K+ and Cl− uptake by cultured oligodendrocytes

1987 ◽  
Vol 65 (5) ◽  
pp. 1033-1037 ◽  
Author(s):  
H. Kettenmann
Keyword(s):  
Membrane Potential ◽  
Equilibrium Distribution ◽  
Negative Charge ◽  
Membrane Conductance ◽  
Input Resistance ◽  
Equilibrium Potential ◽  
Resting Membrane Potential

Cultured oligodendrocytes take up K+ triggered by an increase in [K+]o. Simultaneously [Cl−]i increases in the majority of the oligodendrocytes. This KCl uptake, which is not furosemide sensitive, can be explained by the following model. The first event is the entry of Cl− into the cell driven by the discrepancy between the membrane and Cl− equilibrium potential. As a consequence of the movement of negative charge across the membrane, K+ is driven into the cell. The prerequisites of this model, a passive Cl− distribution at resting membrane potential and a Cl− conductance of the membrane were found to exist in most cultured oligodendrocytes. The chloride equilibrium potential (−61 mV, SD ± 10 mV) was slightly more positive than the membrane potential (−64 ± 8 mV), Since cell input resistance determined with two independent electrodes increased by 11% (SD ± 0.07) when [Cl−]o was reduced to 10 mM, part of the membrane conductance appears to be mediated by Cl−. Differences between membrane potential and Cl− equilibrium potential therefore will lead to Cl− fluxes across the membrane. In contrast with oligodendroyctes, [Cl−]i in astrocytes is significantly increased (from 20 to 40 mM) above the equilibrium distribution owing to the activity of an inward directed Cl− pump; this suggests a different mechanism of K+ uptake in these cells.

scholarly journals The Influence of H+ on the Membrane Potential and Ion Fluxes of Nitella

1968 ◽  
Vol 52 (1) ◽  
pp. 60-87 ◽  
Author(s):  
Hiroshi Kitasato
Keyword(s):  
Membrane Potential ◽  
Membrane Conductance ◽  
Potential Difference ◽  
Potential Change ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Resting Membrane Potential ◽  
Ph Change ◽  
Ph Changes ◽  
External Ph

The resting membrane potential of the Nitella cell is relatively insensitive to [K]o, but behaves like a hydrogen electrode. K+ and Cl- effluxes from the cell were measured continuously, while the membrane potential was changed either by means of a negative feedback circuit or by external pH changes. The experiments indicate that PK and PCl are independent of pH but are a function of membrane potential. Slope ion conductances, GK, GCl, and GNa were calculated from efflux measurements, and their sum was found to be negligible compared to membrane conductance. The possibility that a boundary potential change might be responsible for the membrane potential change was considered but was ruled out by the fact that the peak of the action potential remained at a constant level regardless of pH changes in the external solution. The conductance for H+ was estimated by measuring the membrane current change during an external pH change while the membrane potential was clamped at K+ equilibrium potential. In the range of external pH 5 to 6, H+ chord conductance was substantially equal to the membrane conductance. However, the [H]i measured by various methods was not such as would be predicted from the [H]o and the membrane potential using the Nernst equation. In artificial pond water containing DNP, the resting membrane potential decreased; this suggested that some energy-consuming mechanism maintains the membrane potential at the resting level. It is probable that there is a H+ extrusion mechanism in the Nitella cell, because the potential difference between the resting potential and the H+ equilibrium potential is always maintained notwithstanding a continuous H+ inward current which should result from the potential difference.

Beta-adrenergic actions on membrane electrical properties of dissociated smooth muscle cells

1988 ◽  
Vol 254 (3) ◽  
pp. C423-C431 ◽  
Author(s):  
H. Yamaguchi ◽  
T. W. Honeyman ◽  
F. S. Fay
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Smooth Muscle Cells ◽  
Input Resistance ◽  
Muscle Cells ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Beta Adrenergic

Studies were carried out to determine the effects of the beta-adrenergic agent, isoproterenol (ISO), on membrane electrical properties in single smooth muscle cells enzymatically dispersed from toad stomach. In cells bathed in buffer of physiological composition, the average resting potential was -56.4 +/- 1.4 mV (mean +/- SE, n = 35). The dominant effect of exposure to ISO was hyperpolarization. The hyperpolarization was apparent in all cells studied and averaged 11.6 +/- 1.2 mV (n = 27). In the majority of the cells, hyperpolarization was accompanied by a decreased input resistance (Rin). Often the change in resistance appeared to lag behind the change in membrane potential. The lack of coincident changes in membrane potential and resistance may reflect a superposition of the outward rectification properties of the membrane on beta-adrenergic-induced increases in ionic conductance. In about half of the cells, an initial small depolarization (3.1 +/- 0.3 mV, n = 14) was accompanied by a small but distinct increase in Rin (12 +/- 2.5%). When membrane potential was made more negative than the estimated equilibrium potential for K+ (EK) by injection of current, ISO also produced biphasic effects, an initial hyperpolarization which reversed to a sustained depolarization to a value (-90 mV) near the estimated EK. The hyperpolarization by ISO could be diminished in a time-dependent manner by previous exposure to ouabain. The inhibition by ouabain, however, appeared to be a fortuitous result of glycoside-induced positive shifts in EK. These observations indicate that the dominant electrophysiological effect of beta-adrenergic stimuli is to hyperpolarize the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Ca2+-activated Cl− current in cultured myenteric neurons from murine proximal colon

2003 ◽  
Vol 284 (4) ◽  
pp. C839-C847 ◽  
Author(s):  
Sok Han Kang ◽  
Pieter Vanden Berghe ◽  
Terence K. Smith
Keyword(s):  
Membrane Potential ◽  
Channel Blocker ◽  
Reversal Potential ◽  
Outward Current ◽  
Proximal Colon ◽  
Time Dependent ◽  
Equilibrium Potential ◽  
Resting Membrane Potential ◽  
Myenteric Neurons ◽  
Whole Cell Patch Clamp

Whole cell patch-clamp recordings were made from cultured myenteric neurons taken from murine proximal colon. The micropipette contained Cs+ to remove K+ currents. Depolarization elicited a slowly activating time-dependent outward current ( I tdo), whereas repolarization was followed by a slowly deactivating tail current ( I tail). I tdo and I tail were present in ∼70% of neurons. We identified these currents as Cl− currents ( I Cl), because changing the transmembrane Cl− gradient altered the measured reversal potential ( E rev) of both I tdo and I tail with that for I tailshifted close to the calculated Cl− equilibrium potential ( E Cl). I Cl are Ca2+-activated Cl− current [ I Cl(Ca)] because they were Ca2+dependent. E Cl, which was measured from the E rev of I Cl(Ca) using a gramicidin perforated patch, was −33 mV. This value is more positive than the resting membrane potential (−56.3 ± 2.7 mV), suggesting myenteric neurons accumulate intracellular Cl−. ω-Conotoxin GIVA [0.3 μM; N-type Ca2+ channel blocker] and niflumic acid [10 μM; known I Cl(Ca) blocker], decreased the I Cl(Ca). In conclusion, these neurons have I Cl(Ca) that are activated by Ca2+entry through N-type Ca2+ channels. These currents likely regulate postspike frequency adaptation.

scholarly journals Transmitter Regulation of Plateau Properties in Turtle Motoneurons

1998 ◽  
Vol 79 (1) ◽  
pp. 45-50 ◽  
Author(s):  
Gytis Svirskis ◽  
Jørn Hounsgaard
Keyword(s):  
Membrane Potential ◽  
Metabotropic Glutamate Receptors ◽  
Input Resistance ◽  
Pattern Generation ◽  
Synaptic Activity ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
Type I ◽  
Plateau Potentials ◽  
Inward Current

Svirskis, Gytis and Jørn Hounsgaard. Transmitter regulation of plateau properties in turtle motoneurons. J. Neurophysiol. 79: 45–50, 1998. In motoneurons, generation of plateau potentials is promoted by modulators that block potassium channels. In voltage-clamp experiments with triangular voltage ramp commands, we show that cis-(±)-1-aminocyclopentane-1,3-dicarboxylic acid ( cis-ACPD) and muscarine promote the generation of plateau potentials by increasing the dihydropyridine sensitive inward current, by increasing the input resistance, and by depolarizing the resting membrane potential. Type I metabotropic glutamate receptors (mGluR I) mediate the effects of cis-ACPD. Baclofen suppresses generation of plateau potentials by decreasing the dihydropyridine sensitive inward current, by decreasing the input resistance, and by hyperpolarizing the resting membrane potential. These results suggest that membrane properties of motoneurons are continuously modulated by synaptic activity in ways that may have profound effects on synaptic integration and pattern generation.

Effects of sodium on beta-cell electrical activity

1982 ◽  
Vol 242 (5) ◽  
pp. C296-C303 ◽  
Author(s):  
B. Ribalet ◽  
P. M. Beigelman
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Two Phase ◽  
Sodium Permeability ◽  
Potential Spike ◽  
Presence And Absence

The present studies, designed to evaluate the contribution of Na+ to the mouse pancreatic beta-cell membrane potential, were performed utilizing intracellular microelectrodes. Complete removal of external sodium, in the presence of glucose, did not significantly affect spike peak potential. However, it caused a negative shift of the resting membrane potential, both in the presence and absence of glucose. After this initial hyperpolarization, the membrane gradually depolarized, the rate of depolarization being slower in the absence of glucose. This two-phase hyperpolarization-depolarization pattern remained when ouabain was added, both in the presence and absence of glucose. An increase of input resistance was associated with the slow depolarization. During this depolarization the maximum rate of rise (dV/dtmax) of the action potential (“spike”) decreased. There was no direct relationship between dV/dtmax and [Na]0. Readdition of low [Na]0 (14 mM) to a glucose medium reactivated the postburst hyperpolarization (PBH), even in the presence of ouabain. These observations indicate that there is a significant resting sodium permeability (PNa). However, the action potential (spike) is not generated by activation of a voltage-dependent (gated) sodium channel. The membrane depolarization after Na+ removal reflects concomitant inhibition of the Na+-K+ pump and decrease of potassium permeability (PK). The blockage of PBH in the absence of Na+ is not related to the inhibition of an oscillatory Na+-K+ pump but to the inactivation of a PK. Aside from its effect on the Na+-K+ pump, ouabain may stimulate PNa.

The effects of midazolam on hippocampal dentate gyrus granule neurons from young and old Fischer 344 rats

1989 ◽  
Vol 67 (4) ◽  
pp. 359-362 ◽  
Author(s):  
J. N. Reynolds ◽  
P. L. Carlen
Keyword(s):  
Membrane Potential ◽  
Dentate Gyrus ◽  
Spike Train ◽  
Hippocampal Slices ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Granule Neurons ◽  
Fischer 344 Rats ◽  
Fischer 344 ◽  
Central Neurons

The effects of midazolam (3 nM) perfusion on the membrane and synaptic properties of dentate gyrus granule neurons were examined in hippocampal slices obtained from young adult (4–6 months) and old (24–26 months) Fischer 344 rats. In young neurons, midazolam perfusion resulted in a hyperpolarization of the resting membrane potential with no apparent change in the input resistance. Midazolam perfusion also produced a significant increase in the amplitude of the post-spike train afterhyperpolarization (AHP). In neurons obtained from old animals, midazolam perfusion also produced a hyperpolarization of the resting membrane potential but did not signficantly change the AHP. These effects may result from altered calcium homeostasis in neurons of the aged brain, and suggest that at least some of the direct actions of benzodiazepines on mammalian central neurons are altered during aging.Key words: aging, midazolam, hippocampus, dentate granule neuron, post-spike train afterhyperpolarization.

Development of membrane conductance of chick skeletal muscle in culture

1980 ◽  
Vol 58 (6) ◽  
pp. 600-605 ◽  
Author(s):  
C. M. Thomson ◽  
W. F. Dryden
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Initial Level ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Resting Membrane Potential ◽  
Membrane Conductances ◽  
Rapid Changes ◽  
Fibre Development

Resting membrane potentials and membrane conductances of chick skeletal muscle in culture were determined from the 3rd to the 10th day after plating. The effect of tetraethylammonium (TEA) and of replacement of potassium with caesium on these parameters was investigated. Resting membrane potential (Em) rises during myogenesis in vitro and resting membrane conductance (Gm) falls. The initial level of Gm was relatively high (1.2 mS cm−2) but this fell to a final level around 0.2 mS cm−2. The most rapid changes in both parameters occurred between days 3 and 5 of culture. Both TEA and caesium depressed Em and Gm at all stages of development. On the 3rd day of culture Gm was reduced by 0.2 mS cm−2 by both agents. Thereafter, Gm was depressed by about 0.1 mS cm−2. Caesium does not penetrate potassium channels and the reduction in Gm is attributed to block of these channels. This indicates that resting potassium conductance is relatively constant at 0.1 mS cm−2 throughout muscle fibre development. Because TEA produces changes in Gm similar to those produced by caesium, TEA is concluded to be acting at the potassium channel in a manner similar to caesium.

Electrical properties of frog motoneurons in the in situ spinal cord

1976 ◽  
Vol 39 (3) ◽  
pp. 459-473 ◽  
Author(s):  
P. C. Magherini ◽  
W. Precht
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Rana Temporaria ◽  
Reversal Potential ◽  
Input Resistance ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Spike Initiation

Electrical properties of the spinal motoneurons of Rana temporaria and R. esculenta were investigated in the in situ spinal cord at 20-22 degrees C by means of intracellular recording and current injection. Input resistance values depended on the method of measurement in a given cell but were generally inversely related to axon conduction velocity. The membrane-potential response to a subthreshold current pulse was composed of at least two exponentials with mean time constants of 2.5 and 20 ms. The membrance potential reached by the peak of a spike depended on the mode of spike initiation and membrane potential. Preceding a suprathreshold depolarization by a hyperpolarizing pulse could delay and eliminate spike initiation, similar to effects reported in certain invertebrate neurons. Antidromic invasion frequently failed in motoneurons of normal resting potential. Antidromic spike components (m,IS, SD) were similar to those of cat motoneurons. The delayed depolarization and the long afterhyperpolarization following an antidromic spike had many properties in common with the analogous afterpotentials of cat motoneurons. The reversal potential of the short afterhyperpolarization occurring immediately after the spike varied with resting potential and could not be used to determine potassium equilibrium potential. Sustained rhythmic firing could be evoked by continuous synaptic drive or long pulses of injected current. The plot of firing rate versus current strength had a substantial linear region. Both steady firing and adaptation properties varied markedly with motoneuron input resistance.

Membrane Resting Potential of Thalamocortical Relay Neurons Is Shaped by the Interaction Among TASK3 and HCN2 Channels

2006 ◽  
Vol 96 (3) ◽  
pp. 1517-1529 ◽  
Author(s):  
Sven G. Meuth ◽  
Tatyana Kanyshkova ◽  
Patrick Meuth ◽  
Peter Landgraf ◽  
Thomas Munsch ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Standard Procedure ◽  
Resting Potential ◽  
Immunocytochemical Staining ◽  
Equilibrium Potential ◽  
Resting Membrane Potential ◽  
Hcn Channels ◽  
Extracellular Acidification ◽  
Knock Out ◽  
Task Channels

By combining molecular biological, electrophysiological, immunological, and computer modeling techniques, we here demonstrate a counterbalancing contribution of TASK channels, underlying hyperpolarizing K+ leak currents, and HCN channels, underlying depolarizing Ih, to the resting membrane potential of thalamocortical relay (TC) neurons. RT-PCR experiments revealed the expression of TASK1, TASK3, and HCN1–4. Quantitative determination of mRNA expression levels and immunocytochemical staining demonstrated that TASK3 and HCN2 channels represent the dominant thalamic isoforms and are coexpressed in TC neurons. Extracellular acidification, a standard procedure to inhibit TASK channels, blocked a TASK current masked by additional action on HCN channels. Only in the presence of the HCN blocker ZD7288 was the pH-sensitive component typical for a TASK current, i.e., outward rectification and current reversal at the K+ equilibrium potential. In a similar way extracellular acidification was able to shift the activity pattern of TC neurons from burst to tonic firing only during block of Ih or genetic knock out of HCN channels. A single compartmental computer model of TC neurons simulated the counterbalancing influence of TASK and HCN on the resting membrane potential. It is concluded that TASK3 and HCN2 channels stabilize the membrane potential by a mutual functional interaction, that the most efficient way to regulate the membrane potential of TC neurons is the converse modulation of TASK and HCN channels, and that TC neurons are potentially more resistant to insults accompanied by extracellular pH shifts in comparison to other CNS regions.

Inward rectifier K+ channel Kir2.3 is localized at the postsynaptic membrane of excitatory synapses

2002 ◽  
Vol 282 (6) ◽  
pp. C1396-C1403 ◽  
Author(s):  
Atsushi Inanobe ◽  
Akikazu Fujita ◽  
Minoru Ito ◽  
Hitonobu Tomoike ◽  
Kiyoshi Inageda ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Granule Cells ◽  
Pdz Domain ◽  
Postsynaptic Membrane ◽  
Equilibrium Potential ◽  
K Channel ◽  
Resting Membrane Potential ◽  
Kir Channel ◽  
Anchoring Proteins

Classical inwardly rectifying K+ channels (Kir2.0) are responsible for maintaining the resting membrane potential near the K+ equilibrium potential in various cells, including neurons. Although Kir2.3 is known to be expressed abundantly in the forebrain, its precise localization has not been identified. Using an antibody specific to Kir2.3, we examined the subcellular localization of Kir2.3 in mouse brain. Kir2.3 immunoreactivity was detected in a granular pattern in restricted areas of the brain, including the olfactory bulb (OB). Immunoelectron microscopy of the OB revealed that Kir2.3 immunoreactivity was specifically clustered on the postsynaptic membrane of asymmetric synapses between granule cells and mitral/tufted cells. The immunoprecipitants for Kir2.3 obtained from brain contained PSD-95 and chapsyn-110, PDZ domain-containing anchoring proteins. In vitro binding assay further revealed that the COOH-terminal end of Kir2.3 is responsible for the association with these anchoring proteins. Therefore, the Kir channel may be involved in formation of the resting membrane potential of the spines and, thus, would affect the response of N-methyl-d-aspartic acid receptor channels at the excitatory postsynaptic membrane.

Sign in / Sign up

Export Citation Format

Share Document