Volume‐activated chloride channels in rat parotid acinar cells.

Arreola, Jorge; Melvin, James E.; Begenisich, Ted

doi:10.1113/jphysiol.1995.sp020695

Cited by 72 publications

(70 citation statements)

References 32 publications

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“…A half-unit decrease in pH resulted in an increase in current amplitude while a 0·6 unit increase in pH decreased the amplitude of ICl,IR. Arreola, Melvin & Begenisich (1995) have suggested that there may be negatively charged groups which, under control conditions, normally restrict the flow of chloride ions, but which are neutralized by a decrease in pH. The hyperpolarization-activated chloride current in Aplysia neurons was reported to exhibit the same sensitivity to external pH as was observed in this study and the effects were attributed to shifts in the activation curves (ChesnoyMarchais, 1983).…”

Section: Discussionsupporting

confidence: 58%

“…The characteristics of ICl,IR are completely different to typical volume-activated chloride currents. Such currents are activated rapidly by depolarization, display outward rectification, have a halide selectivity sequence of I¦ > Br¦ > Cl¦ and require ATP (Anderson, Sheppard, Berger & Welsh, 1992;Ackerman, Wickman & Clapham, 1994;Nilius et al 1994;Arreola et al 1995Arreola et al , 1996. A number of currents which share common features with ICl,IR, such as the hyperpolarization-activated chloride currents of rat osteoblastic cells (Chesnoy-Marchais & Fritsch, 1994), mandibular duct cells (Komwatana, Dinudom, Young & Cook, 1995), T84 cells (Fritsch & Edelman, 1997) and the ClC_2-induced chloride current do exhibit sensitivity to changes in the external osmolarity.…”

Section: Discussionmentioning

confidence: 99%

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Characterization of the hyperpolarization‐activated chloride current in dissociated rat sympathetic neurons

Clark

Jordt

Jentsch

et al. 1998

The Journal of Physiology

106

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Dissociated rat superior cervical ganglion (SCG) neurons have been shown to possess a hyperpolarization‐activated inwardly rectifying chloride current. The current was not altered by changes in external potassium concentration, replacing external cations with NMDG (N‐methyl‐D‐glucamine) or by addition of 10 mM caesium or barium ions. The reversal potential of the current was altered by changing external anions. The anion selectivity of the current was Cl− > Br− > I− > cyclamate. All substituted permeant anions also blocked the current. The current was blocked by DIDS (4,4′‐diisothiocyanatostilbene‐2,2′‐disulphonic acid), 9AC (anthracene‐9‐carboxylic acid) and NPPB (5‐nitro‐2‐(3‐phenylpropylamino)benzoic acid) but was unaffected by SITS (4‐acetamido‐4′‐isothiocyanatostilbene‐2,2′‐disulphonic acid) and niflumic acid. The effective blockers were voltage dependent; DIDS and NPPB were more effective at depolarized potentials while 9AC was more effective at hyperpolarized potentials. The current was enhanced by extracellular acidification and reduced by extracellular alkalinization. Reducing external osmolarity was without effect in conventional whole‐cell recording but enhanced current amplitude in those perforated‐patch recordings where little current was evident in control external solution. The current in SCG neurons was blocked by external cadmium and zinc. ClC‐2 chloride currents expressed in Xenopus oocytes were also sensitive to block by these divalent ions and by DIDS but the sensitivity of ClC‐2 to block by cadmium ions was lower than that of the current in SCG neurons. Reverse transcriptase‐polymerase chain reaction (RT‐PCR) experiments showed the presence of mRNA for ClC‐2 in SCG neurons but not in rat cerebellar granule cells which do not possess a hyperpolarization‐activated Cl− current. The data suggest that ClC‐2 may be functionally expressed in rat SCG neurons. This current may play a role in regulating the internal chloride concentration in these neurons and hence their response to activation of GABAA receptors.1. Dissociated rat superior cervical ganglion (SCG) neurons have been shown to possess a hyperpolarization‐activated inwardly rectifying chloride current. The current was not altered by changes in external potassium concentration, replacing external cations with NMDG (N‐methyl‐D‐glucamine) or by addition of 10 mM caesium or barium ions. The reversal potential of the current was altered by changing external anions. The anion selectivity of the current was Cl− > Br− > I− > cyclamate. All substituted permeant anions also blocked the current.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 99%

Characterization of the hyperpolarization‐activated chloride current in dissociated rat sympathetic neurons

Clark

Jordt

Jentsch

et al. 1998

The Journal of Physiology

106

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“…These properties are similar to those of the conductances activated by hypotonic solutions in rat submandibular gland acinar, and other acinar, cells, e.g. rat parotid acinar (Arreola et al 1995) and neonatal rat pancreas (Schmid et al 1998). They are also similar to those of volume-sensitive anion conductances identified in many other cell types (Nilius et al 1996;Strange et al 1996;Okada, 1997).…”

Section: Volume-sensitive Anion Channels In Acinar Cellssupporting

confidence: 72%

“…Expression was also examined in salivary gland acinar cells, which are similar in many respects to lacrimal cells, but are known to express volume-sensitive anion channels (Arreola et al 1995(Arreola et al , 1996.…”

Section: Expression Of Volume-sensitive CLmentioning

confidence: 99%

Expression of volume‐sensitive Cl⁻ channels and ClC‐3 in acinar cells isolated from the rat lacrimal gland and submandibular salivary gland

Majid

Brown

Best

et al. 2001

The Journal of Physiology

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Volume-sensitive anion channels are expressed in most mammalian cells (Nilius et al. 1996;Strange et al. 1996;Okada, 1997). These are channels which, when activated by cell swelling, mediate the efflux of Cl _ , organic anions and amino acids during cell volume regulation. The broad ion and substrate selectivity displayed by these channels has led them to be called volume-sensitive osmolyte and anion channels or VSOAC by some groups (for review see Strange et al. 1996). There is, however, some debate as to whether a single channel mediates the efflux of anions and other osmolytes or whether a group of channel proteins each with similar properties is involved (Mongin et al. 1999;Stutzin et al. 1999; Valverde, 1999).This confusion over the phenotype of the channel or channels involved is further complicated by a lack of precise information about their molecular biology. Several candidate proteins have been identified including p-glycoprotein, pI Cln , ClC-2 and ClC-3 (Okada et al. 1998). However, there is little definitive evidence to support the role of these proteins as volume-sensitive anion channels, and at least one of them, p-glycoprotein, is now thought to function as a channel regulator rather than the actual channel (Okada, 1997). The properties of ClC-3 make it one of the most likely candidate proteins, e.g. it has a structure which is very similar to that of known Cl _ channels (ClC-0 and ClC-1), and it produces an outwardrectifying Cl _ conductance when expressed in Xenopus oocytes (Kawasaki et al. 1994) or mammalian cell lines (Duan et al. 1997; Valverde, 1999;Shimada et al. 2000). However, others have been unable to express ClC-3 in oocytes (for reviews see Jentsch et al. 1999; Valverde, 1999). Furthermore, when transfected into mammalian cells, ClC-3 gives rise to currents in the absence of cell swelling (Duan et al. 1997; Valverde, 1999;Shimada et al. 2000), although cell swelling does appear to further activate the channels (Duan et al. 1997; Valverde, 1999). The role of ClC-3 as a volume-sensitive anion channel is therefore still somewhat controversial.Rat lacrimal gland acinar cells are unusual because volume regulation is not thought to involve volumesensitive anion channels (Strange et al. 1996). Instead, cell swelling causes an increase in intracellular Ca 2+ , which is sufficient to activate Ca 2+ -activated Cl _ channels allowing Cl _ efflux (Kotera & Brown, 1993;Park et al. 1994;Speake et al. 1998). Lacrimal acinar cells may therefore provide a useful natural 'knock-out' in which to study the role of ClC-3, i.e. they can be used to test the hypothesis that ClC-3 is not expressed in cells which do not exhibit volume-sensitive anion channels. The present study has examined the expression of ClC-3 and volume-sensitive anion channels in rat lacrimal acinar cells, using molecular biological and electrophysiological methods 1. The expression of ClC-3 was examined in rat lacrimal gland and submandibular salivary gland cells using RT-PCR and Western analysis. Whole-cell patch clamp methods were u...

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“…In rat parotid acinar cells, extracellular acidosis was indeed reported to potentiate swelling-activated Cl Ϫ currents (2). Interestingly, our data show that the rate of current activation and inactivation by pH is much more rapid than that induced by cell swelling, even though the maximum currents elicited by the two stimuli do not differ.…”

Section: Discussionmentioning

confidence: 47%

Extracellular acidification elicits a chloride current that shares characteristics with I_Cl(swell)

Nobles

Higgins

Sardini

2004

American Journal of Physiology-Cell Physiology

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Nobles, Muriel, Christopher F. Higgins, and Alessandro Sardini. Extracellular acidification elicits a chloride current that shares characteristics with ICl(swell). Am J Physiol Cell Physiol 287: C1426 -C1435, 2004. First published August 11, 2004 doi:10.1152/ ajpcell.00549.2002-A Cl Ϫ current activated by extracellular acidification, ICl(pHac), has been characterized in various mammalian cell types. Many of the properties of ICl(pHac) are similar to those of the cell swelling-activated Cl Ϫ current ICl(swell): ion selectivity (I Ϫ Ͼ Br Ϫ Ͼ Cl Ϫ Ͼ F Ϫ ), pharmacology [ICl(pHac) is inhibited by 4,4Ј-diisothiocyanostilbene-2,2Ј-disulfonic acid (DIDS), 1,9-dideoxyforskolin (DDFSK), diphenylamine-2-carboxylic acid (DPC), and niflumic acid], lack of dependence on intra-or extracellular Ca 2ϩ , and presence in all cell types tested. ICl(pHac) differs from ICl(swell) in three aspects: 1) its rate of activation and inactivation is very much more rapid, currents reaching a maximum in seconds rather than minutes; 2) it exhibits a slow voltage-dependent activation in contrast to the fast voltage-dependent activation and time-and voltage-dependent inactivation observed for ICl(swell); and 3) it shows a more pronounced outward rectification. Despite these differences, study of the transition between the two currents strongly suggests that ICl(swell) and ICl(pHac) are related and that extracellular acidification reflects a novel stimulus for activating I Cl(swell) that, additionally, alters the biophysical properties of the channel.cell swelling-activated chloride current; patch clamp; pH A CHLORIDE CURRENT ACTIVATED by cell swelling (I Cl(swell) ) has been characterized in many different cell types (for review see Refs. 26 and 37), and it is thought to play a role in regulatory cell volume decrease (RVD) in response to hypotonicity. I Cl(swell) exhibits outward rectification, fast voltage-dependent activation, and time-and voltage-dependent inactivation at potentials more positive than ϩ40 mV. The relative anion selectivity for the swelling-activated Cl Ϫ channel is SCN Ϫ Ͼ I Ϫ Ͼ Br Ϫ Ͼ Cl Ϫ Ͼ F Ϫ Ͼ gluconate; this sequence is referred to as "Eisenman sequence I" and indicates a weak interaction between the channel pore and the permeation anion. A number of different substances, including the stilbene derivative 4,4Ј-diisothiocyanostilbene-2,2Ј-disulfonic acid (DIDS) (9, 35), the anti-inflammatory drug niflumic acid (20), the antiestrogen drug tamoxifen (43), diphenylamine-2-carboxylic acid (DPC) (22), and 1,9-dideoxyforskolin (DDFSK) (9), inhibit I Cl(swell) . Furthermore I Cl(swell) is insensitive to changes in calcium concentrations (33). Despite much effort and several candidates, P-glycoprotein (P-gp) (42), pICln (30) and ClC-3 (12), none has stood the test of time, and the molecular identity of the channel responsible for I Cl(swell) and its mechanism of activation remain unknown. Extracellular acidification has been reported to both activate and inhibit anion channel activities in different cell types. Extracellular...

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Volume‐activated chloride channels in rat parotid acinar cells.

Cited by 72 publications

References 32 publications

Characterization of the hyperpolarization‐activated chloride current in dissociated rat sympathetic neurons

Characterization of the hyperpolarization‐activated chloride current in dissociated rat sympathetic neurons

Expression of volume‐sensitive Cl⁻ channels and ClC‐3 in acinar cells isolated from the rat lacrimal gland and submandibular salivary gland

Extracellular acidification elicits a chloride current that shares characteristics with I_Cl(swell)

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Volume‐activated chloride channels in rat parotid acinar cells.

Cited by 72 publications

References 32 publications

Characterization of the hyperpolarization‐activated chloride current in dissociated rat sympathetic neurons

Characterization of the hyperpolarization‐activated chloride current in dissociated rat sympathetic neurons

Expression of volume‐sensitive Cl− channels and ClC‐3 in acinar cells isolated from the rat lacrimal gland and submandibular salivary gland

Extracellular acidification elicits a chloride current that shares characteristics with ICl(swell)

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Expression of volume‐sensitive Cl⁻ channels and ClC‐3 in acinar cells isolated from the rat lacrimal gland and submandibular salivary gland

Extracellular acidification elicits a chloride current that shares characteristics with I_Cl(swell)