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B Soria

Publications and source records attributed to B Soria.

68 records · Page 4Linked to original sources
PubMed1991

Ion channels of glucose-responsive and -unresponsive beta-cells.

To assess whether different electrophysiological characteristics could account for the heterogeneous secretion of individual beta-cells in vitro, we used patch-clamp configurations to study currents in plaque-forming (insulin-secreting) and non-plaque-forming rat pancreatic beta-cells that were distinguished in a reverse hemolytic plaque assay (RHPA) after a 30-min stimulation by 16.7 mM glucose. RHPA showed that the population of single beta-cells under study was stimulated (P less than 0.01-0.001) to secrete insulin by 16.7 mM glucose, 100 microM tolbutamide, 20 microM glyburide, or 30 mM KCl but, under these conditions, also comprised beta-cells that did not secrete detectable amounts of insulin. Under current clamp conditions, secreting and nonsecreting beta-cells showed analogous resting membrane potentials (approximately 60 mV) and were similarly depolarized by 30 mm KCl and 100 microM tolbutamide. Under voltage-clamp conditions, total membrane conductance (approximately 6 nS) was also similar in the glucose-responsive and -unresponsive beta-cells, which, when monitored in the whole-cell configuration after RHPA, showed the following currents: a voltage-dependent Na+ current, a voltage-activated Ba2+ current, a voltage-dependent K+ delayed-rectifier current, a voltage-dependent Ca(2+)-activated K+ current, and a voltage-independent and tolbutamide-sensitive K+ current. In the cell-attached configuration and the presence of 2.8 mM glucose, secreting and nonsecreting beta-cells displayed a similar single-channel activity that was abolished when glucose concentration was raised to 16.7 mM. We conclude that beta-cells studied after RHPA have an electrically normal membrane whether they release insulin in response to 16.7 mM glucose or not.

Animals↗
PubMed1989

Glucose-induced oscillations of intracellular Ca2+ concentration resembling bursting electrical activity in single mouse islets of Langerhans.

Intracellular Ca2+ levels were monitored in single, acutely isolated mouse islets of Langerhans by dual emission Indo-1 fluorometry. High-frequency (3.1 min-1) [Ca2+]i oscillations with a brief rising time (1-2 s) and 10 s half-width ('fast' oscillations) were detected in 11 mM glucose. Raising the glucose concentration to 16.7 mM increased the duration of these oscillations, which were otherwise absent in 5.5 mM glucose. [Ca2+]i waves of lower frequency (0.5 min-1) and longer rising time ('slow' oscillations) were also recorded. The data indicate that "fast" oscillations are directly related to beta-cell bursting electrical activity, and suggest the existence of extensive networks of electrically coupled cells in the islet.

Animals↗
PubMed1989

Voltage-sensitive calcium flux into bovine chromaffin cells occurs through dihydropyridine-sensitive and dihydropyridine- and omega-conotoxin-insensitive pathways.

The fluorescent Ca2+ indicator FURA-2 was used to characterize the depolarization-related intracellular Ca2+ signalling process in bovine adrenal chromaffin cells. Depolarization with high K+ (10-65 mM) gave rise to a very rapid increase in intracellular free Ca2+ concentration, which subsequently decayed slowly towards a "plateau". The size of this initial increase varied sigmoidally with the calculated membrane potential, the relationship being described well by a Boltzmann distribution function for a transition between two states (transition potential, -23 mV). A dihydropyridine calcium channel agonist [(+)202-791, 1 microM] raised intracellular free Ca2+ concentration further in the presence of 30 mM K+, and it enhanced the initial intracellular Ca2+ response to depolarization. Voltage-sensitive calcium channels in chromaffin cells are believed to include the L-type. Several dihydropyridine calcium channel antagonists [(-)202-791, nifedipine, nitrendipine; 1-5 microM], known to be active on L-type channels, caused only modest inhibition of K+ -induced increase in intracellular free Ca2+ concentration: c. 50% (at 30 mM K+) and 25% (at 40-70 mM K+). In addition, omega-conotoxin GVIA (1-10 microM), a blocker of neuronal N- and L-type calcium channels, reduced the initial increase in intracellular free Ca2+ concentration only slightly at 55 mM K+. Further, the dihydropyridine-insensitive component of the intracellular Ca2+ signal was also insensitive to omega-conotoxin, which was otherwise quite active in a central nervous rat in vivo preparation Gd3+ (40 microM), a potent calcium antagonist in the chromaffin cell, blocked the intracellular Ca2+ response to depolarization. When added at different times after K+ stimulation, however, Gd3+ reduced intracellular free Ca2+ concentration to control levels along a slow time course of several minutes. Similar results were obtained when EGTA was added to reduce extracellular Ca2+ concentration to sub-nanomolar levels, in the presence of high K+. We conclude that bovine chromaffin cells are equipped with at least two different classes of voltage-dependent calcium channels, only one of which is likely to be the L-type channel. We also propose that depolarization, in addition to stimulating Ca2+ influx, may also lead to enhancement of Ca2+ release from an intracellular store.

Adrenal Medulla↗
PubMed1988

Evidence that muscarinic potentiation of insulin release is initiated by an early transient calcium entry.

The increased insulin release induced by carbamoylcholine (CbCh) in pancreatic islets requires the presence of extracellular Ca2+. Intracellular recordings demonstrate that CbCh produces a transient increase in Ca2+ channel activity lasting from 30 to 60 s. Thereafter activity decreased to levels lower than in controls. When extracellular Ca2+ was present during this initial period, the stimulatory effects of CbCh were not different from those in which Ca2+ was present throughout. These experiments suggest that during muscarinic potentiation of insulin release extracellular calcium is only needed in the first minute.

Animals↗
PubMed1986

TEA-insensitive K-channels in the crab giant axon.

TTX and TEA-insensitive permeabilities were studied in the crab giant axon under voltage-clamp. Membrane currents in the presence of internal TEA (40 mmol/l) and external TTX (300 nmol/l) may be analyzed as the sum of two components: a linear component, identified as the so-called leakage current, and a non-linear component, identified as a TEA-insensitive potassium channel. Ion permeability ratio of the TTX and TEA insensitive cation channel calculated from reversal potential shows the following sequence pK+:pNa+:pCs+:pRb+:pNH+4 = 1.00:0.16:0.16:0.09:0.06. TEA-insensitive outward currents, carried mainly by Cs+, may be recorded in the presence of different external solutions. Voltage-dependence and equilibrium potential of this channel in physiological conditions allows to postulate its contribution to maintain the cell depolarized during repetitive firing.

Animals↗
PubMed1985

Monovalent cation permeabilities of the potassium systems in the crab giant axon.

Permeability ratios for pairs of monovalent cations permeating the two potassium systems proposed for the giant axon of the crab Carcinus maenas (M.E. Quinta-Ferreira, E. Rojas & N. Arispe, J. Membrane Biol. 66:171-181, 1982b) were estimated from measurements of the reversal potential of the currents under voltage-clamp conditions. With K+ inside the axon, permeability ratios from the reversal potential of the currents through the late channel are: PRb/PK = 0.9, PNH4/PK less than 0.2 and PCS/PK = 0.18. With CS+ inside the ratios are: PK/PCS = 8.7, PRb/PCS = 7.1 and PNH4/PCS = 2.4. The analysis of the inward currents carried by Rb+ or NH+4 showed similar reversal potentials for the early transient component and the late sustained component. Whence, the sequence of permeabilities for the two types of potassium channels is: PK greater than PRb greater than PNH4 greater than PNa = PCS. The time constants for the activation of the two components recorded either in K-, Rb-, or NH4-artificial seawater are twice as large as the corresponding time constants measured in Na-artificial seawater.

Ammonia↗
PubMed1985

Differential blockage of two types of potassium channels in the crab giant axon.

Measurements were made of the kinetic and steady-state characteristics of the potassium conductance in the giant axon of the crabs Carcinus maenas and Cancer pagirus. The conductance increase during depolarizing voltage-clamp pulses was analyzed assuming that two separate types of potassium channels exist in these axons (M.E. Quinta-Ferreira, E. Rojas and N. Arispe, J. Membrane Biol. 66:171-181, 1982). It is shown here that, with small concentrations of conventional K+-channel blockers, it is possible to differentially inhibit these channels. The potassium channels with activation and fast inactivation gating (m3h, Hodgkin-Huxley kinetics) were blocked by external application of 4 amino-pyridine (4-AP). The potassium channels with standard gating (n4, Hodgkin-Huxley kinetics) were preferentially inhibited by externally applied tetraethylammonium (TEA). The differential blockage of the two types of potassium conductance changes suggests that they represent two different populations of potassium channels. It is further shown here that blocking the early transient conductance increase leads to the inhibition of the repetitive electrical activity induced by constant depolarizing current injection in fibers from Cardisoma guanhumi.

4-Aminopyridine↗
PubMed1984

Isonicotinic acid hydrazide: early effects on peripheral nerve conduction velocity.

This report describes the effects of short treatments with isonicotinic acid hydrazide (isoniazid), 300 mg/kg/day, on conduction velocity in the rat tail dorsal nerve trunk. After 6 days of continuous treatment, conduction velocity falls significantly for measurements made at 35 degrees C. After 10 days it falls significantly at both 25 degrees C and 35 degrees C. This appears to be the first electrophysiological corroboration of the early neuropathological changes recently observed in isoniazid treated rats and seems to provide evidence that the temperature at which the experiments are made is important in determining conduction velocity changes.

Animals↗
PubMed1984

Effects of Zn2+ on glucose-induced electrical activity and insulin release from mouse pancreatic islets.

The effects of Zn2+ and CO2+ on glucose-induced beta-cell electrical activity and on insulin release from microdissected mouse pancreatic islets were studied. In 11 mM glucose the electrical activity is characterized by a burst pattern with a bimodal distribution of spike amplitudes along the plateau phase. Zn2+ at 0.05 mM induced a reduction in the number of spikes during the bursts and preferentially blocked the large action potentials. Zn2+ at 0.1 mM and CO2+ at 1.0 mM completely inhibited the electrical activity in response to glucose. Zn2+ inhibition of electrical activity was poorly reversible, whereas CO2+ inhibition was rapidly and completely reversible. Zn2+ and CO2+ inhibited the glucose-stimulated insulin release from microdissected perifused islets. Half-maximal inhibition occurred at about 0.3 mM for both metals. Zn2+ also inhibited K+-induced insulin release in the absence of glucose, indicating that Zn2+ inhibition does not involve glucose metabolism. It is proposed that Zn2+ blocks the voltage-gated Ca2+ channels in pancreatic beta-cells.

Action Potentials↗
PubMed1983

Properties of miniature post-synaptic currents at the Torpedo marmorata nerve-electroplate junction.

The post-synaptic conductance changes induced by spontaneous release of neurotransmitter on the Torpedo marmorata electroplates were studied by focal extracellular recording methods. It was found that miniature post-synaptic currents (m.p.s.c.s) recorded on the innervated and non-innervated faces of the electrocyte are opposite in sense and the distribution of amplitudes is bimodal. The bimodal distribution could reflect the presence of two populations of m.p.s.c.s (smaller and giant m.p.s.c.s). In the smaller m.p.s.c.s the distribution of the ratio (amplitude/decay time constant) shows two populations that probably represent areas with different receptor densities. The value of the mean open-channel lifetime estimated from the decay time constant of the m.p.s.c. is 0.92 +/- 0.67 ms (n = 319, temperature 20 +/- 1 degree C). Prostigmine (10 microM) increases the amplitude, decay time constant and time to peak of the m.p.s.c. A decrease of temperature increases m.p.s.c. decay time, the activation energies found ranging from 8.0 to 12.6 kcal x mol-1. Increasing the external K+ concentration produces a decrease in the decay time constant. High concentrations of divalent ions, particularly Ca2+, increase the decay time constant of the m.p.s.c. Alkaline or acid bathing solution produces a decrease in the decay time constant. An almost total substitution of external Cl- by non-permeant SO42- does not modify the time course of the m.p.s.c.

Animals↗