Transcortical Direct Current Potential Shift Reflects Immediate Signaling of Systemic Insulin to the Human Brain

The Ca2+ mobilization across the neuronal membrane is regarded as a crucial factor in the development of neuronal damage in ischemia. Because glucocorticoids have been reported to aggravate ischemic neuronal injury, the effects of dexamethasone on ischemia-induced membrane depolarization, histologic outcome, and changes in the intracellular Ca2+ concentration in the gerbil hippocampus were examined in vivo and in vitro. The effects of metyrapone, an inhibitor of glucocorticoid synthesis, were also evaluated. Changes in the direct-current potential shift in the hippocampal CA1 area produced by transient forebrain ischemia for 2.5 minutes were compared among animals pretreated with dexamethasone (3 μg, intracerebroventricularly), metyrapone (100 mg/kg, intraperitoneally), and saline. The histologic outcome was evaluated 7 days after ischemia by assessing the delayed neuronal death in the hippocampal CA1 pyramidal cells of these animals. A hypoxia-induced intracellular Ca2+ increase was evaluated by in vitro microfluorometry in gerbil hippocampal slices, and the effect of dexamethasone (120 μg/L in the medium) on the cytosolic Ca2+ accumulation was examined. The effect in a Ca2+-free ischemialike condition was also investigated. Preischemic administration of dexamethasone reduced the onset latency of ischemia-induced membrane depolarization by 22%, and aggravated neuronal damage in vivo. In contrast, pretreatment with metyrapone improved the histologic outcome. The onset time of the increase in the intracellular concentration of Ca2+ provoked by in vitro hypoxia was advanced in dexamethasone-treated slices. The Ca2+-free in vitro hypoxia reduced the elevation compared with that in the Ca2+-containing condition. Treatment with dexamethasone facilitated the increase on both the initiation and the extent in the Ca2+-free condition. Aggravation of ischemic neuronal injury by endogenous or exogenous glucocorticoids is thus thought to be caused by the advanced onset times of both the ischemia-induced direct-current potential shift and the increase in the intracellular Ca2+ concentration.

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Lidocaine Suppresses the Anoxic Depolarization and Reduces the Increase in the Intracellular Ca sup 2+ Concentration in Gerbil Hippocampal Neurons

Anesthesiology ◽

10.1097/00000542-199712000-00026 ◽

1997 ◽

Vol 87 (6) ◽

pp. 1470-1478 ◽

Cited By ~ 30

Author(s):

Keyue Liu ◽

Naoto Adachi ◽

Hisato Yanase ◽

Kiyoshi Kataoka ◽

Tatsuru Arai

Keyword(s):

Direct Current ◽

Hippocampal Slices ◽

Membrane Depolarization ◽

Induced Membrane ◽

Free Condition ◽

Potential Shift ◽

Anoxic Depolarization ◽

Hippocampal Ca1 ◽

Current Potential

Background The movement of ions, particularly Ca2+, across the plasma membrane of neurons is regarded as an initial element of the development of ischemic neuronal damage. Because the mechanism by which lidocaine protects neurons against ischemia is unclear, the effects of lidocaine on the ischemia-induced membrane depolarization, histologic outcome, and the change in the intracellular Ca2+ concentration in the gerbil hippocampus were studied. Methods The changes in the direct-current potential shift in the hippocampal CA1 area produced by transient forebrain ischemia for 4 min were compared in animals given lidocaine (0.8 micromol administered intracerebroventricularly) 10 min before ischemia and those given saline. The histologic outcome was evaluated 7 days after ischemia by assessing delayed neuronal death in hippocampal CA1 pyramidal cells in these animals. In a second study, hypoxia-induced intracellular Ca2+ increases were evaluated by in vitro microfluorometry in gerbil hippocampal slices, and the effects of lidocaine (10, 50, and 100 microM) on the Ca2+ accumulation were examined. In addition, the effect of lidocaine (100 microM) drug perfusion with a Ca2+-free ischemia-like medium was investigated. Results The preischemic administration of lidocaine delayed the onset of the ischemia-induced membrane depolarization (anoxic depolarization) and reduced its maximal amplitude. The histologic outcome was improved by the preischemic treatment with lidocaine. The in vitro hypoxia-induced increase in the intracellular concentration of Ca2+ was suppressed by the perfusion with lidocaine-containing mediums (50 and 100 microM), regarding the initiation and the extent of the increase. The hypoxia-induced intracellular Ca2+ elevation in the Ca2+-free condition was similar to that in the Ca2+-containing condition. Perfusion with lidocaine (100 microM) inhibited this elevation in the Ca2+-free condition. Conclusions Lidocaine helps protect neurons from ischemia by suppressing the direct-current potential shift, by inhibiting the release of Ca2+ from the intracellular Ca2+ stores, and by inhibiting the influx from the extracellular space.

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Effects of Hyperventilation and Hypoventilation on Cochlear Blood Flow and Endocochlear Direct-Current Potential

ORL ◽

10.1159/000276734 ◽

1995 ◽

Vol 57 (4) ◽

pp. 171-176 ◽

Cited By ~ 5

Author(s):

Hirofumi Yamamoto ◽

Kazuo Makimoto ◽

Michiro Kawakami ◽

Yoshimitsu Ohinata ◽

Hiroaki Takahashi

Keyword(s):

Blood Flow ◽

Direct Current ◽

Cochlear Blood Flow ◽

Current Potential

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Eicosanoids in Rat Brain during Ischemia and Reperfusion—Correlation to DC Depolarization

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1990.65 ◽

1990 ◽

Vol 10 (3) ◽

pp. 358-364 ◽

Cited By ~ 23

Author(s):

F. Tegtmeier ◽

C. Weber ◽

U. Heister ◽

I. Haker ◽

D. Scheller ◽

...

Keyword(s):

Arachidonic Acid ◽

Rat Brain ◽

Direct Current ◽

Eicosatetraenoic Acid ◽

Ischemia And Reperfusion ◽

Ischemic Time ◽

Isolated Perfused Rat Brain ◽

Current Potential

The effects of complete ischemia on cerebral arachidonic acid (AA) metabolism were investigated in the isolated perfused rat brain. During 12.5 min of ischemia, AA, 5-hydroxy-6,8,11,14-eicosatetraenoic acid, and 15-hydroxy-5,8,11,13-eicosatetraenoic acid increased 129-, 4-, and 10-fold, respectively, while subsequent reperfusion for 30 min resulted in normalized levels independently of the duration of preceding ischemia. Prostaglandin (PG) F2α, PGE2, PGD2, 6-keto-PGF1α, and thromboxane (Tx) B2 remained at preischemic levels during 12.5 min of complete ischemia. However, at the end of subsequent reperfusion for 30 min, the levels of the prostanoids PGF2α, PGE2, PGD2, 6-keto-PGF1α, and TxB2 increased according to the preceding ischemic time. The levels reached a maximum after 7.5 min of ischemia and were elevated by 7-, 14-, 48-, 3-, and 30-fold, respectively. A prolongation of ischemia of up to 12.5 min was not associated with further increases of prostanoids at the end of reperfusion. The mechanisms underlying the metabolism of eicosanoids are discussed in relation to the changes of cortical direct current potential.

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Enhancement of ion activation and collision induced dissociation by direct current potential in digital ion trap mass spectrometer

International Journal of Mass Spectrometry ◽

10.1016/j.ijms.2018.02.004 ◽

2018 ◽

Vol 428 ◽

pp. 29-34

Author(s):

Fuxing Xu ◽

Chongsheng Xu ◽

Li Ding ◽

Mingfei Zhou ◽

Chuan-Fan Ding

Keyword(s):

Mass Spectrometer ◽

Direct Current ◽

Ion Trap ◽

Collision Induced Dissociation ◽

Ion Activation ◽

Ion Trap Mass Spectrometer ◽

Digital Ion Trap ◽

Current Potential

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Qualitative Study on Cable Breakage of Nb3Sn CICC Based on Direct Current Potential Drop Method

IEEE Transactions on Applied Superconductivity ◽

10.1109/tasc.2021.3108754 ◽

2021 ◽

pp. 1-1

Author(s):

Xiaochuan Liu ◽

Jinggang Qin ◽

Zhenmao Chen ◽

Shuxia Tian

Keyword(s):

Qualitative Study ◽

Direct Current ◽

Potential Drop ◽

Drop Method ◽

Direct Current Potential Drop ◽

Current Potential

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Single-unit pH-sensitive double-barreled microelectrodes for extracellular use

Journal of Applied Physiology ◽

10.1152/jappl.1984.57.3.907 ◽

1984 ◽

Vol 57 (3) ◽

pp. 907-912

Author(s):

S. Javaheri ◽

A. De Hemptinne ◽

I. Leusen

Keyword(s):

Direct Current ◽

Single Unit ◽

Extracellular Fluid ◽

Ph Sensitive ◽

Current Potential

The purpose of this study is to systematically describe the construction of pH-sensitive double-barreled microelectrodes for extracellular use. The most important advantages of these microelectrodes are as follows: the reference and the pH barrels are next to each other, and therefore the measured pH is not affected by asymmetric or slowly spreading direct current potential. The diameter of the tip of the microelectrodes is between 7 and 35 micron. These pH-sensitive microelectrodes are generally stable and Nernstian. They can be used repeatedly both in vivo and in vitro to measure tissue extracellular fluid pH. Some applications are described.

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