ACh-Evoked complex membrane potential changes in mouse submaxillary gland acini
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The effects of hypoxia on hippocampal CA1 neurones in tissue slices of the rat brain were studied in vitro by intracellular recording. In response to superfusion of a hypoxic medium equilibrated with 95%N2-5% CO2, a majority of the neurones showed a transient depolarization followed by a hyperpolarization of 5-15 mV in amplitude and 4-12 min in duration. The hyperpolarization was, in turn, followed by a slow depolarization which within 20 min of hypoxic exposure reached a plateau level of about 25 mV above the prehypoxic resting potential. Both the initial hyperpolarization and subsequent depolarization were associated with a reduction in membrane resistance. The hyperpolarization reversed in polarity at a membrane potential of -83 mV. There was an almost linear relationship between amplitude of the hyperpolarization and membrane potential. The hyperpolarization was markedly enhanced in potassium-free media and was depressed in high-potassium solution. Superfusion of ouabain (5-7 microM)-containing medium in normoxic conditions produced hyperpolarizing and depolarizing responses similar to those elicited by hypoxic exposure. The slow depolarization was also mimicked by elevation of the extracellular potassium concentration to 10-20 mM. Evoked i.p.s.p.s were abolished within 4 min of hypoxic exposure while evoked e.p.s. p.s were maintained for about 20 min of hypoxic superfusion. Soma spikes of the neurones elicited by a depolarizing pulse were also well preserved. Their threshold was, however, raised, concomitant with a decrease in the peak amplitude. In a minority of the neurones the slow depolarization was suddenly followed by a rapid depolarization, after which the neurones showed no functional recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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Valinomycin
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Oscillation (cell signaling)
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1 Effects of pretreatment with isoprenaline (Isop) or noradrenaline (NA) and various ionic environments on the NA-induced or Isop-induced hyperpolarization of guinea-pig liver cells were investigated by means of a microelectrode technique.2 NA (5.9 x 10(-6) M) decreased the membrane resistance, and hyperpolarized the membrane with or without generation of an initial transient small depolarization. The NA-induced initial depolarization was not dependent on the membrane potential and was increased by Isop (4.0 x 10(-6) M) or glucagon (10(-7) M).3 In Ca-free solution, the NA-induced hyperpolarization became transient and a continuous depolarization followed in the presence of NA. Repetitive application of NA resulted in a complete disappearance of the NA-induced hyperpolarization and was replaced by a slowly developing depolarization with or without generation of the initial transient depolarization. In excess [Ca](o), the NA or Isop-induced hyperpolarization was increased.4 Both Isop and glucagon hyperpolarized the membrane and decreased the membrane resistance, to various degrees. Repetitive application of Isop or glucagon resulted in the disappearance of both Isop and glucagon-induced hyperpolarizations. Pretreatment with NA not only resulted in a recovery of both Isop and glucagon-induced hyperpolarizations, but also extensively enhanced the hyperpolarization.5 After pretreatment with Isop, the NA-induced hyperpolarization was decreased in amplitude and duration and was followed by a slowly developing depolarization. After repetitive application of Isop, NA produced only depolarization of the membrane, and in these conditions, Isop, glucagon or ATP also depolarized the membrane. These depolarizations were reversed to hyperpolarizations by pretreatment with excess [Ca](o).6 After treatment with Na-deficient solution, NA depolarized the membrane and decreased the membrane resistance. Excess [Ca](o) restored the NA-induced membrane response from one of depolarization to one of hyperpolarization.7 In the presence of tetraethylammonium 10mM, the NA-induced hyperpolarization became transient or ceased and depolarization occurred with a reduction in the membrane resistance.8 It is postulated that both NA and Isop increase the free [Ca](i) by releasing bound Ca from storage sites and consequently an increase in K conductance follows. NA but not Isop promotes Ca-influx which replenishes the storage site. In Ca-depleted conditions, NA does not elevate the free [Ca](i) to a threshold concentration required for hyperpolarization, probably because NA induces a small release of Ca from storage sites.
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Acinar cell membrane potentials were measured by intracellular micro-electrode recording from isolated segments of mouse pancreas. At the normal resting potential (r. p.) of -40 mV a short lasting pulse of local acetylcholine stimulation (micro-iontophoresis) evoked a monophasic depolarization. At relatively low r. p. biphasic potential changes (depolarization - hyperpolarization) were observed. Strophanthin-G (1 mM) immediately reduced r. p., but had no effect on the secondary hyperpolarization.
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An electrically gated Na+ channel can be made to appear in the membrane of the Xenopus laevis oocyte by simple depolarization. This membrane normally responds passively to imposed transmembrane currents with resting potentials around -60 mV, but when it is held depolarized to more than about +30 mV it becomes possible to obtain long-lasting regenerative depolarizations up to +80 mV; these depolarizations can last as long as 20 min. This potential is due to an "induction" of a Na+-dependent channel that is electrically gated open and closed. Its threshold for opening is about -20 mV and it is selective for Na+ over Cs+ and choline+ but is blocked by relatively small quantities of Li+. When a long voltage clamp step to a positive potential under ENa (+70 to +90 mV) is applied, an inward current is observed for many minutes, implying that this channel does not have an inactivation mechanism. The inward Na+ current is blocked by 0.50 mM tetrodotoxin. When the membrane is held at or near resting potential, the excitability will disappear with time, but it can be made to reappear by again depolarizing the membrane.
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The membrane conductance and reversal potential were determined for neurones in toad dorsal root ganglion (DRG) with intracellular recording technique during depolarization or hyperpolarization induced by noradrenaline (NA). The effects of blocking agents for potassium or calcium channels on NA-induced membrane potential responses were examined. In 15 neurones, the NA-induced depolarization was accompanied by a 32.6% decrease of membrane conductance; in other 4 neurones, the depolarization was accompanied by an initial increase and subsequent decrease in membrane conductance. The NA hyperpolarization was associated with an increase of membrane conductance by 16.2% (n = 8). The mean reversal potential of NA-induced depolarization was -88.5 +/- 0.9 mV (means +/- SE, n = 4). The NA-induced hyperpolarization was nullified at -89 to -92 mV of membrane potentials (n = 3). Tetraethylammonium superfusion enhanced NA depolarization amplitude by 73.7 +/- 11.9% (means +/- SE, n = 7) and depressed NA hyperpolarization amplitude by 40.5% (n = 4). Intracellular injection of CsCl increased phenylephrine-induced depolarization by 34.5% (n = 4). MnCl2 superfusion decreased the amplitudes of NA-induced depolarization by 50.5 +/- 9.9% (means +/- SE, n = 10), and of NA-induced hyperpolarization by 89.5 +/- 4.9% (means +/- SE, n = 7) respectively. The results suggest that the depolarization or hyperpolarization induced by NA might be mediated by the alteration in activation of K+ or Ca2+ channels.
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Tetraethylammonium
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Dorsal root ganglion
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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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