Stimulus-induced changes in extracellular Na+ and Cl− concentration in relation to changes in the size of the extracellular space

Dietzel, Irmgard D.; Heinemann, Uwe; Hofmeier, G.; Lux, H. D.

doi:10.1007/bf00238100

Cited by 204 publications

(126 citation statements)

References 27 publications

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“…Our results suggest that during low isoflurane conditions ongoing inhibitory activities establish a given extracellular Cl ] o is around 150 mM (Dietzel et al, 1982), our recorded difference thus represents a 18% increase. Within seconds of the onset of this increase we recorded the appearance of the first isoelectric episode (Fig.…”

Section: Modification Of Inhibition During Bsmentioning

confidence: 52%

Cortical Inhibition during Burst Suppression Induced with Isoflurane Anesthesia

Ferron¹,

Kroeger²,

Chever³

et al. 2009

J. Neurosci.

123

126

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Isoflurane is a widely used anesthetic which safely and reversibly induces deep coma and associated burst suppression (BS) electroencephalographic patterns. Here we investigate possible underlying causes for the state of cortical hyperexcitability which was recently shown to be one of the characteristics of BS. Our hypothesis was that cortical inhibition is diminished during isoflurane-induced BS. Experiments were performed in vivo using intracellular recordings of cortical neurons to assess their responsiveness to stimulations of connected thalamic nuclei. We demonstrate that during BS EPSPs were diminished by 44%, whereas inhibitory potentials were completely suppressed. This finding was supported by additional results indicating that a decrease in neuronal input resistance normally found during inhibitory responses under low isoflurane conditions was abolished in the BS condition. Moreover, removal of inhibition occasionally revealed excitatory components which were absent during recordings before the induction of BS. We also show that the absence of inhibition during BS is not caused by a blockage of GABA receptors, since iontophoretically applied GABA shows receptor availability. Moreover, the concentration of extracellular chloride was increased during BS, as would be expected after reduced flow of chloride through GABA A receptors. Also inhibitory responses were reinstated by selective blockage of glial glutamate transporters with dihydrokainate. These results suggest that the lack of inhibition during BS is caused by reduced excitation, probably resulting from increased glial uptake of glutamate stimulated by isoflurane, which creates a diminished activation of cortical interneurons. Thus cortical hyperexcitability during BS is favored by suppressed inhibition.

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Section: Modification Of Inhibition During Bsmentioning

confidence: 52%

Cortical Inhibition during Burst Suppression Induced with Isoflurane Anesthesia

Ferron¹,

Kroeger²,

Chever³

et al. 2009

J. Neurosci.

123

126

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“…Our data are compatible with this view. Another mechanism by which K + uptake could occur through Ba 2+ -sensitive channels would be via spatial buffer currents (Orkand et al 1966;Coles and Orkand 1983;Gardner-Medwin 1983;Dietzel et al 1982). According to this view, K + would enter the glial syncytium through K + channels as a result of a spatial potential gradient along the membrane of the electrically coupled glia; the rise of intraglial aC\x would be explained by a redistribution of Cr ions within the linked glial cells.…”

Section: Discussionmentioning

confidence: 99%

“…Several factors such as spatial buffering (Orkandetal. 1966;Dietzel et al 1982;Coles and Orkand 1983;Gardner-Medwin 1983), Na + -K + pump activity (Kukes et al 1976;Walz and Hertz 1982;Grisaretal. 1983), KCl cotransport (Kimelberg and Frangakis 1985;Walz and Hinks 1985), or the presence of Ba 2+ -sensitive K + channels (Walzetal.…”

Section: Introductionmentioning

confidence: 99%

Cellular mechanisms of potassium homeostasis in the mammalian nervous system

Grafe¹,

Ballanyi²

1987

Can. J. Physiol. Pharmacol.

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Double-barrelled ion-sensitive microelectrodes were used to measure changes in the intracellular activities of K+, Na+, and Cl− (aKi, aNai, aCli) in neurones of rat sympathetic ganglia and in glial cells of slices from guinea-pig olfactory cortex. In sympathetic neurones, carbachol and γ-aminobutyric acid (GABA) produced a reversible decrease of aKi. The decrease of aKi during carbachol was accompanied by a rise of aNai, whereas in the presence of GABA decreases of aKi and aCli were seen. The reuptake of K+ released during the action of carbachol was completely blocked by ouabain, whereas furosemide inhibited the aKi recovery after the action of GABA. In glial cells, in contrast to the observations in the sympathetic neurones, aKi and aCli increased, whereas aNai decreased when neuronal activity was enhanced by repetitive stimulation of the lateral olfactory tract. It was found that barium ions and ouabain strongly reduced the activity-related rise of intraglial aKi in slices of guinea-pig olfactory cortex. These data show that mammalian neurones as well as glial cells possess several K+ uptake mechanisms that contribute to potassium homeostasis. Ouabain, furosemide, and Ba2+ are useful pharmacological tools to separate these mechanisms.

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“…Astrocytes are believed to regulate [K + ] o in the brain by (among other mechanisms) K + spatial buffering (13)(14)(15) The high K + conductance of astrocyte endfeet may function to make K + spatial buffering a far more powerful process than previously envisioned. In the absence of a membrane specialization, K + spatial buffering would function to transfer excess K + from the site of a [K + ] o increase to other regions of neural tissue.…”

mentioning

confidence: 99%

High Potassium Conductance in Astrocyte Endfeet

Newman

1986

Science

275

158

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The distribution of potassium conductance over the surface of freshly dissociated salamander astrocytes was determined by monitoring cell depolarizations evoked by focal increases in the extracellular potassium concentration. The specific potassium conductance of the endfoot processes of these cells was approximately tenfold higher than the conductance of other cell regions. This dramatically nonuniform conductance distribution may play an important role in the regulation of extracellular potassium levels by glia in the brain.Although astrocytes outnumber all other types of glial cells and neurons in the vertebrate brain, their membrane properties and functions are not well understood (1,2). Müller cells, the principal glial cells of the retina, resemble astrocytes in many respects. In Müller cells, 95 percent of the total cell membrane conductance is localized to the cell's endfoot process (3, 4). It is not known whether this striking membrane specialization occurs only in these specialized retinal cells or whether membrane conductance is also distributed nonuniformly across the surface of all astrocytes throughout the brain. I have addressed this issue by determining the distribution of potassium conductance over the surface of freshly dissociated astrocytes.Astrocytes were isolated from the optic nerve of the salamander Ambystoma tigrinum. Optic nerves were excised with the meninges intact and partially teased apart before incubation in papain [0.6 mg/ml in Hepes-buffered Ringer solution; see (4) for composition of Ringer solutions] for 30 minutes at 28°C. They were then washed several times in Hepes-Ringer and maintained at 0°C for 3 to 4 hours before the cells were dissociated by gentle trituration. Isolated cells were placed in a recording chamber and perfused with a bicarbonate-buffered Ringer solution (containing 2.5 mM K + ) maintained at 15°C. Experiments were performed on cells within 2 hours of dissociation.The cells isolated with this dissociation procedure all had a similar appearance. They had several stout, branching processes radiating from a prominent soma. These cells were provisionally identified as astrocytes on the basis of their appearance and because astrocytes are the principal cell type found in the salamander optic nerve. [Amphibian optic nerves contain no intrinsic neurons and few myelinated fibers or oligodendrocytes (5,6).] The radial processes of these cells terminated in bulbous enlargements. These were the endfeet, which lie at the ends of astrocyte processes in the intact brain and optic nerve. Cells had from 3 to 17 endfeet each, although the exact number was sometimes difficult to determine (mean = 8.7; n= 30). Some radial processes lacked endfeet, probably because they were broken off during dissociation. Dissociated cells were characterized by immunofluorescent labeling of glial fibrillary acidic protein (GFAP), a characteristic cytoplasmic marker of astrocytes (7). All dissociated cells were labeled heavily with monoclonal antibodies to GFAP (Fig. 1), identifying th...

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Stimulus-induced changes in extracellular Na+ and Cl− concentration in relation to changes in the size of the extracellular space

Cited by 204 publications

References 27 publications

Cortical Inhibition during Burst Suppression Induced with Isoflurane Anesthesia

Cortical Inhibition during Burst Suppression Induced with Isoflurane Anesthesia

Cellular mechanisms of potassium homeostasis in the mammalian nervous system

High Potassium Conductance in Astrocyte Endfeet

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