder and degeneration. 3)Both phenomena induced by glutamate are related to cell injury and death. 4,5) In fact, antagonists for NMDA and non-NMDA glutamate receptors are proven to possess neuroprotective action. [6][7][8] Extract of Ginkgo biloba leaves (EGBL) is expected to treat patients with some neuronal disorders such as dementia and Alzheimer's disease. 9,10) The extract exerts protective action (or antioxidant action) on neurons suffering from oxidative stress induced by hydrogen peroxide, one of ROS, and by overload of intracellular Ca 2ϩ . 7,11,12) EGBL and its constituents inhibit the response mediated by activation of NMDA receptor. 13,14) However, there is limited information concerning the effect of EGBL on response induced by activation of non-NMDA glutamate receptor. Kainate, an agonist for non-NMDA glutamate receptor, increases [Ca 2ϩ ]i in neurons via activations of non-NMDA glutamate receptor and voltage-dependent Ca 2ϩ channel. 15) Therefore, in order to elucidate one of mechanisms for neuroprotective action of EGBL, we examined the effect of EGBL on kainate-induced increase in [Ca 2ϩ ]i in rat brain neurons using a laser microscope with fluorescent Ca 2ϩ -indicator. MATERIALS AND METHODS MaterialsExtract of Ginkgo biloba leaves (EGBL) was obtained from Icho-Ha Sangyo Co., Ltd., Ibaraki, Japan. EGBL was initially dissolved in 50% ethanol. EGBL solution (1-30 mg/ml) was added to bathing solution to achieve appropriate concentrations (1-30 mg/ml). Ethanol as a solvent at 0.05% did not affect any fluorescence measurements from cells. Other chemical reagents except for fluorescent probes were purchased from Sigma Chemical Co. (St. Louis, MO, U.S.A.) unless otherwise mentioned.Cell Preparation Experimental method for dissociation of rat cerebellar neurons was similar to those described in previous studies. 16,17) In brief, the slices of cerebellum dissected from 10-to 16-d-old Wistar strain rats were treated with 1000 protease units/ml dispase (Godo Shusei, Tokyo, Japan) in Tyrode's solution for 50-60 min at a temperature of 32-34°C. After enzymatic treatment, cerebellar neurons were dispersed by triturating in Tyrode's solution. Since the majority of neurons were characterized by small size and spherical shape under microscopic observation, they were ascertained as cerebellar granule cells. These cells responded to kainate, resulting in an increase in [Ca 2ϩ ]i.15) The cells were placed on culture dishes and incubated at 35-36°C in Tyrode's solution for 50-60 min before use. The application of chemicals to neurons was performed by a Y-tube...

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Oxidative Stress-Induced Increase in Intracellular Ca2+ and Ca2+-Induced Increase in Oxidative Stress: An Experimental Model Using Dissociated Rat Brain Neurons

Cited by 25 publications

References 14 publications

Cytoprotective role of the fatty acid binding protein 4 against oxidative and endoplasmic reticulum stress in 3T3‐L1 adipocytes

Cytoprotective role of the fatty acid binding protein 4 against oxidative and endoplasmic reticulum stress in 3T3‐L1 adipocytes

Oxidation Regulates Cloned Neuronal Voltage-Dependent Ca²⁺Channels Expressed inXenopusOocytes

Extract of Ginkgo biloba Leaves Attenuates Kainate-Induced Increase in Intracellular Ca2+ Concentration of Rat Cerebellar Granule Neurons

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Oxidative Stress-Induced Increase in Intracellular Ca2+ and Ca2+-Induced Increase in Oxidative Stress: An Experimental Model Using Dissociated Rat Brain Neurons

Cited by 25 publications

References 14 publications

Cytoprotective role of the fatty acid binding protein 4 against oxidative and endoplasmic reticulum stress in 3T3‐L1 adipocytes

Cytoprotective role of the fatty acid binding protein 4 against oxidative and endoplasmic reticulum stress in 3T3‐L1 adipocytes

Oxidation Regulates Cloned Neuronal Voltage-Dependent Ca2+Channels Expressed inXenopusOocytes

Extract of Ginkgo biloba Leaves Attenuates Kainate-Induced Increase in Intracellular Ca2+ Concentration of Rat Cerebellar Granule Neurons

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Oxidation Regulates Cloned Neuronal Voltage-Dependent Ca²⁺Channels Expressed inXenopusOocytes