Effects of intracellular potassium and sodium injections on the inhibitory postsynaptic potential

Two barrels of double microelectrodes have been filled with different salts so that the electrophoretic injection of Na + and K + ions could be investigated in alternating sequence on the same motoneuron in the cat spinal cord. The effects of these injections on the mechanism generating the IPSP were evaluated by determining the equilibrium potential for the IPSP (the E IPSP ), i. e. the membrane potential at which the IPSP is zero. Such determinations have been made every 5 to 10 s after ion injections and have provided the most direct evidence of the ionic mechanism generating the IPSP . Comparison of the Na + and K + ion injections shows that the former injection always displaced the E IPSP much farther in the depolarizing direction and that recovery was much slower, with a half-time of 70 to 120 s, in contrast to about 20 s after the K + injection. In the discussion and evaluation of these results it was postulated that almost all of the displacement of the E IPSP in the depolarizing direction was due to the increased intracellular Cl - concentration, the (Cl - ) i . Under normal conditions a high (Cl - ) i declines by diffusional exchange across the cell membrane with a half-time of about 20 s, but this decline is much slower when the internal potassium is depleted. An explanation of this difference will be given in the following paper.

1976 ◽  
Vol 231 (4) ◽  
pp. 1214-1219 ◽  
Author(s):  
JF White

Intracellular potassium activity (aKi) has been determined in absorptive cells lining the villi of isolated, stripped proximal segments of Amphiuma small intestine. With single-barreled liquid ion-exchanger microelectrodes aKi = 41.6 +/- 1.5 mM in normal chloride buffer; with double-barreled microelectrodes constructed by a new method aKi = 38.5 +/- 2.4 mM. Also, by the latter approach aKi = 41.1 +/- 2.1 mM in buffer in which potassium was elevated to 5 meq/liter and aKi = 44.2 +/- 1.3 mM in sulfate buffer with the same bath potassium concentration. Since the calculated potassium equilibrium potential exceeds the membrane potential this ion is accumulated by the intestinal absorptive cell. A major portion of cellular potassium is bound or compartmentalized since the intracellular potassium activity coefficient is very low. A layer exists near the villi in which the potassium activity exceeds that in the bath buffer solution.


1966 ◽  
Vol 49 (3) ◽  
pp. 551-563 ◽  
Author(s):  
Ronald J. Poole

Intracellular potentials were measured in beetroot tissue during the steady-state uptake of K+ from various solutions. In solutions containing bicarbonate, the membrane potential becomes up to 70 mv more negative than the estimated equilibrium potential for K+. The uptake of K+ from such solutions is correlated with variations in the potential, both when the bicarbonate concentration is changed and also when the metabolic activity of the tissue is changed by washing in water for various periods. However, the estimated permeability to K+ varies from 0.4 x 10-7 to 1.5 x 10-7 cm·sec-1. It is postulated that the change of potential arises from the metabolic transport of HCO3- into the cell or H+ outwards, and that the associated uptake of K+ is partly or entirely by passive diffusion across the cell membrane. In contrast, K+ uptake from KCl solutions is not accompanied by any significant change in the membrane potential, which remains relatively close to the K+ equilibrium potential. In solutions containing both KHCO3 and KCl, it appears that an amount of K+ equal to the influx of Cl- is taken up independently of the potential, while the component of K+ uptake which is not balanced by Cl- uptake is related to the potential in the manner described. These results suggest that K+ uptake is linked to Cl- uptake in an electrically neutral active transport process.


1976 ◽  
Vol 39 (3) ◽  
pp. 459-473 ◽  
Author(s):  
P. C. Magherini ◽  
W. Precht

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.


1976 ◽  
Vol 67 (6) ◽  
pp. 621-638 ◽  
Author(s):  
S Hagiwara ◽  
S Miyazaki ◽  
N P Rosenthal

The kinetics of the membrane current during the anomalous or inward-going rectification of the K current in the egg cell membrane of the starfish Mediaster aequalis were analyzed by voltage clamp. The rectification has instantaneous and time-dependent components. The time-dependent increase in the K conductance for the negative voltage pulse as well as the decrease in the conductance for the positive pulse follows first-order kinetics. The steady-state conductance increases as the membrane potential becomes more negative and reaches the saturation value at about -40 mV more negative than the K equilibrium potential, V(K). The entire K conductance can be expressed by g(K).n; g g(K) represents the component for the time-independent conductance which depends on V-V(K) and [K+]o, and n is a dimensionless number (1 is greater than or equal to n is greater than or equal to 0) and determined by two rate constants which depend only on V-V(K). Cs+ does not carry any significant current through the K channel but blocks the channel at low concentration in the external medium. The blocking effect increases as the membrane potential is made more negative and the potential-dependent blocking by the external Cs+ also has instantaneous and time-dependent components.


1978 ◽  
Vol 71 (1) ◽  
pp. 69-92 ◽  
Author(s):  
G Waloga ◽  
W L Pak

The ionic mechanism of horizontal cell potentials was investigated in the isolated retina of the axolotl Ambystoma mexicanum. The membrane potentials of both receptors and horizontal cells were recorded intracellularly while the ionic composition of the medium flowing over the receptor side of the retina was changed. The membrane potential of the horizontal cell is highly depender side of the retina was changed. The membrane potential of the horizontal cell is highly dependent on the extracellular concentration of sodium. When the external ion concentration of either chloride or potassium was changed independently of the other, there were shifts in the membrane potential of the horizontal cell which could not be explained by changes in the equilibrium potential of these ions. If the external concentrations of both potassium and chloride ions were varied so that the product of their external concentrations did not change, the shift in the membrane potential of the horizontal cell was in the direction predicted by the Nernst equation. The results are consistent with the suggestion that in the dark the receptors release a synaptic transmitter which increases primarily the sodium conductance of the horizontal cell postsynaptic membrane.


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