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PubMed1982

Long-term synaptic enhancement in hippocampus is not regulated by postsynaptic membrane potential.

The contributions of membrane potential and postsynaptic discharge during afferent fibre tetanization to the generation of long-lasting synaptic enhancement was studied by intra- and extracellular recording in the CAl region of hippocampal slices. Neither parameter affected the magnitude of intracellular synaptic enhancement. Thus, if postsynaptic integration is involved in the control of the enhancement process, the integration must be chemically rather than electrically mediated.

Animals↗
PubMed1973

Membrane potential measurement in parotid acinar cells.

1. Intracellular recording of membrane potential was made from acinar cells of the isolated mouse parotid gland superfused with physiological salt solutions.2. The mean acinar resting membrane potential was - 68.5 mV during superfusion with Krebs-Henseleit solution. Shift of the superfusion solution to one containing ACh or adrenaline (10(-5)M) always caused a transient hyperpolarization (about 10-15 mV).3. The membrane potential was mainly dependent on the extracellular K concentration ([K](o)). Increasing [K](o) tenfold decreased the membrane potential by 50 mV. This depolarization was not mediated by ACh release from depolarized nerve endings, since it was seen in the presence of atropine (1.4 x 10(-6)M) and not caused by the accompanying reduction in [Na](o) to 40 mM caused only a small depolarization (less than 10 mV).4. When the superfusion solution was shifted, during intracellular recording, from a normal Krebs-Henseleit solution ([K] = 4.7 mM) to a K-free solution, a hyperpolarization of about 8 mV was measured. Reintroduction of the normal K-containing solution after a longer period of K deprivation (30-70 min) resulted in a short-lasting pronounced hyperpolarization (about 20 mV) which could be blocked by Strophanthin-G (10(-3)M).5. In contrast to previous reports, the present findings indicate that the membrane potential of salivary acinar cells is similar, with respect to magnitude and K-dependence, to that of cells of more thoroughly investigated tissues, such as muscle and nerve, and that the membrane Na-K pump is electrogenic, at least when the cells have been loaded with Na.

Acetylcholine↗
PubMed1975

Contribution of an electrogenic sodium pump to membrane potential in mammalian skeletal muscle fibres.

1. Relationship between the resting membrane potential and the changes in the intraceullar Na and K concentrations ([Na]i and [K]i) was studied in 'Na-loaded' and K-depleted' soleus (SOL) muscles of rats which had fed a K-free diet for 40 and more days. 2. The extracellular space of the muscles was not significantly different between normal and K-deficient rats. The inulin space in both the 'fresh' and Na-rich' muscles can be determined by the same function relating the space to the muscle weight. 3. Presence of 2-5-15 mM-K in the recovery solution hyperpolarized the 'Na-rich' muscul fibres at the beginning of recovery. The hyperpolarized membrane potential exceeded, beyond the measured potential of 'fresh' muscle fibres, the theoretical potential derived from the ionic theory, or even beyond Ek. Then, the measured membrane potential declined progressively during the immersion in a recovery solution and returned to the steady-state value When a considerable Na extrusion and K uptake took place, the measured membrane potential became equal to Ek. 4.he maximal hyperpolarization occurring immediately after immersion in the recovery solution became smaller and had a shorter duration when increasing the external K concentration ([K]o) from 2-5 to 15mM. 5. The K-sensitive hyperpolarization was completely abolished on exposure to 0mM [K]o, on cooling to ca. 4 degrees C, and in the presence of oubain (10(-4) M). The inhibitory effects were reversed on returning to the control conditions. The membrane potential obtained after inhibition of the electrogenic Na-pump with cooling or ouabain agrees well with that predicted by the 'constant-field' equation. 7. The external Cl ions had a short-circuiting effect on the electrogenic Na-pumping activated on adding K ions. 8. The replacement of Na ions in a recovery solution with Li ions resulted in a faster rate of depolarization from the maximal hyperpolarizationp. It is concluded that the resting membrane potential of 'Na-loaded' and 'K-depleted' SOL muscle fibres is the sum of an ionic diffusion potential predicted by either the Nernst equation or the constant-field equation and of the potential produced by an electrogenic Na-pump.

Animals↗
PubMed1999

Reduced mitochondrial membrane potential and altered responsiveness of a mitochondrial membrane megachannel in p53-induced senescence.

There is accumulating evidence that mitochondrial membrane potential (DeltaPsi(M)) is reduced in aged cells. In addition, a decrease of DeltaPsi(M) has been shown to be an early event in many forms of apoptosis. Here we use a mitochondrial potentiometric dye with in situ laser scanning confocal microscopic (LSCM) imaging to demonstrate that DeltaPsi(M) is dramatically decreased in both the p53-overexpressing, senescent EJ tumor cells and in pre-apoptotic PC12 cells compared to controls. Treatment with cyclosporin A (CSA), which facilitates closure of the mitochondrial permeability transition pore (PTP), was able to reverse the decrease in DeltaPsi(M) in pre-apoptotic PC12 cells but not in the senescent EJ-p53 cells. The capacity to prevent dissipation of DeltaPsi(M) in response to agents that facilitate PTP closure may differentiate cells entering apoptosis from those participating in senescence. Therefore, regulation of the closure of the mitochondrial PTP in the presence of decreased DeltaPsi(M) may be a decisional checkpoint in distinguishing between growth arrest pathways.

Animals↗
PubMedDate not supplied

Plasma membrane potential interferes with the respiratory burst of peripheral granulocytes.

Membrane potential is involved in the regulation of several immune functions developed by granulocytes. The Na(+)/K(+) gradient across the plasma membrane, mainly generated by the Na(+)/K(+) pump, plays a key role in the maintenance of membrane potential. This study is focused on the correlation between plasma membrane potential and the in vitro receptor - triggered respiratory burst of normal human peripheral granulocytes. The respiratory burst was measured as superoxide anion release by the cytochrome c reduction test and plasma membrane potential was modulated by experimental changes of the extracellular potassium concentration. Results show a differentiated cellular response, depending on the in vivo activation state and on the signals received in vitro by granulocytes via CR3 or FcgammaR. Alteration of the membrane potassium gradient modulates the respiratory burst of unstimulated and CR3-activated cells, whilst it does not seem to significantly interfere with the signals delivered by FcgammaR.

Adult↗
PubMed1979

Pancreatic acinar cells: effects of micro-ionophoretic polypeptide application on membrane potential and resistance.

1. Acinar cell membrane potential and resistance were measured from superfused segments of mouse pancreas, in vitro, using intracellular glass micro-electrodes. One or two extracellular micropipettes containing caerulein, bombesin nonapeptide (Bn) or acetylcholine (ACh) were placed near to the surface of the impaled acinus. The secretagogues were ejected rapidly from the micropipettes by ionophoresis.2. Each secretagogue evoked a similar electrical response from the impaled acinar cell: membrane depolarization and a simultaneous reduction in input resistance. The duration of cell activation from caerulein ionophoresis was longer than that observed for ACh and Bn. The cell response to the peptide hormone applications could be repeated in the presence of atropine.3. The minimum interval before the onset of cell depolarization after caerulein ionophoresis was determined. Values ranged between 500 and 1000 msec. The minimum latencies after Bn ionophoresis were 500-1400 msec.4. With two electrodes inserted into electrically coupled acinar cells, direct measurements of the caerulein and Bn null potentials were made. At high negative membrane potentials an enhanced depolarization was evoked by caerulein ionophoresis. At low negative membrane potentials the caerulein stimulation produced a diminished depolarization, and at membrane potentials less than - 10 mV acinar cell hyperpolarizations were observed. A similar series of responses was obtained in experiments where Bn ionophoresis was used. The caerulein and the Bn null potentials were always contained within - 10 to - 15 mV.5. The results describe the almost identical electrical response of acinar cells to stimulation by ACh, caerulein and bombesin. All three secretagogues have similar null potentials and latencies of activation on acinar cells. The bombesin latency responses appear as short as those measured for caerulein and provide electro-physiological evidence that Bn acts directly on acinar cells. The findings support the hypothesis that ACh, caerulein and Bn, though acting on different receptors, evoke the observed changes in electrical properties of acinar cell membranes, through a common pathway.

Acetylcholine↗
PubMed1975

The effect of potassium on the cell membrane potential and the passage of synchronized cells through the cell cycle.

The cell membrane potential of cultured Chinese hamster cells is known to increase at the start of the S phase. The putative role of the cell membrane potential as a regulator of cell proliferation was examined by following the cell cycle traverse of synchronized Chinese hamster cells in the presence or absence of high exogenous levels of potassium. An increase in external potassium levels results in a depressed membrane potential and a reduced rate of cell proliferation. A potassium concentration of 115 mM was used in experiments with synchronized cells since at that level cell proliferation is almost completely halted, recovery of growth is rapid and complete, and the membrane potential is reduced to a level well below that normally found in cells in the G1 phase. A mitotic population was divided into four aliquots and plated in either control medium or medium containing 115 mM K+. Cells placed directly into high K+ medium were retarded in their exit from mitosis and displayed a delayed and abnormal entry into the S phase. If control medium was added after two hours, cell cycle traverse was normal, but delayed by two hours compared to control cells. If the mitotic cells were plated directly into control medium and two hours later were shifted to high K+ medium, the cells entered the S phase in the absence of the normally observed increase in membrane potential and proceeded to the next mitosis normally. It was concluded that the increase in membrane potential observed at the start of the S phase in isolated synchronized cells is not a requirement for the initiation of DNA synthesis. In addition, sensitivity to the high potassium regimen was found at two different times during the cell cycle. In one case, cells were impeded in their transit through mitosis. Such cells displayed an altered chromosome structure which may account for the partial mitotic block. In the second case, synchronized cells displayed a sensitivity to the high potassium regimen in early G1 which appeared to be separate from the block in mitosis and independent of a change in the membrane potential.

Animals↗
PubMed1989

Inhibition by linoleic acid hydroperoxide of alveolar macrophage superoxide production: effects upon mitochondrial and plasma membrane potentials.

Linoleic acid hydroperoxide (LOOH) is a naturally occurring product of lipid peroxidation. Incubation of rat alveolar macrophages with LOOH produced alterations of membrane properties and function at concentrations of LOOH as low as 0.1 microM. These included phorbol myristate acetate (PMA)-stimulated superoxide production, mitochondrial membrane potential, and plasma membrane potentials. These effects were clearly separated from gross loss of structural integrity as measured by lactate dehydrogenase release, in terms of both time of incubation and concentration of LOOH. PMA-stimulated superoxide production measured 15 min after addition of 10 microM LOOH was inhibited approximately 50%; however, addition of this concentration of the hydroperoxide after PMA stimulation was without effect. Superoxide production was also measured in a cell-free system produced by incubation of alveolar macrophages with sodium dodecyl sulfate. Prior incubation of alveolar macrophages with LOOH, H2O2, or t-butyl hydroperoxide, under conditions that significantly inhibited superoxide production by the intact cells, did not produce inhibition of the NADPH-dependent superoxide generating system in the cell-free preparation. These results suggest that the effect of LOOH was upon signal transduction involved in the stimulation of superoxide production rather than on the NADPH oxidase itself. Measurements of membrane potential changes were made using the lipophilic ions, 3,3'-dipentyloxacarbocyanine (DiOC5(3] and bis(3-phenyl-5-oxoisoxazol-4-yl)pentamethineoxonol (oxonol V). On the basis of their charge, DiOC5(3) fluorescence primarily reports mitochondrial potential and oxonol V absorbance reports plasma membrane potential. With 10 microM LOOH, depolarization of the plasma and mitochondrial membranes appeared to occur within seconds. As prior depolarization depresses superoxide production, these hydroperoxide-induced changes in membrane potential may be responsible for decreased PMA-stimulated superoxide production.

Animals↗
PubMed2005

Involvement of adenosine triphosphate-sensitive potassium channels in the response of membrane potential to hyperosmolality in cultured human aorta endothelial cells.

The membrane potential of endothelial cells is an important determinant of endothelial functions, including regulation of vascular tone. We investigated whether adenosine triphosphate-sensitive potassium (K(ATP)) channels were involved in the response of membrane potential to hyperosmolality in cultured human aorta endothelial cells. The voltage-sensitive fluorescent dye, bis-(1,3-diethylthiobarbiturate)trimethine oxonol, was used to assess relative changes in membrane potential semiquantitatively. To investigate the effect of mannitol-, sucrose-, and NaCl-induced hyperosmolality on membrane potential, cells were continuously perfused with Earle's balanced salt solution (285 mOsm/kg H(2)O) containing 200 nM bis-(1,3-diethylthiobarbiturate)trimethine oxonol and exposed to 315 and 345 mOsm/kg H(2)O hyperosmotic medium sequentially in the presence and absence of 1 muM glibenclamide, a well-known K(ATP) channel blocker. Hyperosmotic mannitol significantly induced hyperpolarization of the endothelial cells, which was prevented by 1 microM glibenclamide (n = 6). Estimated changes of membrane potential at 315 and 345 mOsm/kg H(2)O were 13 +/- 8 and 21 +/- 8 mV, respectively. Hypertonic sucrose induced similar changes. However, although hypertonic saline also significantly induced hyperpolarization of the endothelial cells (n = 6), the hyperpolarization was not prevented by 1 muM glibenclamide. In conclusion, K(ATP) channels may participate in hyperosmotic mannitol- and sucrose-induced hyperpolarization, but not in hypertonic saline-induced hyperpolarization in cultured human aorta endothelial cells.

ATP-Binding Cassette Transporters↗
PubMed1982

Dependence of membrane potential on Ca2+ transport in cultured cytotrophoblasts of human immature placentas.

The electrical membrane properties of cultured human cytotrophoblast were examined by means of a standard electrophysiological technique. The mean values of the membrane potential (Rm) and the membrane resistance in a physiological medium were around -49 mV and 12 M omega , respectively. The membrane potential was dependent, to a large extent, on the external Ca2+ concentration ([Ca2+]o). Deprivation of external Ca2+ reduced membrane potential to about -20 mV, and an increase in [Ca2+]o caused a hyperpolarization in a saturable manner. The Ca2+-dependency of membrane potential was affected remarkably by [K+]o, but not by [Na+]o or [Cl-]o. The intracellular Ca2+ injection hyperpolarized the membrane in a Ca2+-free medium. A Ca2+ channel blocker, verapamil, completely abolished the Ca2+-dependent Em. The Ca2+-dependent Em was also suppressed by cooling or by the application of metabolic inhibitors. It is suggested that the Ca2+-dependent Em in cultured human cytotrophoblast is caused by a Ca2+ influx which, in turn, increases the K+ conductance of the cell membrane, presumable due to stimulation of Ca2+-activated K+ channel.

Biological Transport, Active↗
PubMed1994

A possible interpretation for a wide range of resting membrane potentials in human term placental cells.

Membrane potentials of human term placental cells ranged from 0 mV to -85 mV with two peaks. Two different conductances were recognized. One is the inwardly rectifying K conductance which was responsible for one peak at -75 mV. The other one was the outwardly rectifying conductance which was responsible for another peak at -10 mV. The outwardly rectifying current was suggested to be carried mainly by Cl ions because of the reversal potential and a sensitivity to a Cl channel blocker (DIDS). Membrane potentials in human term placental cells were suggested to range between K and Cl equilibrium potentials.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1984

Comparison of the intracellular membrane potentials in crystalline lenses of various frogs.

The intracellular membrane potentials were measured in the individual lens fibers of three kinds of frogs (Rana catesbeiana, Rana pipiens japonica, Rana nigromata) by a conventional glass microelectrode technique, in which the electrode was advanced to a depth of 200 micron from the anterior surface into the lens interior. The maximum intracellular membrane potentials obtained in both anterior and posterior sides of all preparations were between -90 and -95 mV. The measured potentials were nearly close to the EK, and the membrane potentials in in vitro experiments correlated well with in vivo measurements. Low membrane potentials reported previously in various frog lenses were discussed in comparison with the present results.

Animals↗
PubMed1991

Regulation of the proton/electron stoichiometry of mitochondrial ubiquinol:cytochrome c reductase by the membrane potential.

The electron transfer reaction catalysed by mitochondrial ubiquinol:cytochrome c reductase is linked to the outwards translocation of protons with an H+ e- stoichiometry of 1 under non-membrane potential condition. The effect of the electrical membrane potential on the H+/e- stoichiometry was investigated. The enzyme was isolated from Neurospora crassa, reconstituted into phospholipid vesicles and electrical membrane potentials of various values were generated across the membranes by means of the valinomycin-induced potassium-diffusion method. Using lithium ions as counterions for the intravesicular potassium, the induced membrane potential was stable for minutes and was not significantly changed by the protons ejected by the working enzyme. This allowed the assay of steady-state reaction rates at pre-given values of electrical membrane potential. The rate ratio between electron transfer and proton translocation declined from 1 to 0.6 with increase of the membrane potential from 0 to 100 mV. The activity of the quinol/cytochrome c redox reaction followed a parabolic dependence, being activated by low (less than 50 mV) potential and inhibited by high (greater than 100 mV) potential. This apparent non-linear dependence was interpreted in terms of a linear flow/force relationship plus a membrane-potential-dependent slip. Evaluation of the parabolic course by means of a modified linear flow/force relation also indicated a decline of the H+/e- stoichiometry from 1 to 0.5 with increase of the membrane potential from 0 to 120 mV. These observations suggest that the membrane potential controls a change of ubiquinol:cytochrome c reductase between two states that have different reaction routes.

Electron Transport↗
PubMed1983

Rhythmic membrane potential changes in hamster parasympathetic neurons.

Two types of rhythmic membrane potentials in hamster submandibular neurons: (i) slow oscillations of membrane potential (SOMP); and (ii) spontaneous or caffeine-induced rhythmic hyperpolarizing potentials (C-HPs), have been analyzed. SOMPs occurred spontaneously, roughly in sinusoidal forms, between the subthreshold range and the potassium equilibrium potential (EK, approximately -85 mV). The average amplitude of SOMPs from crest to trough was 12 mV with an average crest to crest interval of 6 min. The largest amplitude of SOMPs was seen when their median membrane potentials were between -65 and -70 mV; values outside this range attenuated the amplitude of SOMPs. SOMPs were hardly discernible at or near EK. The membrane resistance was, in general, higher at the crest than at the trough. In eserine-treated preparations, SOMPs of varying durations following postsynaptic potentials were triggered by preganglionic repetitive stimulation. Reduction of extracellular K+ concentration increased the amplitude of SOMP without changing its frequency. This effect was noted at times before K+-free induced membrane depolarization occurred. The amplitude of the SOMP decreased in Ca2+-free saline with concomitant depolarization; conversely, in saline in which the Ca2+ concentration was doubled the membrane potential (Em) was found to be again stable near the EK level. A transient hyperpolarization occurred following intracellular Ca2+ injection when the Em of the preinjected state was between -45 and -60 mV. Among K+-conductance (GK) blockers (TEA, 3- and 4-aminopyridine, Cs+ and Ba2+) examined, only Ba2+ at 5 mM reduced both amplitude and frequency of C-HPs significantly. All Ca2+-conductance (GCa) blockers (Co2+ and Mn2+ at 5 mM, Cd2+ and La3+ at 1 mM, and D-600 at 0.4 mg/ml) prevented synaptic transmission and abolished spike-induced late hyperpolarizing afterpotential. C-HPs were nearly abolished by these agents in 4 mM Ca2+-containing saline. Mitochondrial inhibitors (DNP, CCCP, KCN, NaN3) in a concentration range between 10(-4) M and 10(-5) M, hyperpolarized the membrane before depolarizing and abolishing C-HPs. However, the plasma membrane Na+-pump inhibitor ouabain, at concentrations up to 5 X 10(-4) M, did not affect C-HPs during 1 h perfusion in the majority of neurons; no membrane hyperpolarization was induced, although a gradual depolarization did occur. Both ruthenium red (5 mM) and quinine (5 X 10(-4) M) abolished C-HPs. It is assumed that the two above types of membrane potential changes are generated by the Ca2+-activated GK increase, which, in turn, is under the control of mitochondrial Ca2+ regulatory activity.

Animals↗
PubMed1976

The membrane potential of rat diaphragm muscle fibres and the effect of denervation.

1. Resting membrane potentials of rat diaphragm muscles were measured in vitro after previous denervation for 0-10 days. In some experiments denervated muscles were incubated in vitro for 3 hr while in others they were cultured for 15-24 hr to allow adequate exposure to drugs before recording. 2. It was found that resting membrane potentials, within 2-5 mm of the site of nerve section were significantly lower, within 3 hr, than resting membrane potentials measured more than 9 mm away from site of nerve section. This difference could be reduced or abolished by bathing preparations in solutions containing adrenaline (10 muM), noradrenaline (10 muM) or isoprenaline (10 muM) or dibutyryl cyclic AMP (10 muM-0-25 mM in the presence of 2 mM theophylline). Cyclic AMP (0-5 mM) was ineffective. 3. Application of solutions containing dibutyryl cyclic AMP for 3 hr also raised the resting membrane potential of muscles denervated 4-5 days previously. Culture studies showed that this effect was sustained when the time of incubation was 24 hr. 4. Incubating freshly denervated preparations with cycloheximide (22 mug/ml.) or actinomycin D (1 mug/ml.) did not prevent the development of the early (3 hr) fall in resting membrane potential despite a concomitant inhibition of RNA or protein synthesis. Culturing freshly denervated muscles in solutions containing cycloheximide (10 or 25 mug/ml.) which blocked 93% of protein synthesis, did not prevent the expected drop in resting membrane potential after 15 or 24 hr. 5. It was found that exposure to ouabain (1 or 5 mM) produced a rapid (15 min) fall in resting membrane potential in innervated and denervated preparations treated with dibutyryl cyclic AMP but not denervated preparations. After 5 days denervation cyclic AMP levels in muscle were increased by about 40%. 6. It is suggested that upon denervation an electrogenic action of a NA+-pump is blocked and that dibutyryl cyclic AMP and catecholamines are capable of stimulating this pump.

Animals↗
PubMed1984

Membrane-potential-dependent changes of the lipid microviscosity of mitochondria and phospholipid vesicles.

The effects of a transmembrane potential difference upon the lipid microviscosity of cytochrome oxidase vesicles (COVs) and rat liver mitochondria (RLM) were investigated. COVs and RLM were labelled with the fluorescent probe 1,6-diphenylhexa-1,3,5-triene (DPH). The fluorescence polarization of the probe was then measured when potentials of different magnitudes were induced across the membranes of these particles. It was shown that the absolute value of the microviscosity changes to quite a significant extent, owing to the imposition of large membrane potentials. On relaxation of the membrane potential the lipid microviscosity was also shown to return to the value before the induction of the potential. The largest change in lipid microviscosity was observed when coupled respiration was initiated. This occurred in both the COV system and the RLM system. The absolute value of the lipid microviscosity was shown to change by as much as 22% with the induction of membrane potentials, owing to respiration. To confirm the viscosity measurements made with DPH, lipid microviscosity was also measured with the spin-labelled fatty acid 5-doxyl stearate. Measurements of the order parameters indicated that, in agreement with the results of fluorescence experiments, viscosity changes occurred that were due to the induction of a membrane potential. The significance of these findings to the regulation of metabolism is briefly discussed, the main conclusion being that, although there is certainly a significant variation of lipid microviscosity with electric field, mechanistic interpretations will require further studies.

Animals↗
PubMedDate not supplied

Membrane potential fluctuations determine the precision of spike timing and synchronous activity: a model study.

It is much debated on what time scale information is encoded by neuronal spike activity. With a phenomenological model that transforms time-dependent membrane potential fluctuations into spike trains, we investigate constraints for the timing of spikes and for synchronous activity of neurons with common input. The model of spike generation has a variable threshold that depends on the time elapsed since the previous action potential and on the preceding membrane potential changes. To ensure that the model operates in a biologically meaningful range, the model was adjusted to fit the responses of a fly visual interneuron to motion stimuli. The dependence of spike timing on the membrane potential dynamics was analyzed. Fast membrane potential fluctuations are needed to trigger spikes with a high temporal precision. Slow fluctuations lead to spike activity with a rate about proportional to the membrane potential. Thus, for a given level of stochastic input, the frequency range of membrane potential fluctuations induced by a stimulus determines whether a neuron can use a rate code or a temporal code. The relationship between the steepness of membrane potential fluctuations and the timing of spikes has also implications for synchronous activity in neurons with common input. Fast membrane potential changes must be shared by the neurons to produce synchronous activity.

Action Potentials↗
PubMed1981

Measurement of delta pH and membrane potential in isolated neurosecretory vesicles from bovine neurohypophyses.

The steady state concentration ratios of [3H]methylamine and [14C]SCN- were measured to determine the pH gradient and electrical potential, respectively, across the membrane of purified, intact, neurosecretory vesicles from bovine posterior pituitary. The intravesicular pH was 5.8 when the medium pH was 7. Varying the external pH had only a small effect on the intravesicular pH and resulted in a change in the pH gradient. Extrapolation to zero pH gradient yielded a value of 5.5 for the intravesicular pH. When the medium pH was 7, the pH gradient collapsed in the presence of ammonium sulfate or the combination of nigericin and K+. Measurement of the thiocyanate distribution across the vesicle membrane suggested the existence of an inside negative membrane potential. Mg2+ ATP caused a marked shift in the potential to +50 mV (inside positive) without altering the intravesicular pH. This shift was inhibited by carbonyl cyanide p-trifluoromethoxyphenylhydrazone. The possible roles of the large pH gradient and membrane potential in the storage of peptide hormones and their secretion is discussed.

Adenosine Triphosphate↗