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E Syková

Publications and source records attributed to E Syková.

At least 19 recordsLinked to original sources
PubMed1992

K+ and pH homeostasis in the developing rat spinal cord is impaired by early postnatal X-irradiation.

Activity-related transient changes in extracellular K+ concentration ([K+]e) and pH (pHe) were studied by means of ion-selective microelectrodes in neonatal rat spinal cords isolated from pups 2-14 days of age. Pups 1 to 2 days old were X-irradiated to impair gliogenesis and spinal cords were isolated 2-13 days postirradiation (PI). In 2- to 14-day-old pups PI stimulation produced ionic changes that were the same as those in 3- to 6-day-old control (non-irradiated) pups; e.g. the [K+]e increased by 4.03 +/- 0.24 mM (mean +/- S.E.M., n = 30) at a stimulation frequency of 10 Hz and this was accompanied by an alkaline shift of 0.048 +/- 0.004 pH units (mean +/- S.E.M., n = 32) pH units. By contrast, stimulation in non-irradiated 10- to 14-day-old pups produced smaller [K+]e changes, of 1.95 +/- 0.12 mM (mean +/- S.E.M., n = 30), and an acid shift of 0.035 +/- 0.003 pH units which was usually preceded by a scarcely discernible initial alkaline shift, as is also the case in adult rats. Our results show that the decrease in [K+]e ceiling level and the development of the acid shift in pHe are blocked by X-irradiation. Concomitantly, typical continuous development of GFAP-positive reaction was disrupted and densely stained astrocytes in gray matter of 10- to 14-day-old pups PI revealed astrogliosis. In control 3- to 6-day-old pups and in pups PI the stimulation-evoked alkaline, but not the acid, shift was blocked by Mg2+ and picrotoxin (10(-6) M). The acid shift was blocked, and the alkaline shift enhanced, by acetazolamide, Ba2+, amiloride and SITS. Application of GABA evoked an alkaline shift in the pHe baseline which was blocked by picrotoxin and in HEPES-buffered solution. By contrast, the stimulus-evoked alkaline shifts were enhanced in HEPES-buffered solutions. The results suggest a dual mechanism of the stimulus-evoked alkaline shifts. Firstly, the activation of GABA-gated anion (Cl-) channels induces a passive net efflux of bicarbonate, which may lead to a fall in neuronal intracellular pH and to a rise in the pHe. Secondly, bicarbonate independent alkaline shifts may arise from synaptic activity resulting in a flux of acid equivalents.

Animals↗
PubMed1992

Extracellular K+, pH, and volume changes in spinal cord of adult rats and during postnatal development.

Activity-related transient changes in extracellular K+ concentration ([K+]c), extracellular pH (pHc), and extracellular volume (EC volume) were studied by means of ion-selective microelectrodes in the adult rat spinal cord in vivo and in neonatal rat spinal cords isolated from pups 3-14 days of age. Repetitive electrical nerve stimulation (10-100 Hz) in adults elicited increases in [K+]c by about 2.0-3.5 mM, followed by a poststimulation K+ undershoot and triphasic alkaline-acid-alkaline changes in pHc. In 3- to 6-day-old pups, the [K+]c increased by as much as 6.5 mM at a stimulation frequency of 10 Hz, and this was accompanied by an alkaline shift. Increases in [K+]c as large as 1.3-2.5 mM accompanied by an alkaline shift were evoked by a single electrical stimulus. Stimulation in 10- to 13-day-old pups produced smaller [K+]c change and an acid shift, which was preceded by a small initial alkaline shift, as in adult rats. We conclude that glial cells buffer the activity-related [K+]c increase and alkaline pHc shifts. Mg2+ blocked the alkaline but not the acid shift. Acetazolamide had no effect on the alkaline shift but blocked the acid shift. The alkaline shift was enhanced and the acid shift blocked by Ba2+, amiloride, 4-acetamido-4'-isothiocyanotostilbene-2,2'-disulfonic acid (SITS), and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). Activity-related acid shifts therefore have a complex mechanism, which includes Na+H+ exchange, Cl-/HCO3- exchange, or Na+/Cl-/H+/HCO3- antiport, Na(+)-HCO3- cotransport, and H+ efflux through voltage-sensitive H+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Extracellular space volume changes in the rat spinal cord produced by nerve stimulation and peripheral injury.

Double-barrelled potassium and tetramethylammonium-sensitive microelectrodes were used in diffusion studies with tetramethylammonium ions, which remain essentially extracellular during the measurements. Activity-related changes in the extracellular space (ECS) volume fraction (alpha), ECS tortuosity (lambda) and the dynamics of the ECS volume changes were examined in the spinal dorsal horns of rats. The alpha and lambda in L4 and L5 segments of unstimulated rats were alpha = 0.24 +/- 0.01 (i.e. ECS occupied 24 +/- 1% of the total spinal cord volume) and lambda = 1.54 +/- 0.04 (mean +/- S.D. of mean, n = 21). The values were not significantly different throughout the dorsal horn. Repetitive electrical stimulation of peripheral nerves at 3-100 Hz increased extracellular potassium concentration [( K+]e) and ECS volume in Rexed laminae III-V by 15.8 +/- 2.7% (n = 5). After the end of stimulation, when the [K+]e decreased below the original baseline (K+ undershoot), the ECS volume decreased by 20-45%. The magnitude and duration of ECS volume decrease were positively related to the stimulation frequency and duration. The ECS volume decrease was maximal at 2-10 min after the stimulation had been discontinued, and it returned to the prestimulation values in 15-40 min. The ECS volume decreased by 20-50% after injury of the ipsilateral hind paw evoked either by subcutaneous injection of turpentine (n = 5), or by thermal injury (n = 6). The maximal changes were found in Rexed laminae III-V, 5-10 min after injection of turpentine and 10-25 min after thermal injury, and persisted for more than 120 min and 30 min, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Role of glia in K+ and pH homeostasis in the neonatal rat spinal cord.

Stimulation-evoked transient changes in extracellular potassium ([K+]e) and pH (pHe) were studied in the neonatal rat spinal cords isolated from 3-13-day-old pups. In unstimulated pups the [K+]e baseline was elevated and pHe was more acid than that in Ringer's solution (3.5 mM K+, pH 7.3-7.35). The [K+]e and pHe in 3-6-day-old pups was 3.91 +/- 0.12 mM and pHe 7.19 +/- 0.01, respectively, while in 10-13-day-old pups it was 4.35 +/- 0.15 mM and 7.11 +/- 0.01, respectively. The [K+]e changes evoked in the dorsal horn by a single electrical stimulus were as large as 1.5-2.5 mM. Such changes in [K+]e are evoked in the adult rat spinal cord with stimulation at a frequency of 10-30 Hz. The maximal changes of 2.1-6.5 mM were found at a stimulation frequency of 10 Hz in 3-6-day-old animals. In older animals the [K+]e changes progressively decreased. The poststimulation K(+)-undershoot was found after a single stimulus as well as after repetitive stimulation. In 3-8-day-old pups, the stimulation evoked an alkaline shift, which was followed by a smaller poststimulation acid shift when the stimulation was discontinued. In pups 3-4-days-old the stimulation evoked the greatest alkaline shifts, i.e., by as much as 0.05 pH units after a single pulse and by about 0.1 pH units during stimulation at a frequency of 10 Hz. In 5-8-day-old pups, the alkaline shift became smaller and the poststimulation acid shift increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1991

Molecular mechanisms of memory formation.

Studies with neonate chicks, trained on a passive avoidance task, suggest that at least two shorter-term memory stages precede long-term, protein synthesis-dependent memory consolidation. Posttetanic neuronal hyperpolarization arising from two distinct mechanisms is postulated to underlie formation of these two early memory stages. Maintenance of the second of these stages may involve a prolonged period of hyperpolarization brought about by phosphorylation of particular proteins. A triggering mechanism for long-term consolidation is postulated to occur at a specific time during the second stage, and may involve reinforcement-contingent release of neuronal noradrenaline stimulating cAMP-dependent intracellular processes. The possibility that astroglia may have a critical role to play in these early stages of memory processing is raised.

Animals↗
PubMed1990

Extracellular alkaline-acid-alkaline transients in the rat spinal cord evoked by peripheral stimulation.

Regional differences in extracellular pH (pHe) were found in unstimulated rat spinal cord using double-barrel pH-sensitive microelectrodes. The pHe in the lower dorsal horn (laminae III-VII) was about 7.15, i.e. by about 0.2 pH units lower than that measured in the cerebrospinal fluid. Transient acid shifts in pHe by 0.01-0.05 pH units were found when acute nociceptive stimuli (pinch, press, heat) were applied to the hind paw. Chemical or thermal injury evoked by subcutaneous injection of turpentine or by application of 1-3 ml of hot oil onto the hindpaw produced a long-term decrease in pHe base line in the lower dorsal horn by about 0.05-0.1 pH units. The decrease in pHe began 2-10 min after injury and persisted for more than 2 h. Electrical nerve stimulation (10-100 Hz, 20-60 s) elicited biphasic (acid-alkaline) or triphasic (alkaline-acid-alkaline) changes in pHe which have a similar depth profile as the concomitantly recorded increase in [K+]e. An initial alkaline shift by about 0.005 pH units was found to be significantly decreased by La3+, an H+ channel blocker. The dominating acid shift by about 0.1-0.2 pH units was accelerated and increased by acetazolamide (carbonic anhydrase inhibitor) showing that the high buffering capacity of the extracellular fluid may hamper the resolution of acid perturbations. Stimulation-evoked acid shifts were blocked by amiloride, SITS, DIDS and La3+ and therefore have a complex mechanism which includes Na+/H+ exchange, Cl-/HCO3- cotransport and/or Na+/Cl-/H+/HCO3- antiport and H+ efflux through voltage-sensitive H+ channels. The poststimulation alkaline shift (alkaline undershoot) was blocked by ouabain and reflects coupled clearance of K+ and H+ by active transport processes.

Acetazolamide↗
PubMed1989

Stimulus-related potassium changes in the organ of Corti of guinea-pig.

1. Potassium concentration was measured with double-barrelled K+-selective microelectrodes within the organ of Corti in the first turn of the guinea-pig cochlea. 2. Penetration of the electrode from scala tympani through the basilar membrane was accompanied by an increase in K+ resting level from 3.0 mmol/l in perilymph to 3.4 mmol/l in cortilymph (n = 8). K+ resting level was not significantly different in various extracellular regions of the organ of Corti. On penetration of the cuticular plate, the K+ level reached 140 mmol/l simultaneously with the occurrence of a +80 mV endocochlear potential. Impalement of hair cells and supporting cells was accompanied by an increase in K+ level, but intracellular K+ level was not systematically measured. 3. Stimulation with pure tones over the frequency range 500 Hz to 25 kHz produced changes in the K+ level in the organ of Corti. The magnitude of these changes was dependent on stimulus frequency and intensity. At high sound intensities the K+ level in the tunnel of Corti could increase by typically 1 mmol/l, while a maximum increase of 3 mmol/l with respect to the resting level was observed immediately adjacent to inner hair cells. 4. During brief exposures to moderate intensity, pure tone acoustic stimulation (10 s, less than 80 dB SPL (sound pressure level] of frequency 4 kHz or greater the K+ level in the extracellular fluid of the organ of Corti rose monotonically to a steady peak level. On cessation of the stimulus the K+ level fell monotonically with a time constant of about 2 s to a level close to the pre-stimulus level. In some cases this level was slightly above the pre-stimulus level. 5. For brief exposures to moderate intensity sound (10 s, less than 80 dB SPL) the extracellular potential in the organ of Corti became more positive. The amplitude of this sound-evoked change adapted during stimulation to a level approximately one-fifth of its initial value. Upon cessation of the stimulus the potential fell transiently below its pre-stimulus level, before recovering to that level. The time constant of these changes was between 2 and 3 s. 6. Iso-response tuning curves for the sound-evoked elevation in K+ level in the organ of Corti in animals in good condition were similar to iso-rate tuning curves for primary afferent fibres reported previously.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗
PubMed1988

Increase in extracellular potassium level in rat spinal dorsal horn induced by noxious stimulation and peripheral injury.

Changes in extracellular K+ concentration ([K+]e) in dorsal horn were studied by means of double-barrel K+-sensitive microelectrodes in rats anesthetized with Nembutal. Acute nociceptive stimuli (pinch, press, heat) applied to the hind paw induced a transient increase in [K+]e of about 0.1-0.5 mM which persisted for 5-30 s. Regional variations in [K+]e were found in unstimulated rat spinal cords. The K+ level in the lower dorsal horn (laminae III-V) was by about 0.4 +/- 0.06 mM higher than that in more superficial laminae and in the ventral horn. Chemical or thermal injury was evoked by: s.c. injection of 0.1-0.5 ml formalin or turpentine into the hind paw, by application of mustard oil onto the skin, or by thermal injury of the hind paw. These produced a long-term increase in [K+]e in the lower dorsal horn by 0.3-3.0 mM in 75% of animals (n = 27). The increase in [K+]e began 5-15 min after injury and persisted for more than 2 h. In the rest of the animals, occasional elevation in [K+]e of 0.1-0.3 mM were observed. The K+ increases evoked by acute nociceptive stimuli as well as by injury were blocked by preinjecting the hind paw with 1% procaine. However, when procaine was applied 20 min or later after injury, the evoked long-term rise in [K+]e was not affected. This shows that the long-term K+ accumulation results from self-sustained abnormal neuronal firing induced in the dorsal horn by injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Extracellular pH and stimulated neurons.

The use of ion-sensitive microelectrodes enabled us to follow the dynamic changes in extracellular pH (pHe) together with those in the extracellular concentration of some biologically important ions, particularly K+ and Ca2+. Activity-related changes in pHe were studied in isolated spinal cords of frogs and in spinal cords of rats in vivo. Repetitive electrical stimulation of an afferent input led either to triphasic alkaline-acid-acid changes (90% of frogs) or to triphasic alkaline-acid-alkaline changes (10% of frogs and rats) with the greatest changes in the lower dorsal horns. The transient acid shift by as much as 0.15-0.25 pH units is dominant and builds up during the stimulation. The changes in pHe were also found in response to various adequate stimuli applied to the skin on the hind limb. Using specific inhibitors of Na+/H+ exchange, K+-Cl- co-transport, Cl-/HCO3- exchange, the Na+/K+ pump and carbonic anhydrase, we found pHe homeostasis to be impaired and stimulation-induced changes in pHe decreased. We conclude that the pHe changes evoked by electrical or adequate stimulation of an afferent input are not determined by changes in extracellular strong ion concentration differences due to accumulation of lactate, since we found no effect of NaF, a metabolic blocker of lactate production. However, lactate accumulation has been demonstrated during seizures, spreading depression and anoxia. Recently, it has been recognized that the observed pHe changes can affect permeability of membrane ionic channels, neuronal excitability and glial cell function.

Acid-Base Equilibrium↗
PubMed1988

Effects of carbon dioxide on extracellular potassium accumulation and volume in isolated frog spinal cord.

A 6-10-fold increase in pCO2 in the superfusing Ringer solution increased the volume of the extracellular space (ECS) and changed the spatial distribution and amplitude of the extracellular K+ accumulation which resulted from dorsal root stimulation. Using the increase in tetraethylammonium concentration [( TEA+]) resulting from iontophoretic injection of that ion in the extracellular fluid as an indication of the volume of the ECS, it was found that in high pCO2 the ECS volume in spinal dorsal horn increased by more than 60%. In addition, in the presence of raised pCO2 we also observed the following: (1) The rate of diffusion of TEA+ into the dorsal horn increased. (2) The accumulation of K+ evoked by single or tetanic stimulation of the dorsal root was less. (3) The clearance of K+ was slowed down. (4) The regions where K+ accumulated were more restricted. (5) The K+ evoked depolarization of the primary afferent fibres decreased. (6) In contrast to TEA+, the rate of diffusion of K+ into the dorsal horn decreased. The effects of an increase in pCO2 on K+ accumulation and clearance appear to result from an increase in ECS volume and a possible decrease in glial electrical coupling which interferes with glial spatial buffering of K+.

Animals↗
PubMed1988

Stimulation-evoked changes in extracellular pH, calcium and potassium activity in the frog spinal cord.

Double-barrel ion-sensitive microelectrodes were used to measure activity-related changes in extracellular pH (pHe), potassium and calcium concentration ([K+]e and [Ca2+]e) in the spinal dorsal horns of frogs. Repetitive stimulation (30-100 Hz) of the dorsal root evoked transient acidification in the lower dorsal horn by 0.25 pH units, which was accompanied by an increase in [K+]e by 4-5 mmol/l and a decrease in [Ca2+]e by 0.5 mmol/l. The pHe changes were found to have a typical depth profile and increased with the stimulation frequency, intensity and duration. The maximum of pHe changes was reached in 25-30 s of stimulation, and when stimulation continued further no greater pHe changes were achieved. Similarly as the K+ and Ca2+ transients, the pHe reached a ceiling level, which was 0.2-0.25 pH units more acid than the pH of the Ringer solution. The poststimulation K+ undershoot below the resting K+ level (3 mmol/l) was accompanied by an alkaline shift before the original pH base line. The rise time of the pHe changes was slower than that of [K+]e and [Ca2+]e changes. However, the redistribution of all the ionic changes had a similar time course. The clearance of changes in [K+]e and pHe was slowed by ouabain. The depression of the acid shift required higher concentrations of ouabain than the depression of the alkaline shifts. Acetazolamide, a carbonic anhydrase inhibitor, depressed the acid and enhanced the alkaline shift. Superfusion of the cord with elevated [K+]e was accompanied by a prompt and progressive acid shift, the lowering of [K+]e by an alkaline shift. The stimulus-evoked K+ increase and acid shift were depressed during the elevated [K+]e, while the alkaline shift was enhanced. Spontaneous elevations of [K+]e were accompanied by acid shifts of a similar time course. The results are discussed in terms of stimulus-evoked changes in extracellular strong ion differences [SID]e, and of their possible physiological significance.

Acetazolamide↗
PubMed1987

Longitudinal flow of endolymph measured by distribution of tetraethylammonium and choline in scala media.

Longitudinal endolymph flow rate in the guinea pig cochlea was measured by determining the rate of migration of extrinsic ions, tetraethylammonium chloride (TEA) or choline, with a potassium sensitive ion-selective microelectrode (ISM). Low concentrations of iontophoretically injected TEA were detected with the ISM at various distances from the injection electrode. The results were variable when the ISM was used to record spread of TEA from turn II to turn I and vice versa. However, consistent data were obtained when the TEA spread was measured at different electrode separations (0.2, 0.5, 0.7 mm) within turn II. Electrode locations were systematically exchanged without changing their distance, i.e. the ISM electrode was placed basally or apically with respect to the TEA electrode. Comparison of data with a model, which combines the bulk diffusion of TEA and the flow of endolymph, is consistent with a rate of endolymph flow in turn II of about 0.2 mm/min, apex to base. A similar value was also obtained with the iontophoretic injection of choline. The endolymph flow rate may be different in turn I as indicated by measurements of compound action potential (CAP) changes. However, the results of experiments when TEA spread is measured at large distances must be interpreted cautiously because TEA may enter cellular walls of the cochlear duct and alternative routes of transport may be involved.

Action Potentials↗
PubMed1987

Modulation of spinal cord transmission by changes in extracellular K+ activity and extracellular volume.

The neuronal activity in spinal cord in response to electrical or adequate stimulation of afferent fibres increases extracellular K+ activity. The increase during a stimulation can reach 9-10 mM (so-called ceiling level) and persists for some time even when a stimulation is discontinued. The activation of a neuronal Na-K pump is a limiting factor in stimulation-evoked increase in extracellular K+ activity and in the time course of its recovery to the resting level. Drugs that affect either the neuronal activity (picrotoxin, strychnine, GABA, 5-HT) or activity of Na-K ATPase (oubain, naloxone, morphine, enkephalins) substantially change the K+ transience. Repetitive electrical stimulation of low threshold cutaneous afferents at frequency 1-100 Hz induced transient shrinkage of extracellular space in spinal dorsal horns by 5-75%. The increase in extracellular K+ activity depolarizes the membranes of neurones, glial cells, and primary afferent fibres and may eventually lead to either facilitation or inhibition of synaptic transmission. It is also suggested that the transient poststimulation changes in extracellular volume may alter synaptic potency in spinal cord.

Animals↗
PubMed1985

Changes in extracellular potassium accumulation produced by opioids and naloxone in frog spinal cord: relation to changes of Na-K pump activity.

Superfusion of the isolated spinal cord of the frog with Ringer solution containing ouabain or naloxone elevated resting [K]e and depolarized the dorsal roots, while the application of enkephalins or morphine decreased [K]e and hyperpolarized the dorsal roots. During repetitive electrical stimulation (10-100 Hz) ouabain and naloxone increased the transient changes of [K]e and enhanced dorsal root potentials. When stimulation stopped, the clearance of K+ was slowed, the poststimulation K+ undershoot disappeared and poststimulation hyperpolarization of dorsal roots was diminished. The opposite effects were found during the application of enkephalins or morphine. Our results imply that the activity of the membrane Na-K pump is reduced after application of naloxone, while opioids enhance it.

Animals↗