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

Sykové, Eva

doi:10.1007/978-3-642-76937-5

Cited by 49 publications

(50 citation statements)

References 322 publications

(501 reference statements)

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“…This study revealed progressive shrinkage of the ECS to -50% (to a = 0.12 ± 0.04, mean ± SD), but no significant changes occurred in tortuosity or nonspecific tetramethylammonium ion (TMA + ) up take during exposure to hypoxic media with contin ual availability of glucose. The relatively small in crease in extracellular K + concentration by 7.7 ± 1.2 rnM in this study, which is in contrast to the large K + increases observed during hypoxia in vivo (for review see Sykova, 1983Sykova, , 1992, suggests that only mild hypoxia has been evoked and/or that the changes in vivo may be different. Diffusion param eters during anoxia have not yet been sufficiently studied in vivo.…”

contrasting

confidence: 74%

Extracellular Volume Fraction and Diffusion Characteristics during Progressive Ischemia and Terminal Anoxia in the Spinal Cord of the Rat

Syková

Svoboda

Polák

et al. 1994

J Cereb Blood Flow Metab

166

121

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Summary: Extracellular space (ECS) volume fraction(IX), ECS tortuosity (A), and nonspecific uptake (k'), three parameters affecting the diffusion of substances in ner vous tissue, were studied during ischemia and anoxia in the rat spinal cord gray matter in vivo. Progressive isch emia evoked by exsanguination, as well as anoxia evoked by respiratory or cardiac arrest, produced prominent ex tracellular K + and pH changes closely related to a de crease in blood pressure and amplitude of field potentials. With use of ion-selective microelectrodes, the changes in the diffusion parameters were measured by quantitative analysis of concentration-time profiles of tetramethylam monium (TMA +) applied by iontophoresis concomitantly with ionic shifts. Under normoxic conditions (in rats with blood pressure of 80-110 mm Hg) diffusion parameters in the dorsal hom gray matter at depth 500-900 fLm were as follows: IX = 0.20 ± 0.019, A = 1.62 ± 0.12, k' = 4.6 ± 2.5 x 10-3 s -1 (mean ± SD, n = 39). Extracellular K +, pH, and diffusion properties gradually changed during progressive ischemia. As the blood pressure fell to 50-60 mm Hg and field potential amplitude to 20-60%, K + rose to 6-12 mM, pHe fell by -0.05-0.1 pH unit, and volume fraction of the ECS significantly decreased, to IX = 0.16 ± 0.019 (n = 22). Even though the tortuosity remained vir tually constant, the nonspecific uptake significantly de creased to k' = 3.4 ± 1.8 x 10-3 S-I. As the blood pressure fell to 20-30 mm Hg and field potential ampli tude to 0-6%, K + rose to 60-70 mM, pHe fell by -0.6-0.8 pH unit, and all three diffusion parameters significantly 301changed. The ECS volume fraction decreased to a = 0.05 ± 0.021, tortuosity increased to A = 2.00 ± 0.24, and TMA + uptake decreased to k' = 1.5 ± 1.6 x 10 -3 S -1 (n = 12). No further increase in extracellular K + or changes in the IX were found during and up to 120 min after the death of the animal. However, there was a further signif icant increase in A = 2.20 ± 0.14 and decrease in k' = 0.4 ± 0.3 x 10-3 s -1 (n = 24). The acid shift reached its maximum level at -5-10 min after respiratory arrest and then the pHe gradually increased by -0.2 unit. Full re covery to "normoxic" diffusion parameters was achieved after reinjection of the blood or after an injection of nor adrenaline during severe ischemia, if this resulted in a rise in blood pressure above 80 mm Hg and a decrease in extracellular K + below 12 mM. At -10 and 30 min after this recovery, the ECS volume fraction significantly in creased above "normoxic" values, to IX = 0.25 ± 0.016 (n = 7) and IX = 0.30 ± 0.021 (n = 6), respectively. The A and k' were not significantly different from the values found under normoxic conditions. Our data represent the first detailed in vivo measurements of diffusion parame ters IX, A, and k' during and after progressive ischemia and anoxia. The observed substantial changes in the diffusion parameters could affect the diffusion and aggravate the accumulation of ions, neurotransmitters, metabolic sub stances, and drugs ...

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contrasting

confidence: 74%

Extracellular Volume Fraction and Diffusion Characteristics during Progressive Ischemia and Terminal Anoxia in the Spinal Cord of the Rat

Syková

Svoboda

Polák

et al. 1994

J Cereb Blood Flow Metab

166

121

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“…An initial small acid shift corresponded to a rise in [K+]e of 1-2 mM and a subsequent larger acid shift corresponded to a rise in [K+]c of 50-70 mM. When [K+]c was stable, pHe revealed a second acid shift of 0.3-0.5 pH units that was separated from the first one by a small alkaline shift, presumably akin to SD (for re view, see Sykova, 1992). Figure 3 further shows that the second acid shift was accompanied by an increase in the TMA + baseline, indicating that this acidosis was accompanied by further cellular swelling and changes in ECS diffusion parameters.…”

Section: Changes In Ecs Diffusion Parameters In Gm Andwmmentioning

confidence: 99%

“…Neuronal and glial cell swelling during an energy deficit is the consequence of transmembrane ionic shifts resulting in the intracellular accumulation of K+, Ca2+, or Na+ and accompanied by an influx of water due to osmotic imbalance (for reviews see Sy kova, 1983;Kimelberg and Ransom, 1986;Sykova, 1992;Walz et aI., 1993). Anoxia/ischemia and, to a lesser degree, hypoxia or partial ischemia result in a dramatic decrease in extracellular space (ECS) vol ume and a decrease in the apparent diffusion coeffi cient (ADC) of tetramethylammonium (TMA +) or tetraethylammonium (TEA +) Lundbaek and Hansen, 1992;Sykova et aI., 1994b;Perez-Pinzon et aI., 1995) or ADC of water (Van der Toorn et aI., 1996), apparently due to cellu lar swelling.…”

mentioning

confidence: 99%

“…It has been recognized that ECS size and geometry affect movement and accumulation of substances within the CNS. Movement of substances in the ECS by diffusion is the underlying mechanism of nonsynaptic transmission (Bach-y-Rita, 1993;Bjelke et aI., 1995;Fuxe and Agnati, 1991;Nicholson and Rice, 1991;Sykova, , 1992. Compensatory shrinkage of the ECS during the pathological states leading to cellular swelling may further contribute to functional deficits and CNS damage.…”

mentioning

confidence: 99%

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Ischemia-Induced Changes in the Extracellular Space Diffusion Parameters, K⁺, and pH in the Developing Rat Cortex and Corpus Callosum

Voříšek

Syková

1997

J Cereb Blood Flow Metab

128

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“…Parallel water fluxes were suggested to be coupled to the transglial K ϩ fluxes (Nagelhus et al, 1999). The K ϩ and water fluxes, generated by neuronal activity and mediated by glial cells, are accompanied by swelling of cells and shrinkage of the extracellular space caused by the decreased extracellular osmolality (Dietzel et al, 1980;Jendelová and Syková, 1991;Syková, 1991). Cell volume alterations are important, particularly under pathological conditions such as epilepsy and ischemia in which overexcited neurons release large amounts of glutamate and K ϩ (Adachi et al, 1972;Glass and Dragunow, 1995;Nicholson and Syková, 1998).…”

Section: Introductionmentioning

confidence: 99%

Glutamate-Evoked Alterations of Glial and Neuronal Cell Morphology in the Guinea Pig Retina

Uckermann¹,

Vargová²,

Ulbricht³

et al. 2004

J. Neurosci.

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Neuronal activity is accompanied by transmembranous ion fluxes that cause cell volume changes. In whole mounts of the guinea pig retina, application of glutamate resulted in fast swelling of neuronal cell bodies in the ganglion cell layer (GCL) and the inner nuclear layer (INL) (by ϳ40%) and a concomitant decrease of the thickness of glial cell processes in the inner plexiform layer (IPL) (by ϳ40%) that was accompanied by an elongation of the glial cells, by a thickening of the whole retinal tissue, and by a shrinkage of the extracellular space (by ϳ18%). The half-maximal effect of glutamate was observed at ϳ250 M, after ϳ4 min. The swelling was caused predominantly by AMPAkainate receptor-mediated influx of Na ϩ into retinal neurons. Similar but transient morphological alterations were induced by high K ϩ and dopamine, which caused release of endogenous glutamate and subsequent activation of AMPA-kainate receptors. Apparently, retinal glutamatergic transmission is accompanied by neuronal cell swelling that causes compensatory morphological alterations of glial cells. The effect of dopamine was elicitable only during light adaptation but not in the dark, and glutamate and high K ϩ induced stronger effects in the dark than in the light. This suggests that not only the endogenous release of dopamine but also the responsiveness of glutamatergic neurons to dopamine is regulated by light-dark adaptation. Similar morphological alterations (neuronal swelling and decreased glial process thickness) were observed in whole mounts isolated immediately after experimental retinal ischemia, suggesting an involvement of AMPA-kainate receptor activation in putative neurotoxic cell swelling in the postischemic retina.Key words: glutamate; dopamine; ATP; neuroglia; circadian phase; ischemia; retina IntroductionGlial cells play crucial roles in supporting neuronal survival and information processing (Newman and Reichenbach, 1996): they regulate the extracellular homeostasis of relevant ions including K ϩ , control the water content of the extracellular space, and mediate the rapid termination of neuronal activity by transmitter uptake from the synaptic cleft (Matsui et al., 1999). In the retina, neuronally released K ϩ , water, and glutamate are cleared from the extracellular space mainly by the radial glial (Müller) cells. Retinal glial cells display a complex pattern of K ϩ channel expression in their plasma membranes that directs the flow of neuronally released K ϩ into the glial cell bodies and farther into the vitreous and the blood vessels (Kofuji et al., 2002). Parallel water fluxes were suggested to be coupled to the transglial K ϩ fluxes (Nagelhus et al., 1999). The K ϩ and water fluxes, generated by neuronal activity and mediated by glial cells, are accompanied by swelling of cells and shrinkage of the extracellular space caused by the decreased extracellular osmolality (Dietzel et al., 1980;Jendelová and Syková, 1991;Syková, 1991). Cell volume alterations are important, particularly under pathological conditions such as ...

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

Cited by 49 publications

References 322 publications

Extracellular Volume Fraction and Diffusion Characteristics during Progressive Ischemia and Terminal Anoxia in the Spinal Cord of the Rat

Extracellular Volume Fraction and Diffusion Characteristics during Progressive Ischemia and Terminal Anoxia in the Spinal Cord of the Rat

Ischemia-Induced Changes in the Extracellular Space Diffusion Parameters, K⁺, and pH in the Developing Rat Cortex and Corpus Callosum

Glutamate-Evoked Alterations of Glial and Neuronal Cell Morphology in the Guinea Pig Retina

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

Cited by 49 publications

References 322 publications

Extracellular Volume Fraction and Diffusion Characteristics during Progressive Ischemia and Terminal Anoxia in the Spinal Cord of the Rat

Extracellular Volume Fraction and Diffusion Characteristics during Progressive Ischemia and Terminal Anoxia in the Spinal Cord of the Rat

Ischemia-Induced Changes in the Extracellular Space Diffusion Parameters, K+, and pH in the Developing Rat Cortex and Corpus Callosum

Glutamate-Evoked Alterations of Glial and Neuronal Cell Morphology in the Guinea Pig Retina

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Ischemia-Induced Changes in the Extracellular Space Diffusion Parameters, K⁺, and pH in the Developing Rat Cortex and Corpus Callosum