Fall in intracellular pH mediated by GABAA receptors in cultured rat astrocytes

Kaila, Kai; Panula, Pertti; Karhunen, Tuula; Heinonen, Erkki

doi:10.1016/0304-3940(91)90358-z

Cited by 41 publications

(33 citation statements)

References 24 publications

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“…In our study, steady-state pHi (in C0,-free NaHEPES buffer) of C6 cells was 7.39, similar to the previously reported value of 7.35 in this cell line (Jean et al, 19861, while steady-state pHi of rat astrocytes was 7.15, somewhat higher than the average of previously reported values for mammalian astrocytes, between 6.89 and 7.02 (Boyarsky et al, 1993;Chow et al, 1991;Kaila et al, 1991;MellergArd et al, 1992). In mouse astrocytes, a very low value of 6.68 has been reported (Wuttke and Walz, 1990), but this value was measured with double-barrelled microelectrodes and might reflect cell damage.…”

Section: Discussionsupporting

confidence: 91%

Intracellular pH regulation in primary rat astrocytes and C6 glioma cells

Shrode

Putnam

1994

Glia

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We used the pH-sensitive fluorescent dye BCECF to study intracellular pH (pHi) regulation in primary cultures of rat astrocytes and C6 glioma cells. Both cell types contain three pH-regulating transporters: 1) alkalinizing Na+/H+ exchange; 2) alkalinizing Na+ + HCO3-/Cl- exchange; and 3) acidifying Cl-/HCO3- exchange. Na+/H+ exchange was most evident in the absence of CO2; recovery from acidification was Na+ dependent and amiloride sensitive. Exposure to CO2 caused a cell alkalinization that was inhibited by DIDS, dependent on external Na+, and inhibited 75% in the absence of Cl- (thus mediated by Na+ + HCO3-/Cl- exchange). When pHi was increased above the normal steady-state pHi, a DIDS-inhibitable and Na(+)-independent acidifying recovery was evident, indicating the presence of Cl-/HCO3- exchange. Astrocytes, but not C6 cells, contain a fourth pH-regulating transporter, Na(+)-HCO3- cotransport; in the presence of CO2, depolarization caused an alkalinization of 0.12 +/- 0.01 (n = 8) and increased the rate of CO2-induced alkalinization from 0.23 +/- 0.02 to 0.42 +/- 0.03 pH unit/min. Since C6 cells lack the Na(+)-HCO3- cotransporter, they are an inferior model of pHi regulation in glia. Our results differ from previous observations in glia in that: 1) Na+/H+ exchange was entirely inhibited by amiloride; 2) Na+ + HCO3-/Cl- exchange was present and largely responsible for CO2-induced alkalinization; 3) Cl-/HCO3- exchange was only active at pHi values above steady state; and 4) depolarization-induced alkalinization of astrocytes was seen only in the presence of CO2.

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Section: Discussionsupporting

confidence: 91%

Intracellular pH regulation in primary rat astrocytes and C6 glioma cells

Shrode

Putnam

1994

Glia

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“…In particular, activation of glial GABA receptors, which are permeable to Cl-and HC03 (51 ), results in acidification of glial pH, accompanied by a more alkaline shift of pHo (52)(53)(54)(55). Similarly, activation of glial glutamate receptors decreases pH, by --0.2 to 0.3 pH units, suggesting that these cation channels are also permeable to H+ (56).…”

Section: Glial Modulation Of [K+]omentioning

confidence: 95%

Review : Glial Neuronal Interactions: A Physiological Perspective

Sontheimer

1995

Neuroscientist

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Throughout the nervous system, neurons are closely surrounded by glial cells, leaving only a 20-nm wide extracellular space filled with interstitial fluid. Ions, transmitters, hormones, nutrients, and waste products all share this narrow diffusion pathway. Because the interstitial space occupies only a small volume, neuronal activity can lead to appreciable changes in the extracellular concentration of ions, protons, and neurotransmitters. These changes can affect neuronal activity and are believed to be influenced by glial cells. The proximity of glial processes to synapses and axons make glial cells ideal partners to sequester ions and transmitters released by neurons. The failure of glial cells to perform such essential homeostatic functions can have profound effects, and these homeostatic activities may constitute one way in which glial cells can influence neuronal signaling. In addition, glial cells, which, unlike most neurons, are coupled to each other through gap-junctions, communicate with each other and possibly also with adjacent neurons through propagated intracellular Ca 2+ waves. The importance of such interglial signaling is not understood. Additionally, glial cells and neurons mutually modulate their expression of ion channels, most likely through factors released into the extracellular space. The range of responses observed in glial cells and their intimate anatomical relationship with neurons suggest a broader role for glia than is currently appreciated. It also emphasizes the importance of a better understanding of glial-neuronal interactions to an understanding of brain function. The Neuroscientist 1: [328][329][330][331][332][333][334][335][336][337] 1995

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“…This process leads to extracellular alkalinization. As shown by Kaila et al (1991) it is dependent upon activation of GABA, receptors. Both processes require intracellular as well as extracellular carbonic anhydrase activity.…”

Section: Carbsnf C Anhydresementioning

confidence: 95%

“…A receptor-activated mechanism for extracellular alkalinization has been established and thorouoghly studied by Kaila et al (1990Kaila et al ( , 1991Kaila et al ( , 1992. It operates by causing an efflux of bicarbonate ions through activated GABAA channels, which have keen found to be relatively permeable also to bicarbonate ions in cultured rat astrocytes (Kaila et ial.…”

Section: Carbsnf C Anhydresementioning

confidence: 96%

“…B990), with that suggested above for generation of intracellular alkalinization in astrocytes. However, in the GABA-operated mechanism it is the bicarbonate ions, not the protons, that are extruded, and this mechanism is not stimulated by an increased extracellular Kf concentration (Kaila et al 1991). Astrocytes are able to carry out a SITS-inhibited HCO:/Clexchange (Kimelberg t.t 01.…”

Section: Carbsnf C Anhydresementioning

confidence: 99%

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Ions, water, and energy in brain cells: A synopsis of interrelations

Hertz¹,

Code²,

Syková³

1992

Can. J. Physiol. Pharmacol.

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A brief summary is given of some of the key points of the individual contributions at this International Brain Research Organization satellite meeting, presenting up-to-date, expert knowledge of energy metabolism, ionic turnover, and cell swelling at the cellular level of the mammalian central nervous system. On the basis of this material, we are also suggesting a unified concept of reciprocal interactions between metabolism, ion carriers, and ion channels, which are of crucial importance for the function of the central nervous system.

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Fall in intracellular pH mediated by GABAA receptors in cultured rat astrocytes

Cited by 41 publications

References 24 publications

Intracellular pH regulation in primary rat astrocytes and C6 glioma cells

Intracellular pH regulation in primary rat astrocytes and C6 glioma cells

Review : Glial Neuronal Interactions: A Physiological Perspective

Ions, water, and energy in brain cells: A synopsis of interrelations

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