Extracellular potassium regulates the chloride reversal potential in cultured hippocampal neurons
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Hyperpolarization
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The mechanisms by which K+ relaxes circular muscles of pig duodenum were investigated, and compared with the response of the longitudinal muscles to K+. Circular muscles were concentration-dependently relaxed by 8.3-23.6 mM K+, but contracted by 47.2-143.4 mM K+. Longitudinal muscles were contracted by 11.8-94.4 mM K+. The relaxation of circular muscles was correlated with hyperpolarization (4 mV), but evoked Ca2+ spikes were not suppressed. Neither ouabain (0.14 microM) nor phentolamine (10 microM) blocked the relaxation, but tetrodotoxin (TTX, 0.63 microM) blocked both the relaxation and hyperpolarization. Mesaconitine (0.16 microM) increased the relaxation. Inhibitory junction potentials and concomitant relaxations were also blocked by TTX. The results suggest that K+-induced relaxation is caused by the release of a non-adrenergic inhibitory transmitter.
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1. Two types of after‐potentials in the stretch receptor neurone of crayfish are described. 2. A short‐duration after‐hyperpolarization associated with a single spike or a few spikes is diminished and reversed on applying hyperpolarizing currents. However, a much longer‐lasting post‐tetanic hyperpolarization (PTH) is enhanced by conditioning hyperpolarization; thus, no reversal potential can be obtained. 3. No changes in membrane conductance occur during PTH. 4. Reducing K concentration in the bathing fluid diminishes PTH, while it shifts the reversal potential of the short after‐potential toward greater negativity. 5. Replacement of Na with Li, or addition of 2,4‐dinitrophenol in the bathing fluid suppresses PTH in a reversible manner. 6. Electrophoretic injection of Na into the cell induces a long‐lasting hyperpolarization. 7. No change in K‐equilibrium potential, as indicated by the reversal point of the short after‐potential, is detected during PTH. 8. It is concluded that the short after‐potential is caused by a permeability increase for potassium ion, whereas PTH is produced by an electrogenic Na‐pump.
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Abstract In the presence of Ba ++ , an increase in the bath HCO at constant CO 2 (i.e., Variable bath pH) produced a hyperpolarization. The hyperpolarizing effect of adding HCO 3 − /CO 2 at constant bath pH was not significantly affected by the presence of 50 μmol/l strophanthidin. In the absence of Ba ++ , addition of HCO 3 − /CO 2 at constant bath pH produced a Na + ‐dependent hyperpolarization. Therefore, CO 2 movements, electrogenic Na + /K + pump activity and changes in Ba ++ binding do not contribute significantly to the hyperpolarization induced by HCO 3 − . These results along with the results of previous studies (Astion et al: J Gen Physiol 93:731, 1989) strongly suggest that the hyperpolarization induced by the addition of HCO 3 − is due to an electrogenic Na + /HCO 3 − cotransporter, which transports Na + , HCO 3 − (or its equivalent), and net negative charge across the glial membrane. To study the role of electrogenic Na + /HCO cotransport in the regulation of pHi in glial cells, we used intracellular double‐barreled, pH‐sensitive microelectrodes. At a bath pH of 7.5, the mean initial intracellular pH (pH i ) was 7.32 (SD 0.03, n = 6) in HEPES‐buffered Ringer's solution and 7.39 (SD 0.1, n = 6) in HCO 3 − /CO 2 buffered solution. These values for pH i are more than 1.2 pH units alkaline to the pH i predicted from a passive distribution of protons; thus, these cells actively regulated pH i . Superfusion and with‐drawal of 15 mmol/l NH 4 + induced an acidification of 0.2 to 0.3 pH units, which recovered toward the original steady‐steady‐state pH i . Recovery from acidification was stimulated by adding HCO 3 − /CO 2 at constant pH. In HCO 3 − /CO 2 ‐buffered solutions, the recovery was Na + ‐dependent, inhibited by 4‐acetamido‐4′‐isothiocyanato‐stilbene‐2,2′‐disulfonic acid (SITS), and associated with a hyperpolarization of the membrane. Thus it appears that the electrogenic Na + /HCO 3 − cotransporter helps maintain the relatively alkaline pH i of glial cells and also contributes to the ability of glial cells to buffer changes in pH in the neuronal microenvironment.
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Intracellular recordings were made from neurones of the myenteric plexus of the guinea-pig ileum.The slow after-hyper- polarization which followed an action poten- tial in some neurones was abolished by Mn++, La+++ and by solutions which contained no Ca++.In these neurones, the action potential and the slow after-hyperpolarization persisted in Na+-free solutions or in the presence of tetrodotoxin (2 ,M).The findings suggest that an inward Ca++ current during the action potential is essential for the slow after- hyperpolarization.
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A slow hyperpolarization‐activated inwardly rectifying K + current ( I K(SHA) ) with novel characteristics was identified from the mouse embryonic hippocampus x neuroblastoma cell line HN9.10e. The non‐inactivating current activated negative to a membrane potential of −80 mV with slow and complex activation kinetics ( τ act ≈ 1–7 s) and a characteristic delay of 1–10 s (−80 to −140 mV) that was linearly dependent on the membrane potential. Tail currents and instantaneous open channel currents determined through fast voltage ramps reversed at the K + equilibrium potential ( E K ) indicating that primarily K + , but not Na + , permeated the channels. I K(SHA) was unaffected by altering the intracellular Ca 2+ concentration between ∼0 and 10 μ m , but was susceptible to block by 5 m m extracellular Ca 2+ , Ba 2+ ( K 1 = 0.42 m m ), and Cs + ( K 1 = 2.77 m m ) In cells stably transformed with M2 muscarinic receptors, I K(SHA) was rapidly, but reversibly, suppressed by application of micromolar concentrations of muscarine. At the single channel level K(SHA) channel openings were observed with the characteristic delay upon membrane hyperpolarization. Analysis of unitary currents revealed an inwardly rectifying I–V profile and a channel slope conductance of 7 pS. Channel activity persisted in the inside‐out configuration for many minutes. It is concluded that I K(SHA) m HN9.10e cells represents a novel K + current, which is activated upon membrane hyperpolarization. It is functionally different from both classic inwardly rectifying I kir currents and other cationic hyperpolarization‐activated 7 H currents that have been previously described in neuronal or glial cells.
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1. Effects of membrane polarization and of reduction in external K and Cl concentration on the inhibitory potential were investigated in the guinea‐pig taenia coli. 2. Depolarization of the membrane increased the inhibitory potential while hyperpolarization decreased it. The relationship between the degree of membrane polarization and the amplitude of inhibitory potential was linear. The inhibitory potential was abolished or slightly reversed in polarity, when the membrane was hyperpolarized by 25–40 mV in different preparations. 3. Removal of external K ion depolarized the membrane for about 5 min and increased the inhibitory potential more than could be accounted for by the depolarization. Readmission of K transiently hyperpolarized the membrane, probably due to an activation of the Na‐K pump, and reduced the inhibitory potential, but no reversal of polarity in the inhibitory potential was observed during this hyperpolarizing phase. 4. The membrane was transiently depolarized when the external Cl concentration was reduced by substituting with isethionate. Hyperpolarization was produced by restoring the external Cl concentration to normal. Changes in the amplitude of inhibitory potentials during alterations in Cl concentration occurred as expected from the shift of the membrane potential. 5. From the results, it is concluded that the membrane conductance is increased during the inhibitory potential, and that an increase in the K permeability is the main factor for hyperpolarization of the membrane.
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