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At least 1,099 records · Page 61Linked to original sources
PubMed1998

Macroscopic and single-channel chloride currents in neuropile glial cells of the leech central nervous system.

In patch-clamp experiments we characterized four Cl- channels (42 pS, 70 pS, 80 pS and 229 pS) underlying the large Cl- conductance of leech neuropile glial cells. They differed with respect to their gating, their rectification and their activity in the cell-attached configuration, showed the selectivity sequence I->Cl->/=Br->F- and were impermeable to SO42-. The four channels were blocked by NPPB, DPC, niflumic acid and DIDS and exhibited either three or four sublevel states. The outward rectifying 42 pS, 70 pS and 80 pS Cl- channels were classified as intermediate conductance Cl- channels and they could contribute to the high Cl- conductance of the glial membrane, which stabilizes the glial membrane potential. The inward rectifying 229 pS Cl- channel is very similar to vertebrate high conductance Cl- channels, which are assumed to be part of an emergency system that is activated under pathophysiological conditions. In voltage-clamp experiments we calculated that the Cl- conductance amounts to one-third of the total membrane conductance. Reduction of this Cl- conductance by Cl- channel inhibitors markedly depolarized the glial cell membrane. These prominent depolarizations depended on Na+ influx and in most cases the glial cells failed to regulate their membrane potential following wash-out of the inhibitors.

Animals↗
PubMed1998

Volatile anesthetics and a volatile convulsant differentially affect GABA(A) receptor-chloride channel complex.

1. General anesthetics at clinical concentrations are known to affect neurotransmitter-gated ion channels in postsynaptic membranes. 2. Volatile anesthetics suppress excitatory transmissions, whereas they potentiate inhibitory chloride currents evoked by GABA or glycine. Hexafluorodiethyl ether (a volatile convulsant) markedly depresses the GABA(A) response but not the glycine-evoked chloride current or the glutamate-induced excitatory response. 3. Molecular biology has revealed that GABA(A) receptor is a heteromeric pentamer composed of alpha, beta, gamma, delta, and/or rho subunits. In baculovirus-Sf9 expression system, the gamma subunit was crucial for potentiation of the GABA-induced chloride current by volatile anesthetics. 4. Following sustained presence of GABA and high concentrations of isoflurane, simultaneous washout of both agents evoked a slowly decaying surge current, whose nature is controversial.

Anesthetics, Inhalation↗
PubMed1985

Voltage sensitive, high-conductance chloride channels in the luminal membrane of cultured pulmonary alveolar (type II) cells.

The properties of ion channels in patches from the luminal membrane of cultured monolayers of type II alveolar epithelial cells from adult rat lung have been studied. In excised patches, prepared as described to yield the "outside-out" configuration (with cesium ions in the bathing solutions to suppress currents arising from potassium channels), we observed anion-selective channels with a conductance of 350-400 pS, and burst lengths lasting seconds. When patches were bathed in solutions with equal chloride concentrations, channels opened and closed spontaneously at membrane voltages close to zero, but tended to close when the potential was shifted by +/- 10 mV, particularly in the negative direction. Other anions could pass through these channels with a permeability sequence of I(1.5) greater than Br(1.02) = greater than Cl(1.00) greater than NO3(0.9) greater than gluconate(0.6) but there was a very low permeability for sodium (PNa/PCl = 0.015 +/- 0.006). Calcium ions reduced channel conductance. The channels probably have a role to play in salt absorption by this epithelium, but insufficient information is available about how sodium crosses it for the role of the anion channels in transport to be defined with confidence.

Animals↗
PubMed1991

gamma-Aminobutyric acid-activated chloride channels in rats selectively bred for differential acute sensitivity to alcohol.

Effects of various sedative hypnotic agents on GABA-mediated chloride flux were evaluated in whole brain membrane vesicles (microsacs) prepared from rats selectively bred for high (HAS) and low sensitivity (LAS) to an acute hypnotic dose of alcohol. The HAS rats were more sensitive to the effects of pentobarbital, phenobarbital, flunitrazepam, and ethanol on GABA-mediated chloride flux compared with the LAS rats. No differences between the lines in GABA-stimulated chloride flux were observed. Modulation of 1-[3H]-phenyl-4-butyl-2,6,7-trioxabicyclo(2.2.2)octane ([3H]-TBOB) and [3H]-diazepam binding also was measured. The lines did not differ in inhibition of [3H]-TBOB binding by pentobarbital, phenobarbital, muscimol or picrotoxin. Although the lines displayed almost identical KD and Bmax for [3H]-diazepam binding, the GABA agonist, muscimol, was a more potent stimulator of [3H]-diazepam binding in membranes prepared from HAS rats than from LAS rats. These findings are discussed in light of previous work using other selected lines.

Alcohol Drinking↗
PubMed2005

Chloride channel diseases resulting from impaired transepithelial transport or vesicular function.

The transport of anions across cellular membranes is crucial for various functions, including the control of electrical excitability of muscle and nerve, transport of salt and water across epithelia, and the regulation of cell volume or the acidification and ionic homeostasis of intracellular organelles. Given this broad range of functions, it is perhaps not surprising that mutations in Cl- channels lead to a large spectrum of diseases. These diverse pathologies include the muscle disorder myotonia, cystic fibrosis, renal salt loss in Bartter syndrome, kidney stones, deafness, and the bone disease osteopetrosis. This review will focus on diseases related to transepithelial transport and on disorders involving vesicular Cl- channels.

Animals↗
PubMed1999

Chloride channels and salivary gland function.

Fluid and electrolyte transport is driven by transepithelial Cl- movement. The opening of Cl- channels in the apical membrane of salivary gland acinar cells initiates the fluid secretion process, whereas the activation of Cl- channels in both the apical and the basolateral membranes of ductal cells is thought to be necessary for NaCl re-absorption. Saliva formation can be evoked by sympathetic and parasympathetic stimulation. The composition and flow rate vary greatly, depending on the type of stimulation. As many as five classes of Cl- channels with distinct gating mechanisms have been identified in salivary cells. One of these Cl- channels is activated by intracellular Ca2+, while another is gated by cAMP. An increase in the intracellular free Ca2+ concentration is the dominant mechanism triggering fluid secretion from acinar cells, while cAMP may be required for efficient NaCl re-absorption in many ductal cells. In addition to cAMP- and Ca(2+)-gated Cl- channels, agonist-induced changes in membrane potential and cell volume activate different Cl- channels that likely play a role in modulating fluid and electrolyte movement. In this review, the properties of the different types of Cl- currents expressed in salivary gland cells are described, and functions are proposed based on the unique properties of these channels.

Absorption↗
PubMed1999

Bimodal kinetics of a chloride channel from human fibroblasts.

Excised patches were used to study the kinetics of a Cl channel newly identified in cultured human fibroblasts (L132). The conductance of ca. 70 pS in 150 mm symmetrical Cl, and the marked outward rectification ascribe this channel to the ICOR family. Long single-channel recordings (>30 min) revealed that the channel spontaneously switches from a kinetic mode characterized by high voltage dependence (with activity increasing with depolarization; mode 1), into a second mode (mode 2) insensitive to voltage, and characterized by a high activity in the voltage range +/-120 mV. On patch excision the channel always appeared in mode 1, which was maintained for a variable time (5-20 min). In most instances the channels then switched into mode 2, and never were seen to switch back, in spite of the eight patches that cumulatively dwelled in this mode 2.33-fold as compared to mode 1. Stability plots of long recordings showed that the channel was kinetically stable in both modes, allowing standard analysis of steady-state kinetics to be performed. Open and closed time distributions of mode 1 and mode 2 revealed that the apparent number of kinetic states of the channel was the same in the two modes. The transition from mode 1 into mode 2 was not instantaneous, but required a variable time in the range 5-60 sec. During the transition the channel mean open time was intermediate between mode 1 and mode 2. The intermediate duration in the stability plot however is not to be interpreted as if the channel, during the transition, rapidly switches between mode 1 and mode 2, but represents a distinct kinetic feature of the transitional channel.

Cell Line↗
PubMed1994

A GTP-binding protein inhibits a gastric housekeeping chloride channel via intracellular production of superoxide.

A housekeeping basolateral Cl- channel of rabbit gastric parietal cells, the single channel conductance of which is about 0.3 picosiemens, is opened by prostaglandin E2 and closed by intracellular application of guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S). In the present patch clamp study, we found a novel GTP gamma S-dependent regulatory mechanism of the Cl- channel. GTP gamma S significantly decreased the open probability of the single Cl- channel without altering unit conductance. An intracellular application of superoxide dismutase (SOD; 100 units/ml) inhibited the GTP gamma S (50 microM)-induced closure of the Cl- channel. SOD plus catalase (100 units/ml) also inhibited the GTP gamma S-induced effect, while catalase alone did not inhibit it. In the absence of GTP gamma S, an intracellular application of hydrogen peroxide (H2O2; 30 microM) did not affect the Cl- channel current. Desferrioxamine (50 microM) which inhibits hydroxyl radical (.OH) production was without effect on the GTP gamma S-induced closure. These results suggest that the GTP gamma S-induced closure of the Cl- channel was due to intracellular production of superoxide (O2.-), but not due to .OH or H2O2. Furthermore, an artificial production of O2.- inside the cell by lumazine (50-100 microM) plus xanthine oxidase (0.5-1 milliunit/ml) in the absence of GTP gamma S also closed the channel. The lumazine/xanthine oxidase-induced closure of the channel was inhibited by SOD, but not by catalase or desferrioxamine. We conclude from these results that GTP-binding protein-coupled production of O2.- leads to closure of the Cl- channel in rabbit gastric parietal cells.

Animals↗
PubMed1993

Characterization of cAMP dependent CFTR-chloride channels in human tracheal gland cells.

Human tracheal gland cells are believed to be a major site at the origin of cystic fibrosis. Since this disease is due to mutations in a protein called CFTR, we looked for the activity of CFTR in human tracheal gland cells in culture. We have identified CFTR-like chloride-selective channels as having a linear current voltage relationship and unitary conductance of 7 pS in these cells. In cell-attached patches, theophylline (1 mM), IBMX (1 mM), or a cocktail of dibutyryl cAMP (1 mM) and IBMX (0.1 mM) promoted the opening of channels. The unitary current had a reversal potential close to the cell resting potential. Replacement of choline by K+ or Na+ in the pipette solution was without effect on the current-voltage relationship, the reversal potential or the unitary conductance, which is consistent with the chloride selectivity of the channel. Channels were always found clustered and their opening probability was not noticeably dependent on membrane potential. This work therefore represents the first observation of a CFTR-like channel activity in submucosal gland cells.

Base Sequence↗