Membrane potential changes associated with pinocytosis of serum lipoproteins in L cells

Tsuchiya, Wakoh; Okada, Yasunobu; Yano, Jun; Murai, Atsushi; Miyahara, Tadao; Tanaka, Tomoji

doi:10.1016/0014-4827(81)90005-7

Cited by 19 publications

(10 citation statements)

References 17 publications

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“…Since under certain conditions a sustained hyperpolarization can be produced Tsuchiya et al 1981 b), the depolarizing phase of the potential oscillation is unlikely to result from spontaneous inactivation of the K+ channel. Inactivation of the Ca2+ pump by flavones resulted in a prolongation of the hyperpolarizing phase of the potential oscillation or a sustained hyperpolarization Stimu lus [Ca].…”

Section: Discussionmentioning

confidence: 99%

“…L cells, an established line of mouse fibroblasts, exhibit oscillations of membrane potential composed of spontaneously repeated hyperpolarizing responses (Okada, Doida, Roy, Tsuchiya, Inouye & Inouye, 1977 a) and respond with a hyperpolarizing response to a mechanical, electrical (Nelson, Peacock & Minna, 1972;Okada et al 1977 a) or chemical stimulus (Tsuchiya, Okada, Yawo, Yada & Yano, 1979; Tsuchiya, Okada, Yano, Murai, Miyahara & Tanaka, 1981 b; Okada, Machida, Yada, Ohno & Ueda, 1982). These hyperpolarizing responses have been suggested to be related to endocytic activity (Okada, Tsuchiya, Yada, Yano & Yawo, 1981 a) and membrane motility (Tsuchiya, Okada, Yano, Inouye, Sasaki & Doida, 1981 a) of the cells.…”

Section: Introductionmentioning

confidence: 99%

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Calcium channel and calcium pump involved in oscillatory hyperpolarizing responses of L‐strain mouse fibroblasts

Okada

Tsuchiya

Yada

1982

The Journal of Physiology

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SUMMARY1. In fibroblastic L cells, spontaneously repeated hyperpolarizing responses (oscillation of membrane potential) and hyperpolarizing responses evoked by electrical stimuli were suppressed by the external application of a K+ channel blocker, nonyltriethylammonium (C9). This hydrophobic TEA-analogue also inhibited the hyperpolarization induced by intracellular Ca2+ injection.2. Quinine or quinidine, known inhibitors of the Ca2+-activated K+ channel of red cells, instantaneously inhibited these hyperpolarizations. Thus, these hyperpolarizations are likely to be caused by the operation of Ca2+-sensitive K+ channels.3. Azide, which is known to inhibit the mitochondrial Ca2+ uptake in fibroblasts, and caffeine, dantrolene Na and oxalate, which affect the microsomal Ca2+ transport, did not exert any effects upon the electrical potential profiles.4. On the other hand, Ca2+ channel blockers (nifedipine, D 600 and Co2+) suppressed the hyperpolarizing responses, but not the hyperpolarizations produced by intracellular Ca2+ injection, suggesting that the calcium ions responsible for the hyperpolarizing responses are mainly derived from outside the cell through Ca2+ channels.5. Flavones of plant origin, which are known to inhibit Ca2+-ATPase, prolonged the duration of the hyperpolarizing phase of the oscillation or produced a sustained hyperpolarization.6. It is concluded that the Ca2+ channel and the Ca2+ pump play essential roles in the generation of the hyperpolarizing response and of the membrane potential oscillation in L cells, and that these hyperpolarizations are brought about by a transient elevation of cytosolic Ca2+ level which, in turn, activates Ca2+-dependent K+ channels.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Calcium channel and calcium pump involved in oscillatory hyperpolarizing responses of L‐strain mouse fibroblasts

Okada

Tsuchiya

Yada

1982

The Journal of Physiology

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“…It is not known, however, whether the oscillatory hyperpolarizations occur in undisturbed cells or as a result of impalement by a micro-electrode. None the less, properties of L cells, such as phagocytosis (Okada, Tsuchiya, Yada, Yano & Yawo, 1981), cell motility (Tsuchiya, Okada, Yano, Inouye, Saski & Doida, 1981 a), and pinocytosis (Tsuchiya, Okada, Yano, Murai, Miyahara & Tanaka, 1981 b) have been associated with such hyperpolarizations, and in macrophages these hyperpolarizations have been associated with chemotaxis (Gallin & Gallin, 1977) and phagocytosis (Kouri, Noa, Diaz & Niubo, 1980). Recently, we analysed the fast potential transient seen after impalement (Lassen, Nielson, Pape & Simonsen, 1971) into macrophages and found (Ince, Ypey, Van Furth & Verveen, 1983b) that penetratation by a microelectrode induces a leakage conductance across the membrane and that the membrane potentials of macrophages (mean -40 mV) are two to three times more negative than has generally been thought on the basis of sustained potential measurements (-15 to -25 mV).…”

Section: Introductionmentioning

confidence: 99%

Oscillatory hyperpolarizations and resting membrane potentials of mouse fibroblast and macrophage cell lines.

İnce¹,

Leijh²,

Meijer³

et al. 1984

The Journal of Physiology

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SUMMARY1. L cells (a mouse fibroblast cell line) and macrophages have been reported to exhibit slow oscillatory hyperpolarizations and relatively low membrane potentials, when measured with glass micro-electrodes. This paper describes the role of microelectrode-induced leakage in these oscillations for L cells and a mouse macrophage cell line (P388D1).2. Both L cells and macrophages showed fast negative-going peak-shaped potential transients upon micro-electrode entry. This shows that the micro-electrode introduces a leakage conductance across the membrane.3. The peak values of these fast transients were less negative for L cells (-17 mV) than for macrophages (-39 mV), although their sustained resting membrane potentials were about equal (-13 mV). This indicates that the pre-impaled membrane potential of macrophages is more negative than that of L cells.4. Ionophoretic injection of Ca2+ into the P388D1 macrophages showed the existence of a Ca2+-dependent hyperpolarizing conductance presumed to be involved in the oscillatory hyperpolarizations of L cells and macrophages.5. Cells increased in size by X-ray irradiation to reduce membrane input resistances were still found to be susceptible to micro-electrode-induced leakage.6. Impalement transients upon entry of a second electrode during a hyperpolarization evoked by a first electrode, were often step-shaped instead of peak-shaped due to the high membrane conductance associated with hyperpolarization.7. Since peak-shaped impalement transients were always seen with the first impalement both in oscillating and non-oscillating cells, oscillatory hyperpolarizations cannot be regarded as spontaneously occurring in the unperturbed cells but are induced by micro-electrode penetration.8. Since the hyperpolarizing response can be evoked by ionophoretic injection of Ca2+, and oscillatory as well as single hyperpolarizing responses are absent in a Ca2+-free medium, it is concluded that the Ca2+ needed intracellularly to activate the hyperpolarizing responses enters the cell via the leakage pathway introduced by the measuring electrode.t To whom correspondence should be addressed.

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“…It has been reported that potential oscillations may be related to Ca2+-dependent membrane-mobile activities of fibroblasts such as endocytosis (Okada et al, 1981;Tsuchiya, 1981b) and chemotaxis (Okada et al, , 1984Oiki & Okada, 1988). Thus, the membrane potential oscillation and/or the responsible oscillation of intracellular free Ca 2 § are likely to be endogenous in nature in activated fibroblasts participating in wound healing.…”

Section: Discussionmentioning

confidence: 97%

Factors responsible for oscillations of membrane potential recorded with tight-seal-patch electrodes in mouse fibroblasts

Oiki

Okada

1988

J. Membrain Biol.

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In giant fibroblastic L cells, penetration of a conventional microelectrode brought about marked decreases in the membrane potential and input resistance measured with a patch electrode under tight-seal whole-cell configuration, and repeated hyperpolarizations were often observed upon penetration. Therefore, the question arose whether such leakage artifact is a causal factor for generation of the membrane potential oscillation even in giant L cells. During whole-cell recordings, however, regular potential oscillations were observed in the cells that had not been impaled with a conventional microelectrode, as far as the Ca2+ buffer was not strong in the pipette solution. Oscillatory changes in the intracellular potential were detected by extracellular recordings with a tight-seal patch electrode in the cell-attached configuration. Thus, the potential oscillation occurs even in the absence of penetration-induced leakage or without rupture of the patch membrane. Withdrawal of a micropipette from one cell was often found to induce marked cell damage and elicit oscillatory hyperpolarizations in a neighboring cell with a certain time lag. The longer the distance between the injured and recorded cells, the greater was the time lag. Application of the cell lysate on the cell surface also gave rise to oscillatory hyperpolarizations. After repeated applications of the lysate, the membrane became unresponsive (desensitized), suggesting the involvement of receptors for the lysate factor. The lysates of different cell species (mouse lymphoma L5178Y cells or human epithelial Intestine 407 cells) produced similar effects. The effective component was heat stable and distinct from ATP. Lysate-induced hyperpolarizations were inhibited by deprivation of extracellular Ca2+ and by application of a Ca2+ channel blocker (nifedipine) or a K+ channel blocker (quinine) in the same manner as spontaneous oscillatory hyperpolarizations. It is concluded that the mouse fibroblast exhibits membrane potential oscillations, when the cell was activated, presumably via receptor systems, by some diffusible factors released from damaged cells.

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Membrane potential changes associated with pinocytosis of serum lipoproteins in L cells

Cited by 19 publications

References 17 publications

Calcium channel and calcium pump involved in oscillatory hyperpolarizing responses of L‐strain mouse fibroblasts

Calcium channel and calcium pump involved in oscillatory hyperpolarizing responses of L‐strain mouse fibroblasts

Oscillatory hyperpolarizations and resting membrane potentials of mouse fibroblast and macrophage cell lines.

Factors responsible for oscillations of membrane potential recorded with tight-seal-patch electrodes in mouse fibroblasts

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