Intracellular chloride activity in glial cells of the leech central nervous system.

Ballanyi, Klaus; Schlue, Wolf-Rüdiger

doi:10.1113/jphysiol.1990.sp017915

Cited by 21 publications

(20 citation statements)

References 23 publications

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“…That the response of fetal motoneurons in the present study depends on Cl Ϫ is evident from the observation that Cl Ϫ -free solution, which causes initially a positive shift of the Cl Ϫ equilibrium potential (E C l ) (Ballanyi et al, 1987;Ballanyi and Schlue, 1990), greatly potentiated the agonist-evoked [Ca 2ϩ ] i rise . Our results are in accordance with findings on immature spinal neurons Wang et al, 1994;Serafini et al, 1995;Rohrbough and Spitzer, 1996), including identified motoneurons (Wu et al, 1992;Gao and Ziskind-Conhaim, 1995).…”

Section: Ionic Mechanism Of the Gaba-and Glycine-induced [Ca 2؉ ] I Risementioning

confidence: 70%

“…As also evident from the recording of Figure 6C, recovery from the agonist-induced [Ca 2ϩ ] i transients in Cl Ϫ -free solution was incomplete in ϳ30% of cases. The observation that the [Ca 2ϩ ] i increases persisted in the absence of extracellular (and thus intracellular) Cl Ϫ (Ballanyi et al, 1987;Ballanyi and Schlue, 1990) indicated that another anion substitutes for Cl Ϫ to produce the GABA-or glycine-induced depolarizations. Receptor-coupled anion channels are permeable to several anions, including HCO 3 Ϫ (Bormann et al, 1987;Kaila and Voipio, 1987;Fatima-Shad and Barry, 1993;Staley et al, 1995 Fig.…”

Section: ؉ ] I Risesmentioning

confidence: 99%

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Role of Bicarbonate and Chloride in GABA- and Glycine-Induced Depolarization and [Ca²⁺]_iRise in Fetal Rat MotoneuronsIn Situ

2000

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Ca2ϩ imaging and (perforated) patch recording were used to analyze the mechanism of GABA-and glycine-induced depolarizations in lumbar motoneurons of spinal cord slices from fetal rats. In fura-2 ester-loaded cells, the agonist-induced depolarizations increased [Ca 2ϩ ] i by up to 100 nM. The GABA-and glycine-evoked [Ca 2ϩ ] i transients were suppressed by bicuculline and strychnine, respectively. Their magnitude decreased by ϳ50% between embryonic days 15.5 and 19.5. Ϫ efflux has a major contribution to depolarizations mediated by GABA A and glycine receptor-coupled anion channels in prenatal neurons. We hypothesize that the HCO 3 Ϫ -dependent depolarizing component, which is likely to produce an intracellular acidosis, might play an important role during the early postnatal period when the Cl Ϫ -dependent component gradually shifts to hyperpolarization. Key words: bicarbonate; calcium; chloride pump; development; imaging; motor neurons; neuronal maturationThe principal hyperpolarizing and thus inhibitory neurotransmitters GABA and glycine exert a depolarizing action during development of neuronal structures (Ben-Ari et al., 1989;Obrietan and van den Pol, 1995). In the immature hippocampus, depolarizing GABAergic IPSPs inhibit synaptic responses of CA3 pyramidal neurons (Psarropoulou and Descombes, 1999;Palva et al., 2000), but periodic GABA release produces a "giant" neuronal depolarization and action potential discharge (Ben-Ari et al., 1989). The rise in the concentration of free intracellular Ca 2ϩ ([Ca 2ϩ ] i ) associated with the GABA-induced depolarization (Leinekugel et al., 1995;Garaschuk et al., 1998) might be implicated in trophic or hebbian modulation of developing synapses and activity-dependent formation of the hippocampal network Leinekugel et al., 1999).In motoneurons that are among the earliest neurons to differentiate within the brain, activity-related rises of [Ca 2ϩ ] i are also supposed to have a trophic effect. Suppression of neurite outgrowth in developing motoneurons (Owen and Bird, 1997; Metzger et al., 1998) appears to be causally related with an increase of [Ca 2ϩ ] i attributable to activation of Ca 2ϩ -permeable glutamate receptors (Metzger et al., 2000). Accordingly, maturation of motoneurons of cultured lumbar spinal cord is retarded upon blockade of glutamatergic neurotransmission (Xie and Ziskind-Conhaim, 1995). One week before birth, the isolated spinal cord of rats generates rhythmic nerve activity that is impaired by blockers of glycine and GABA A receptors (Nishimaru et al., 1996). It was found previously that GABA and glycine depolarize lumbar motoneurons that provide the output of this rhythmically active network in the fetus (Obata et al., 1978;Wu et al., 1992;Gao and Ziskind-Conhaim, 1995). The latter studies indicated a major role of Cl Ϫ ions in this depolarization. However, it is yet not clear whether efflux of HCO 3 Ϫ through the receptor-coupled anion pore (Bormann et al., 1987;Fatima-Shad and Barry, 1993) contributes to the GABA-and glycine-evoked r...

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Section: Ionic Mechanism Of the Gaba-and Glycine-induced [Ca 2؉ ] I Risementioning

confidence: 70%

Section: ؉ ] I Risesmentioning

confidence: 99%

Role of Bicarbonate and Chloride in GABA- and Glycine-Induced Depolarization and [Ca²⁺]_iRise in Fetal Rat MotoneuronsIn Situ

2000

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“…If there is indeed a high permeability, the E Cl will follow the new potential within seconds. In some invertebrate glia in which there is a high chloride conductance (e.g., leech or drone retina), E Cl follows E M within 30 s (Coles and Orkand, 1984;Ballanyi and Schlue, 1990). On unidentified glial cells in guinea pig olfactory bulb slices (mentioned above) Ballanyi et al (1987), demonstrated a passive distribution of chloride and a fast (within seconds) equilibration of chloride after a change in the driving force.…”

Section: Resting Chloride Conductance Of the Cell Membranesmentioning

confidence: 99%

Chloride/anion channels in glial cell membranes

Walz

2002

Glia

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At least seven different chloride/anion currents have now been identified in astrocytes, oligodendrocytes/Schwann cells, and microglia. Only for two of these currents is the corresponding gene known. One of these genes is not encoding for a chloride channel, but for a class of mitochondria-like pores also found in cell membranes. Astrocytes and oligodendrocytes differ in their resting properties: astrocytes accumulate chloride but do not have a significant permeability. Oligodendrocytes have a close to passive distribution and a significant permeability. Under certain circumstances, astrocytes can express a resting chloride conductance. Reactive and neoplastic astrocytes as well as astrocytes with an altered shape exhibit a resting conductance. The function of these channels certainly involves volume regulation. Other possible functions are potassium homeostasis, migration, proliferation (in microglia), and involvement in spreading depression waves. Of greatest interest are two phenomena discovered in situ: The ClC-2 channel is only found in astrocytic endfeet near blood capillaries adjacent to neuronal GABA A receptors. In the supraoptic nucleus of the hypothalamus, there is an osmosensitive astrocytic taurine release. This released taurine interacts with glycine receptors in neighboring neurons, causing inhibition. It is assumed that with the future availability of more in situ, rather than in vitro, studies, an increased number of such complex interactions between glial cells, neurons, and blood vessels will be discovered.

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“…Hence, the cell membrane surface is very large. The electrical input resistance of this glial cell is relatively low (200-500 kfl), due to large resting conductances to K+ and Cl- (Walz & Schlue, 1982;Ballanyi & Schlue, 1990;Wuttke, 1990 (Deitmer, 1991(Deitmer, , 1992b C02-HC03--free saline could be as large as 10 mV, assuming a residual HCO3-flux in nominally C02-HC03--free saline of 15 % of that in C02-HC03--buffered saline. This would still favour a stoichiometry of 2 HC03-: 1 Nae, because the Erev would still be more negative than -60 mV, i.e.…”

Section: Voltage Clamp Of the Glial Cellmentioning

confidence: 99%

Sodium‐bicarbonate cotransport current in identified leech glial cells.

Munsch

Deitmer

1994

The Journal of Physiology

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1. The membrane current associated with the cotransport of Na+ and HC03-was investigated in neuropil glial cells in isolated ganglia of the leech Hirudo medicinalis L. using the twoelectrode voltage-clamp technique. 2. The addition of 5 % C02-24 mm HC03-evoked an outward current, which slowly decayed, and which was dependent upon the presence of external Na+. Removal of C02-HC03-elicited a transient inward current. Re-addition of Na+ to Na+-free saline in the presence of C02-HC03-also produced an outward current. Under these conditions an intracellular alkalinization and a rise in intracellular [Na+] were recorded using triple-barrelled, ionsensitive microelectrodes. Addition or removal of HCO3-, in the absence of external Na+, caused little or no change in membrane voltage, membrane current and intracellular pH, indicating that the glial membrane has a very low HC03-conductance. 3. Voltage steps revealed nearly linear current-voltage relationships both in the absence and presence of C02-HCO3-, with an intersection at the assumed reversal potential of the HCO3--dependent current. These results suggest a cotransport stoichiometry of 2 HC03-: 1 Na+. The HC03--dependent current could be inhibited by diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS). 4. Simultaneous recording of current and intracellular pH showed a correlation of the maximal acid-base flux with the transient HC03--dependent current during voltage steps in the presence of CO2-HCO3-. The maximum rate of acid-base flux and the HC03--dependent peak current showed a similar dependence on membrane voltage. Lowering the external pH from 7-4 to 7 0 produced an inward current, which increased twofold in the presence of CO2-HCO3-. This current was largely inhibited by DIDS, indicating outward-going electrogenic Na'-HCO3-cotransport during external acidification.5. When external Na+ was replaced by Li', a similar outward current and intracellular alkalinization were observed in the presence of C02-HC03-. The Li'-induced intracellular alkalinization was not inhibited by amiloride, a blocker of Na+(Li+)-H+ exchange, but was sensitive to DIDS. These results suggest that Li' could, at least partly, substitute for Na+ at the cotransporter site. 6. Our results indicate that the Na+-HCO3-cotransport produces a current across the glial cell membrane in both directions with a reversal potential near the membrane resting potential, rendering pH, a function of the glial membrane potential.Glial cells play an important role in maintaining ion homeoThe transport mechanism responsible for the efficient stasis in nervous systems. We have recently shown that shift of acid-base equivalents across the glial membrane is a glial cells actively regulate their intracellular pH (Deitmer & Na+-HCO3-cotransport, which has been identified in epi- Schlue, 1987Schlue, , 1989 and also participate in pH regulation of thelial tissue (see Boron & Boulpaep, 1989), in glial cells of extracellular spaces in the nervous tissue by uptake and invertebrates (Deitmer & Schlue, 1987, 1989 and v...

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Intracellular chloride activity in glial cells of the leech central nervous system.

Abstract: SUMMARY1. Chloride-sensitive double-barrelled microelectrodes were used to measure the intracellular Cl-activity (a 1) and membrane potential (Em)

Cited by 21 publications

References 23 publications

Role of Bicarbonate and Chloride in GABA- and Glycine-Induced Depolarization and [Ca²⁺]_iRise in Fetal Rat MotoneuronsIn Situ

Role of Bicarbonate and Chloride in GABA- and Glycine-Induced Depolarization and [Ca²⁺]_iRise in Fetal Rat MotoneuronsIn Situ

Chloride/anion channels in glial cell membranes

Sodium‐bicarbonate cotransport current in identified leech glial cells.

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Intracellular chloride activity in glial cells of the leech central nervous system.

Abstract: SUMMARY1. Chloride-sensitive double-barrelled microelectrodes were used to measure the intracellular Cl-activity (a 1) and membrane potential (Em)

Cited by 21 publications

References 23 publications

Role of Bicarbonate and Chloride in GABA- and Glycine-Induced Depolarization and [Ca2+]iRise in Fetal Rat MotoneuronsIn Situ

Role of Bicarbonate and Chloride in GABA- and Glycine-Induced Depolarization and [Ca2+]iRise in Fetal Rat MotoneuronsIn Situ

Chloride/anion channels in glial cell membranes

Sodium‐bicarbonate cotransport current in identified leech glial cells.

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Product

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Role of Bicarbonate and Chloride in GABA- and Glycine-Induced Depolarization and [Ca²⁺]_iRise in Fetal Rat MotoneuronsIn Situ

Role of Bicarbonate and Chloride in GABA- and Glycine-Induced Depolarization and [Ca²⁺]_iRise in Fetal Rat MotoneuronsIn Situ