Slow inward current in aggregates of neonatal rat heart cells and its contribution to the steady state current-voltage relationship

1983 ◽  
Vol 397 (4) ◽  
pp. 265-271 ◽  
Author(s):  
A. C. G. van Ginneken ◽  
H. J. Jongsma
1997 ◽  
Vol 77 (1) ◽  
pp. 221-228 ◽  
Author(s):  
Anita Lüthi ◽  
Beat H. Gähwiler ◽  
Urs Gerber

Lüthi, Anita, Beat H. Gähwiler, and Urs Gerber. 1 S,3 R-ACPD induces a region of negative slope conductance in the steady-state current-voltage relationship of hippocampal pyramidal cells. J. Neurophysiol. 77: 221–228, 1997. Synaptic responses mediated by metabotropic glutamate receptors (mGluRs) display a marked voltage-dependent increase in amplitude when neurons are moderately depolarized beyond membrane potential. We have investigated the basis for this apparent nonlinear behavior by activatingmGluRs with 1 S,3 R-1-aminocyclopentane-1,3-dicarboxylate(1 S,3 R-ACPD; 10 μM) in CA3 pyramidal cells from rat hippocampal slice cultures with the use of the single-electrode voltage-clamp technique. Under control conditions, cells depolarized from resting potential by 10–20 mV responded with delayed outwardly rectifying currents due to activation of voltage- and Ca2+-dependent K+ conductances. In contrast, in the continuous presence of 1 S,3 R-ACPD, small depolarizations (10–20 mV) induced a delayed inward current. The steady-state current-voltage relationship for this response displayed a region of negative slope conductance at potentials between −55 and −40 mV. The reversal potential of the corresponding 1 S,3 R-ACPD-sensitive tail currents (−93.0 ± 2.2 mV, mean ± SE) was close to the potassium reversal potential, consistent with an mGluR-mediated suppression of K+ current. When external K+ concentration was increased to 8 mM, there was a positive shift in reversal potential to −76.9 ± 5.1 mV. The depolarization-induced inward current in the presence of 1 S,3 R-ACPD was blocked by Ba2+ (1 mM). The response was not dependent on changes in intracellular Ca2+ concentration and was insensitive to bath-applied Cs+ (1 mM), ruling out a contribution of Ca2+-dependent currents or the inward rectifier I Q. Furthermore, the effect of 1 S,3 R-ACPD was not mimicked by inhibiting afterhyperpolarizing current and M current with low-Ca2+ saline (0.5 mM Ca2+, 10 mM Mg2+) containing 10 mM tetraethylammonium chloride. A comparison of the responses induced by 1 S,3 R-ACPD and N-methyl-d-aspartate showed that both induce an inward current with small depolarizations from resting potential but with different kinetics and Mg2+ sensitivity. These results indicate that the suppression of K+ currents in response to activation of mGluRs is markedly voltage dependent, increasing at depolarized potentials and decreasing at hyperpolarized potentials. The negative slope conductance at membrane voltages positive to resting potential may underlie the amplification of mGluR-mediated responses when the membrane potential approaches action potential threshold.


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


1979 ◽  
Vol 58 (2) ◽  
pp. 117-123 ◽  
Author(s):  
Klara Csete ◽  
Marie-Claude Auclair ◽  
Paul Lechat

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