Effects of inhibitors and adenosine on (HCO3−/CO2)-stimulated swelling and Cl− uptake in brain slices and cultured astrocytes

Bourke, Robert S.; Kimelberg, Harold K.; Dazé, M.A.

doi:10.1016/0006-8993(78)91072-7

Cited by 41 publications

(10 citation statements)

References 27 publications

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“…Enlargement was reversible and was accompanied by an increase in tissue respiration. Bourke et al (1976Bourke et al ( , 1978 were the first to show that the incubation of brain slices in medium with a high K + concentration (50 mmol/l), in the presence of bicarbonates, led to enlargement of astroglia volume. The size of volume changes after repetitive stimulation (Dietzel et al 1980(Dietzel et al , 1982Ransom et al 1985a,b;Sykova 1987;Svoboda et al 1989Svoboda et al , 1991 can be deduced from changes in tissue osmolarity and from ion shifts across cell membranes.…”

Section: Volume Changes Induced By Changes In Extracellular Osmolaritymentioning

confidence: 99%

Ionic and Volume Changes in the Microenvironment of Nerve and Receptor Cells

Sykové¹

1992

Progress in Sensory Physiology

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Section: Volume Changes Induced By Changes In Extracellular Osmolaritymentioning

confidence: 99%

Ionic and Volume Changes in the Microenvironment of Nerve and Receptor Cells

Sykové¹

1992

Progress in Sensory Physiology

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“…The presence of Cl--HC03-and Na+-H+ transport across the cell membrane of cultured astrocytes has been inferred from recent studies using radioactive ion flux measurements (Bourke, Kimelberg & Daze, 1978; Kimelberg, Biddlecome & Bourke, 1979). However, there are no previous reports of direct measurements of intracellular pH in glial cells.…”

Section: Introductionmentioning

confidence: 99%

The regulation of intracellular pH by identified glial cells and neurones in the central nervous system of the leech.

Deitmer

Schlue

1987

The Journal of Physiology

135

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SUMMARY1. Double-barrelled, neutral-carrier pH-sensitive micro-electrodes were used to measure the intracellular pH (pHi) and the pHi regulation of neuropile glial (n.g.) cells and of identified neurones of the leech Hirudo medicinalis.2. The distribution of H+ in the n.g. cells and in the neurones was found not to be in electrical equilibrium. The mean pHi ofthe n.g. cells was 6-87 + 0 13 (mean + S.D.of mean here and for all following data n = 27) in HEPES-buffered leech saline (pHo = 7 4) and 7418 + 0-19 (n = 13) in 2 % C02-11 mM-HC03--saline. The mean pHi was 7'28+0-1 (n = 20) in Retzius neurones and 7-32+0415 (n = 12) in noxious neurones in HEPES-buffered leech saline, and 7-20+0415 (n = 10) and 7-27 +016 (n = 6) in 2 % C02-1 1 mM-HC03--buffered saline in these two types of neurones, respectively.3. The cytoplasmic buffering power, as calculated by the change in pHi following the change from 2 % C02-11 mM-HC03-to 5 % C02-22 mM-HCO.-in the leech saline, was 20-30 mM/pH unit in the n.g. cells and between 12 and 33 mM/pH unit in the neurones.4. The recovery of pHi in n.g. cells from an experimentally induced acidification (addition and removal of 20 mm-NH4Cl) was dependent on the presence of external Na+. Independent of the buffer system used, pHi recovery was inhibited when external Na+ was exchanged by N-methyl-D-glucamine. Amiloride (2-3 mM) reduced the rate of pHi recovery by about 50 % in these n.g. cells.5. In CO2-HCO3--free saline, or in the presence of the anion exchange blocker 4-acetamido-4'-isothiocyanostilbene-2, 2'-disulphonic acid (SITS, 0 5 mM), pHi recovery from an acid load was often slowed by up to 50 % in n.g. cells. This suggests that there is a significant contribution of a HC03--dependent membrane transport to pHi regulation in n.g. cells.6. When a HEPES-buffered saline was exchanged by a 2 % C02-11 mM-HCO3-buffered saline, the pHi of n.g. cells increased by 0-31 pH units. This alkaline shift was reversible upon removal of the CO2-HC03-and was absent in the Na+-free saline. It was not inhibited by 1 mM-furosemide or by 0 5 mM-SITS. Successive addition of first Na+ and then CO2-HCO3-to an Na+-free HEPES-buffered saline produced two separate phases of intracellular alkalization, suggesting two different pHi regulation transport systems.J. W. DEITMER AND W.-R. SCHLUE 7. In sensory and Retzius neurones pHi recovery from acidification was also dependent on external Na+, both in the presence and in the absence of CO2-HC03-.The rate of pHi recovery was reversibly reduced by 2 mM-amiloride by up to 90 % in these neurones.8. In conclusion, bicarbonate buffer affects n.g. cell pHi differently from the way in which it affects neuronal pHi. The regulation of pHi depends on the presence of external Na+ in both n.g. cells and neurones. The experiments suggest the presence of an Na+-H+ exchange and a SITS-sensitive HCO3--and Na+-dependent acid extrusion mechanism across n.g. (and nerve cell) membranes and another, SITSinsensitive HC03-and Na+-dependent transport system only in n.g. cells.

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“…1975), which is known to antagonize adenosine actions (Fredholm 1980;Rall 1980). There is good evidence that adenosine is able to cause swelling in cerebral gray matter by causing a coupled chloride-cation transport which leads to the influx of an osmotic equivalent of water (Bourke et al 1978(Bourke et al & 1981. The interesting possibility emerges that some vasodilator substances, e.g.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Some Drugs with Purported Antianoxic Effect on Veratridine‐induced Purine Release from Isolated Rat Hypothalamic Synaptosomes

Fredholm

Lindgren

Lindström

et al. 1983

Acta Pharmacologica et Toxicologica

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Several drugs claimed to protect against anoxic damage to the brain and/or to aleviate symptoms of senility were tested for their ability to influence purine overflow from hypothalamic synaptosomes. Theophylline did not influence the total purine release but tended to decrease the nucleoside and increase the nucleotide release. Cyclic nucleotide phosphodiesterase inhibitors were ineffective, whereas drugs that inhibit carrier mediated nucleoside transport inhibited veratridine‐induced purine release. Some ergot derivatives, some vinca‐analogues and the vasodilator ifenprodil also decreased stimulated purine release, but their effect could not be attributed to adenosine transport inhibition. The results suggest that drugs that are reported to aleviate symptoms of anoxic damage or senility may inhibit the release of adenosine and related compounds in the central nervous system. Some possible reasons why a decreased purine release may protect against ischaemic brain damage are discussed.

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Effects of inhibitors and adenosine on (HCO3−/CO2)-stimulated swelling and Cl− uptake in brain slices and cultured astrocytes

Cited by 41 publications

References 27 publications

Ionic and Volume Changes in the Microenvironment of Nerve and Receptor Cells

Ionic and Volume Changes in the Microenvironment of Nerve and Receptor Cells

The regulation of intracellular pH by identified glial cells and neurones in the central nervous system of the leech.

The Effect of Some Drugs with Purported Antianoxic Effect on Veratridine‐induced Purine Release from Isolated Rat Hypothalamic Synaptosomes

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