Activation of K+ currents in cultured Schwann cells is controlled by extracellular pH

Hoppe, D.; Lux, H. D.; Schachner, Melitta; Kettenmann, Helmut

doi:10.1007/bf00373137

Cited by 22 publications

(31 citation statements)

References 27 publications

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“…9B). Contrary to results in rabbit and rat cultured Schwann cells (Howe & Ritchie, 1989) and similarly to Hoppe, Lux, Schachner & Kettermann, (1989) in the same preparation as ours, no sign of an inward Na+ current was found with this protocol in any of the twenty-five cells tested. Among the different criteria proposed by Hagiwara & Byerly (1981) for identifying voltage-dependent Ca21 channels, are listed: persistence of the signal when Ca2+ in the external solution is replaced by Ba2+ or strontium (Sr2+), insensitivity of the signal to high concentrations of tetrodotoxin (TTX) and blockage of the signal by Co2+.…”

Section: Lack Of Na+ Current In Mouse Schwann Cellscontrasting

confidence: 92%

“…1987 (Shrager et al 1985), rabbits (Chiu et al 1984) and mice (Konishi, 1989a). In the same preparation as ours, Hoppe et al (1989) reported the presence of voltage-dependent and pH-sensitive K+ currents. According to differences in voltage dependence, inactivation kinetics and pharmacological properties, we conclude that mouse Schwann cells in our cultures display two types of K' currents.…”

Section: Discussionsupporting

confidence: 67%

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Voltage‐dependent calcium and potassium channels in Schwann cells cultured from dorsal root ganglia of the mouse.

Amédée

Ellie

Dupouy

et al. 1991

The Journal of Physiology

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SUMMARY1. Whole-cell patch clamp studies were carried out on Schwann cells in organotypic cultures of dorsal root ganglia (DRG) from OFI mice embryos (18-19 days).2. In standard external solution, from a holding potential of -70 mV, two types of voltage-dependent K+ currents were recorded: a fast transient current and a delayed sustained current. With a holding potential of -30 mV, only the delayed sustained current could be evoked.3. Both K+ currents were inhibited by tetraethylammonium chloride (TEA) and 4-aminopyridine (4-AP) in a dose-dependent manner. For the transient current the half-maximal effective dose was 100 mm for TEA and 13 mm for 4-AP. For the delayed sustained current the half-maximal effective dose was 11 mm for TEA and 4 mM for 4-AP. Both currents were insensitive to external Ca2".4. The delayed sustained current, isolated by use of a holding potential of -30 mV displayed a 'cumulative inactivation' which was removed by hyperpolarizing the membrane to -70 mV between each test pulse.5. In K+-free external and pipette solutions, with 10 mM-external Ca2+, from a holding potential of -70 mV voltage-dependent Ca21 channel currents were recorded. The threshold for activation was -453 + 5-4 mV (mean + S.D., n = 5) and the current inactivated fully at the end of the test potential. The current was unaffected by 2 /IM-tetrodotoxin (TTX) and totally blocked by 5 mM-Co2+.6. Equimolar replacement of external Ca2' by Ba2+ did not significantly modify the voltage dependence (threshold for activation -428+64 mV, n = 7) or the magnitude of the inward current. Ca2+ and Ba2+ were equally permeant. The fully inactivating current was insensitive to both nifedipine and Bay K 8644 (1 1aM each). Increasing the external Ba2+ concentration from 10 to 89 mm enhanced the Ba2c urrent and shifted the voltage dependence of the current (threshold for activation, -30 5 + 7-3 mV, n = 9) along the voltage axis as expected for altered external surface potential.7. In 89 mM-external Ba2+ solution, some cells displayed an additional slowly decaying current which was totally blocked by nifedipine (1 1M).*To whom correspondence and reprint requests should be sent. M5S 91422-2 36 T. AMEDEE, E. ELLIE, B. DUPOUTY AND J. D. VINCENT 8. Ca2" channel currents were recorded only when DRG neurons were present in the culture, as excision of explants and subsequent axonal degeneration led to loss of detectable Ca2" channel currents. This phenomenon was never observed for K+ currents.9. We conclude that mouse Schwann cells in organotypic culture possess voltagedependent K+ and Ca2" channels. The fast transient K+ current is similar to 'A' currents described in numerous neuronal cells. The delayed sustained current is similar to the delayed rectifier K+ current widely distributed among excitable cells. Two types of Ca2" channel currents are present on mouse Schwann cells: a fully inactivating current which resembles the T-type current more particularly described in neuronal cells and a slowly decaying current similar to the L-type current. DRG ...

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Section: Lack Of Na+ Current In Mouse Schwann Cellscontrasting

confidence: 92%

Section: Discussionsupporting

confidence: 67%

Voltage‐dependent calcium and potassium channels in Schwann cells cultured from dorsal root ganglia of the mouse.

Amédée

Ellie

Dupouy

et al. 1991

The Journal of Physiology

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“…Conversely, in non-inactivating channels the mean open probability continuously increased with depolarization. The heterogeneity in time-dependence of single channel behaviour is also reflected in a heterogeneity of whole cell currents recorded from different Schwann cells (Hoppe et al, 1989). Eighty-four percent of cells inactivated, and the time constant of inactivation and its voltage dependence were similar to the values obtained from averaged single channel recordings (Fig.…”

Section: Time Dependent Gating Properties Of Single K + Channelsmentioning

confidence: 78%

Single K⁺ channel properties in cultured mouse Schwann cells: Conductance and kinetics

Verkhratsky¹,

Hoppe²,

Kettenmann³

1991

J of Neuroscience Research

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Cultured Schwann cells are characterized by a strong outward rectification of the membrane; the threshold of the outward currents is close to the resting membrane potential of about -50 mV (Gray et al.: In Ritchie, Keynes (eds): Ion Channels in Neural Membranes. New York: Alan R. Liss, Inc., pp 145-157, 1986). These outward currents show up a heterogeneity among the cultured Schwann cells: some cells displayed inactivating, others non-inactivating outward currents (Hoppe et al.: Pflügers Arch 415:22-28, 1989). In this study we characterized the single channel currents using the patch-clamp technique in the intact patch recording configuration. The conductance of all recorded channels was 10-12 pS (5.6 mM [K+]o). These channels were K+ selective since changes in extracellular [K+] resulted in changes of the reversal potential as predicted for an exclusively K+ selective pore. The reversal potentials also predicted an intracellular [K+] of 60 mM indicating that the K+ equilibrium potential is slightly negative to the membrane potential. Analysis of the kinetic behavior of the channels resolved two different types of behaviour: 40% inactivated during a depolarizing voltage step, the others showing no sign of inactivation. The analysis of open probability and gating properties in the steady state showed up more differences between these two channel types: mean open probability peaked at about 10 mV for inactivating channels, while it continuously increased for non-inactivating channels. The inactivation time constants of averaged single channel and whole cell currents were similar and showed both a similar voltage dependency. We conclude that cultured Schwann cells express either two types of K+ channels with similar conductance or a channel which can acquire two functional states and that these channels can account for the different types of K+ currents observed in these cells.

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“…In opossum kidney cells, inwardly rectifying K+ channels were activated by a more alkaline pH (Ohno-Shosaku, Kubota, Yamaguchi & Fujimoto, 1990): the potassium current of cultured Schwann cells was also inhibited by external H+ (Hoppe, Lux, Schachner & Kettenmann, 1989). All these channels were influenced by changes within the physiological pHi range, whereas in the cardiac KATP channel, it was blocked by a strong acidic pHi below 6-0.…”

Section: Effects Of H+ On Katp Channels In Atp-free Solutionmentioning

confidence: 97%

ATP‐regulated K+ channels are modulated by intracellular H+ in guinea‐pig ventricular cells.

Koyano

Kakei

Nakashima

et al. 1993

The Journal of Physiology

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SUMMARY1. The ATP-regulated potassium channel (KiATP) was investigated with respect to modulation by intracellular pH (pHi) by using the inside-out membrane patch clamp technique in ventricular cells isolated from the heart of the guinea-pig. Channels which had been closed by internal ATP (0 3-3 mM) were dose-dependently activated by decreasing the pHi over the range of pH 7-6-6-0. However, the channel was conversely inhibited when the pHi was further decreased below 6-0. Inwardly rectifying K+ channels were also decreased in activity when pHi fell from 7-2 to 6-0.2. The channel activation was also observed with constant concentration of free Ca2+ (1 nM) and Mg2+ (1 mM) in the bathing solution, suggesting that a change in divalent cation concentration is not involved in channel modulation by pHi.3. When the dose-response relations of the channel activity for ATP concentrations at different pHi were examined, the channel activity obtained at 1 /tM ATP was increased by decreasing pH from 7-2 to 6-4. The half-maximal inhibition for ATP concentration at pH 7-2 and 6-4 was 20 and 40 ,(M, respectively, and the Hill coefficient was 2-5 in both curves.4. In the absence of ATP, internal H+ was able to reactivate run-down channels but it had less effect on the channel as long as the activity was maintained at a higher level. The increase in the channel activity by H+ was facilitated with a proceeding of the run-down. However, after the channel was completely inactivated by a long exposure of the membrane patch to ATP-free solution, a reduction of pH could not activate the channel.5. The decrease of pH from 7-2 to 6-4 reduced single channel conductance from 89-0 to 77-7 pS in the absence of Mg2+, whereas it reduced the conductance only at the negative membrane potentials in the presence of 2 mm Mg2+.6. Mean open and closed times within the burst-like openings of the channel remained unaffected during the change in pHi.7. We conclude that the cardiac KATP channel is modulated by a change in the intracellular pH. The channel modulation consisted of the increase in the channel * To whom offprints should be requested. MS 9964T. KOYANO AND OTHERS activity and a decrease in the permeability. The former effect was due to the decrease in the sensitivity of the channel to ATP and the reactivation of the channel which is during the process of run-down in activity.

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Activation of K+ currents in cultured Schwann cells is controlled by extracellular pH

Cited by 22 publications

References 27 publications

Voltage‐dependent calcium and potassium channels in Schwann cells cultured from dorsal root ganglia of the mouse.

Voltage‐dependent calcium and potassium channels in Schwann cells cultured from dorsal root ganglia of the mouse.

Single K⁺ channel properties in cultured mouse Schwann cells: Conductance and kinetics

ATP‐regulated K+ channels are modulated by intracellular H+ in guinea‐pig ventricular cells.

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Activation of K+ currents in cultured Schwann cells is controlled by extracellular pH

Cited by 22 publications

References 27 publications

Voltage‐dependent calcium and potassium channels in Schwann cells cultured from dorsal root ganglia of the mouse.

Voltage‐dependent calcium and potassium channels in Schwann cells cultured from dorsal root ganglia of the mouse.

Single K+ channel properties in cultured mouse Schwann cells: Conductance and kinetics

ATP‐regulated K+ channels are modulated by intracellular H+ in guinea‐pig ventricular cells.

Contact Info

Product

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Single K⁺ channel properties in cultured mouse Schwann cells: Conductance and kinetics