Current-Voltage Relationship Considering Electrode Degradation Using Sm-Doped Ceria Electrolytes in SOFCs

2019 ◽  
Vol 35 (1) ◽  
pp. 583-592 ◽  
Author(s):  
Tomofumi Miyashita
Keyword(s):  
Doped Ceria ◽  
Electrode Degradation ◽  
Current Voltage ◽  
Current Voltage Relationship ◽  
Voltage Relationship

scholarly journals Plasticity of calcium-permeable AMPA glutamate receptors in Pro-opiomelanocortin neurons

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Shigetomo Suyama ◽  
Alexandra Ralevski ◽  
Zhong-Wu Liu ◽  
Marcelo O Dietrich ◽  
Toshihiko Yada ◽  
...  
Keyword(s):  
Food Deprivation ◽  
High Fat Diet ◽  
Receptor Complex ◽  
High Fat ◽  
Fasted State ◽  
Linear Current ◽  
Current Voltage ◽  
Relationship Of ◽  
Current Voltage Relationship ◽  
Voltage Relationship

POMC neurons integrate metabolic signals from the periphery. Here, we show in mice that food deprivation induces a linear current-voltage relationship of AMPAR-mediated excitatory postsynaptic currents (EPSCs) in POMC neurons. Inhibition of EPSCs by IEM-1460, an antagonist of calcium-permeable (Cp) AMPARs, diminished EPSC amplitude in the fed but not in the fasted state, suggesting entry of GluR2 subunits into the AMPA receptor complex during food deprivation. Accordingly, removal of extracellular calcium from ACSF decreased the amplitude of mEPSCs in the fed but not the fasted state. Ten days of high-fat diet exposure, which was accompanied by elevated leptin levels and increased POMC neuronal activity, resulted in increased expression of Cp-AMPARs on POMC neurons. Altogether, our results show that entry of calcium via Cp-AMPARs is inherent to activation of POMC neurons, which may underlie a vulnerability of these neurons to calcium overload while activated in a sustained manner during over-nutrition.

Capsaicin and nicotine both activate a subset of rat trigeminal ganglion neurons

1996 ◽  
Vol 270 (6) ◽  
pp. C1807-C1814 ◽  
Author(s):  
L. Liu ◽  
S. A. Simon
Keyword(s):  
Trigeminal Ganglion ◽  
Acetylcholine Receptors ◽  
Ganglion Cells ◽  
Whole Cell Patch Clamp ◽  
Current Voltage ◽  
Trigeminal Ganglion Neurons ◽  
Ganglion Neurons ◽  
Relationship Of ◽  
Current Voltage Relationship ◽  
Voltage Relationship

Nicotine and capsaicin produce many similar physiological responses that include pain, irritation, and vasodilation. To determine whether neuronal nicotine acetylcholine receptors (nAChR) are present on capsaicin-sensitive neurons, whole cell patch-clamp recordings were performed on rat trigeminal ganglion cells. It was found that approximately 20% of the total number of neurons tested was activated by both 100 microM nicotine and 1 nM capsaicin. Other subsets of neurons were activated by only one of these compounds, whereas a fourth subset was not activated by either compound. At -60 mV, the magnitude of the capsaicin-activated currents was about three times larger than the magnitude of the nicotine-activated currents. The current-voltage relationship of the nAChR exhibited marked rectification, such that for voltages > or = 0 mV the current was essentially zero. In contrast, the current-voltage relationship of the capsaicin-activated current was ohmic from +/- 60 mV. These data indicate the existence of subsets of capsaicin-sensitive afferent neurons.

Simulation of Na/K Pump Current-Voltage Relationship

1992 ◽  
Vol 671 (1 Ion-Motive AT) ◽  
pp. 449-451 ◽  
Author(s):  
X.-Y. LIU ◽  
T. A. KINARD ◽  
J. R. STIMERS
Keyword(s):  
Pump Current ◽  
Current Voltage ◽  
Current Voltage Relationship ◽  
Voltage Relationship

scholarly journals Ionic Basis of Membrane Potential and of Acetylcholine-evduced Currents in the Cell Body of the Cockroach Fast Coxal Depressor Motor Neurone

1990 ◽  
Vol 151 (1) ◽  
pp. 21-39 ◽  
Author(s):  
JONATHAN A. DAVID ◽  
DAVID B. SATTELLE
Keyword(s):  
Cell Body ◽  
Outward Current ◽  
Motor Neurone ◽  
Resting Potential ◽  
Inward Current ◽  
Current Voltage ◽  
Low K ◽  
Current Voltage Relationship ◽  
Ionic Basis ◽  
Voltage Relationship

The ionic basis of the resting potential and of the response to acetylcholine (ACh) has been investigated in the cell body membrane of the fast coxal depressor motor neurone in the metathoracic ganglion of the cockroach Periplaneta americana. By means of ion-sensitive microelectrodes, intracellular concentrations of three ion species were estimated (mmoll−1): [K+]i, 1443; [Na+]i, 9±1; [Cl−], 7±1. The resting potential of continuously superfused cells was −75.6±1.9mV at 22° C. A change in resting potential of 42.0±2.5mV accompanied a decade change in [K+]o. Experiments with (10−4moll−1) ouabain, Na+ injection, low temperature (10°C) and non-superfused cells indicated the presence of an electrogenic sodium pump. Under current-clamp, the cell body membrane was depolarized by sequentially applied, ionophoretic pulses (500ms duration) of ACh. Under voltage-clamp, such doses of ACh resulted in an inward current which was abolished in low-Na+ saline. Ion-sensitive electrodes revealed an increase in [Na+]i but no change in [Cl−1]j in response to externally applied ACh. The ACh-induced current-voltage relationship was shifted in a negative direction by low-K+ saline. The AChinduced inward current was usually followed by a delayed outward current which reversed at Ek. Low-K+ saline had the same effect on this outward component as depolarizing the membrane. This suggests that the outward current component is carried by K+. The ACh-induced inward current and the delayed outward current were potentiated either when [Ca2+]i was lowered by injecting the calcium chelator BAPTA or by exposure of the cell to low-Ca2+ saline. High-Ca2+ saline reduced the inward component of the response and produced a negative shift in the AChinduced current-voltage relationship. The amplitude of the delayed outward

Current-voltage relationship of the basolateral membrane of a tight epithelium

1979 ◽  
Vol 555 (3) ◽  
pp. 519-523 ◽  
Author(s):  
Nancy K. Wills ◽  
Douglas C. Eaton ◽  
Simon A. Lewis ◽  
Mark S. Ifshin
Keyword(s):  
Basolateral Membrane ◽  
Current Voltage ◽  
Relationship Of ◽  
Current Voltage Relationship ◽  
Voltage Relationship ◽  
Tight Epithelium

Citrate decreases contraction and Ca current in cardiac muscle independent of its buffering action

1991 ◽  
Vol 260 (5) ◽  
pp. C900-C909 ◽  
Author(s):  
D. M. Bers ◽  
L. V. Hryshko ◽  
S. M. Harrison ◽  
D. D. Dawson
Keyword(s):  
Cardiac Muscle ◽  
Dipicolinic Acid ◽  
Reversal Potential ◽  
Cell Voltage ◽  
Nitrilotriacetic Acid ◽  
Ca Current ◽  
Current Voltage ◽  
Protonated Forms ◽  
Current Voltage Relationship ◽  
Voltage Relationship

Extracellular Ca (Cao) depletions that occur during cardiac muscle contractions are indicative of net Ca entry. Buffering Cao concentration ([Ca]o) with citrate can limit the magnitude of these Cao depletions [e.g., Shattock and Bers. Am. J. Physiol. 256 (Cell Physiol. 25): C813-C822, 1989] which theoretically would allow more Ca entry and consequently greater force at the same free [Ca]o. However, Shimoni and Ginsburg [Am. J. Physiol. 252 (Cell Physiol. 21): C248-C252, 1987] have shown that citrate inhibits cardiac contractions and suggested that this was due to its Ca-buffering action (i.e., dissipating a local elevation of [Ca] at the outer sarcolemmal surface and thereby decreasing Ca influx). To examine the effects of Ca buffering per se, we compared the effects of four low-affinity Ca buffers [citrate, nitrilotriacetic acid (NTA), dipicolinic acid (DPA), and acetamidoiminodiacetic acid (ADA)] on several cardiac preparations. In Mg-free medium with 2 mM free Ca (measured using murexide), citrate, DPA, and ADA (10 mM) decreased the force of twitch contractions in rabbit ventricle to 76 +/- 2, 60 +/- 2, and 85 +/- 2%, respectively, but 10 mM NTA increased force slightly to 105 +/- 2%. No simple correlation was observed between the Ca affinity of the buffer and its effect on tension. These effects were not due to changes in sarcoplasmic reticulum (SR) Ca loading because rapid cooling contractures were not affected and similar results were observed in the presence of caffeine or ryanodine. The depressant effects of citrate and ADA on tension were greater at pH 5.5-6 and ADA had no effect at pH 8.5. Thus the depressant effect is stronger with more protonated forms of citrate and ADA, which are also poorer Ca buffers. Citrate (but not NTA) decreased Ca current in whole cell voltage clamp and shifted the current-voltage relationship and reversal potential to more negative potentials. Citrate decreased Ca current more effectively at higher citrate and lower Ca concentrations. We conclude that citrate (and some other weak Ca buffers) may directly decrease Ca current and contraction in a manner independent of Ca buffering ability.

scholarly journals Spadin Modulates Astrocytic Passive Conductance via Inhibition of TWIK-1/TREK-1 Heterodimeric Channels

2020 ◽  
Vol 21 (24) ◽  
pp. 9639
Author(s):  
Yeonju Bae ◽  
Jae Hyouk Choi ◽  
Kanghyun Ryoo ◽  
Ajung Kim ◽  
Osung Kwon ◽  
...  
Keyword(s):  
Brain Slices ◽  
Specific Inhibitor ◽  
Excitable Cells ◽  
Cultured Astrocytes ◽  
Current Voltage ◽  
Molecular Machinery ◽  
Hippocampal Astrocytes ◽  
Current Voltage Relationship ◽  
The Brain ◽  
Voltage Relationship

Astrocytes, the most abundant cell type in the brain, are non-excitable cells and play critical roles in brain function. Mature astrocytes typically exhibit a linear current–voltage relationship termed passive conductance, which is believed to enable astrocytes to maintain potassium homeostasis in the brain. We previously demonstrated that TWIK-1/TREK-1 heterodimeric channels mainly contribute to astrocytic passive conductance. However, the molecular identity of astrocytic passive conductance is still controversial and needs to be elucidated. Here, we report that spadin, an inhibitor of TREK-1, can dramatically reduce astrocytic passive conductance in brain slices. A series of gene silencing experiments demonstrated that spadin-sensitive currents are mediated by TWIK-1/TREK-1 heterodimeric channels in cultured astrocytes and hippocampal astrocytes from brain slices. Our study clearly showed that TWIK-1/TREK-1-heterodimeric channels can act as the main molecular machinery of astrocytic passive conductance, and suggested that spadin can be used as a specific inhibitor to control astrocytic passive conductance.

Sign in / Sign up

Export Citation Format

Share Document