Action of Lindane on the Current-Voltage Relationship in the Plasma Membrane of Elodea under Passive Conditions

1979 ◽  
Vol 34 (11) ◽  
pp. 1072-1074 ◽  
Author(s):  
Kurt Schefczik ◽  
Wilhelm Simonis

Abstract Side effects of the chlorinated hydrocarbon insecticide Lindane on the plasma membrane of the submerged macrophytic fresh-water plant Elodea densa were studied. Single glass microelectrodes were inserted into single cells and membrane potential, membrane resistance and electrode resistance were recorded using a new designed electrophysiological monitoring system (“ELM 2”). The current-voltage relationship in the plasma membrane of Elodea cells under passive conditions is nearly linear for relaxing current pulses up to 10-8 amperes. Lindane treatment, produced first (3.5 hours) a strong nonlinearity in current-voltage relationship with increased membrane resistance for inward current flow, and later (24.5 hours) an increased membrane resistance both for inward and outward current flow. It is discussed that the earlier reported lowering of the potassium selectivity in the plasma membrane of Elodea after Lindane treatment will be the reason for the alterations of current-voltage relationship.

1990 ◽  
Vol 151 (1) ◽  
pp. 21-39 ◽  
Author(s):  
JONATHAN A. DAVID ◽  
DAVID B. SATTELLE

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


1998 ◽  
Vol 79 (3) ◽  
pp. 1230-1238 ◽  
Author(s):  
Paul Schweitzer ◽  
Samuel G. Madamba ◽  
George R. Siggins

Schweitzer, Paul, Samuel G. Madamba, and George R. Siggins. Somatostatin increases a voltage-insensitive K+ conductance in rat CA1 hippocampal neurons. J. Neurophysiol. 79: 1230–1238, 1998. Somatostatin (SST) is a neuropeptide involved in several central processes. In hippocampus, SST hyperpolarizes CA1 pyramidal neurons and augments the K+ M current ( I M). However, the limited involvement of I M at resting potential in these cells suggests that the peptide also may modulate another channel to hyperpolarize hippocampal pyramidal neurons (HPNs). We studied the effect of SST on noninactivating conductances of rat CA1 HPNs in a slice preparation. Using MK886, a specific inhibitor of the enzymatic pathway that leads to the augmentation of I M by SST, we have uncovered and characterized a second conductance activated by the peptide. SST did not affect I M when applied with MK886 or the amplitudes of the slow Ca2+-dependent K+ afterhyperpolarization-current and the cationic Q current but still caused an outward current, indicating that SST acts upon another conductance. In the presence of MK886, SST elicited an outward current that reversed around −100 mV and that displayed a linear current-voltage relationship. Reversal potentials obtained in different external K+ concentrations are consistent with a conductance carried solely by K+ ions. The slope of the current-voltage relationship increased proportionately with the extracellular K+ concentration and remained linear. This suggests that SST opens a voltage-insensitive leak current ( I K(L)) in HPNs not an inwardly rectifying K+ current as reported in other neuron types. A low concentration of extracellular Ba2+ (150 μM) only slightly decreased the SST-induced effect in a voltage-independent manner, whereas a high concentration of Ba2+ (2 mM) completely blocked it. Extracellular Cs+ (2 mM) did not affect the outward SST current but inhibited the inward component. We conclude that SST inhibits HPNs by activating two different K+ conductances: the voltage-insensitive I K(L) and the voltage-dependent I M. The hyperpolarizing effect of SST at resting membrane potential appears to be mainly carried by I K(L), whereas I M dominates at slightly depolarized potentials.


1991 ◽  
Vol 6 (1) ◽  
pp. 69-74
Author(s):  
Lawrence H. Pinto ◽  
Akimichi Kaneko

AbstractTotal RNA was purified from freshly isolated retinas of adult carp and injected into oocytes of Xenopus laevis (stage 5–6). Two to six days after injection, depolarizing voltage-clamp steps evoked a slowly activated outward currents as large as 3 μA. This current inactivated slowly with a single time constant (τ= 3.1 ± 0.24 S.E.M., for Vm= +30 mV). The current was inhibited by tetraethylammonium (3.8 mM for half-maximal inhibition). In the presence of Co2+ (1 mM) or barium methanesulfonate (40 mM), the current-voltage relationship shifted to slightly more depolarized values (5–10 mV); the maximal value of the current that was sensitive to Co2+ or Ba2+ treatments was only a small fraction (about 10%) of the TEA-sensitive current, and its current-voltage relationship was similar to that for uninjected oocytes. The reversal potential of the membrane current was studied with [K+]0 of 1–77 mM. For [K+]0 > 20 mM, the reversal potential changed with a slope of 63 mV (±;2 mV S.E.M.) per 10-fold change in [K+]0. The conductance was induced half-maximally at 17 mV (±;0.9 mV s.e.m.). The depolarization required for an e−fold increase in conductance was 13 mV (±;0.6 mV s.e.m.). From these results, we conclude that the injection of total RNA from carp retinas induces the formation of a membrane K+ channel in Xenopus oocytes. The channel formed has many of properties reported for the maintained outward current of goldfish horizontal and bipolar cells.


eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Shigetomo Suyama ◽  
Alexandra Ralevski ◽  
Zhong-Wu Liu ◽  
Marcelo O Dietrich ◽  
Toshihiko Yada ◽  
...  

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.


1996 ◽  
Vol 270 (6) ◽  
pp. C1807-C1814 ◽  
Author(s):  
L. Liu ◽  
S. A. Simon

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.


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

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