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Biomedical subjects

E Syková

Publications and source records attributed to E Syková.

At least 91 records · Page 5Linked to original sources
PubMed1985

Role of endogenous opiates and extracellular K+ accumulation in the inhibition of frog spinal reflexes by electrical skin stimulation.

Electrical skin stimulation of the hind limb (10-100 Hz, 30 s-5 min) at the intensity which leads only to the excitation of low threshold afferents depressed (for 1-30 min) the flexor reflex evoked in spinal frogs by nociceptive stimuli. The inhibition, which lasted for longer than 5 min was blocked by naloxone. Short-term poststimulation effects were associated with an increase of extracellular K+ concentration (delta [K]e) and were not blocked by naloxone. Enkephalins or morphine applied to the spinal cord surface increased the threshold for flexor reflexes while naloxone decrease their threshold. The stimulation was followed by short-term hyperpolarization of primary afferents (PAH; 1-5 min) and by depression of dorsal root potentials (DPRs) which had a similar time course to the delta [K]e, and were not blocked by naloxone. This period was frequently followed by longlasting PAH and enhancement of DRPs (5-30 min), which were abolished by naloxone. Superfusion of the isolated spinal cord with opioids produced PAH and enhanced DRPs evoked by nociceptive stimuli, while naloxone or increase of [K] in Ringer solution depolarized primary afferents and depressed DRPs. It is suggested that the antinociceptive effects of electrical stimulation of low threshold cutaneous afferents in spinal frogs involves at least two mechanisms. The short-term effect may result from delta [K]e, especially at high stimulus strength and is equally effective against noxious and non-noxious stimuli. The longlasting effects selectively affecting nociceptive transmission appear to be produced by endogenous opioids.

Animals↗
PubMed1983

Elevated extracellular potassium concentration in unstimulated spinal dorsal horns of frogs.

The extracellular K+ concentration, [K+]e, was studied in unstimulated spinal cords in situ or in isolated spinal cords of frogs. The [K+]e in the dorsal horn at a depth of 150-500 microM exceeded the [K+]e found in the submeningeal fluid, in most of the upper dorsal horn and in the ventral horn by as much as 2.0 mmol . 1(-1). A substantially higher [K+]e, by 0.5-1.0 mmol . 1(-1) was also found in the intermediate region. The blockade of synaptic activity and of spontaneous activity in isolated spinal cords superfused by Ringer solution with high Mg2+ or Mn2+ concentrations decreased [K+]e in the dorsal horn and intermediate region to about 3.0 mmol . 1(-1). Similarly, the increase of spontaneous activity evoked in the isolated cords by changing the temperature of the Ringer solution, was associated with an increase of [K+]e in the dorsal spinal horn. The data suggest that the high [K+]e in the unstimulated dorsal horn results from K+ accumulation during spontaneous activity of interneurones, and its possible physiological role is discussed.

Animals↗
PubMed1981

Extracellular potassium accumulation in the frog spinal cord induced by stimulation of the skin and ventrolateral columns.

1. Changes in extracellular K(+) concentration (Delta[K](e)), dorsal root potentials (DRPs) and single unit activity were studied in the frog spinal cord in response to stimulation of the skin of the hindlimb by touch, pressure, hot water (heat), single electrical pulses and to stimulation of the ventrolateral columns (LC).2. Single electrical pulses, various types of adequate stimulation applied to the skin of the hind limb for 1-2 s as well as single volleys of LC led to a Delta[K](e) of up to 0.2 mmol.l(-1). Stimuli which evoked larger Delta[K](e) also produced larger DRPs in the same frog preparation.3. The briefest heat stimuli, which lasted about 1-2 s, led to more prolonged activity in dorsal horn interneurones than did a single volley or a single tactile stimulus and the Delta[K](e) were longer and larger and had a slower rise time.4. The ;slow' second component of dorsal root depolarization (presumably mediated by K(+)) was observed after electrical and heat stimulation of the skin on the hind limb corresponding to the time course of Delta[K](e).5. The maximum Delta[K](e) induced by nociceptive stimulation occurred in the grey matter of the dorsal horn at a depth of 300-600 mum from the dorsal surface. The maximum response to single stimuli applied to the skin occurred at a depth of 400-800 mum, while that evoked by LC stimulation in the ventral horn at a depth of 1000-1400 mum.6. Repetitive and more prolonged nociceptive stimulation (5-20 s) produced a Delta[K](e) of up to 1 mmol.l(-1). The Delta[K](e) in response to repetitive tactile stimulation does not exceed 0.2 mmol.l(-1). Repetitive stimulation (100 Hz) of LC fibres led to an increase in [K](e) of up to 9-10 mmol.l(-1) in the ventral horn; this level was similar to that achieved in the intermediate region by electrical repetitive stimulation of the skin (100 Hz). Tetanic stimulation of the ventral root led to a Delta[K](e) of only about 0.05 mmol.l(-1) at a depth of 500-700 mum and no measurable Delta[K](e) within the ventral horn.7. Spontaneous Delta[K](e) associated with spontaneous DRPs and VRPs were observed during the decay phase of Delta[K](e) at various intervals from several seconds to one minute after nociceptive or electrical stimulation of the skin, suggesting the occurrence of a longlasting increase in excitability.8. The depolarization of dorsal root fibres evoked by nociceptive stimulation, tetanic stimulation of the LC and single or tetanic stimulation of the skin was followed by a dorsal root hyperpolarization. Its size, as well as that of Delta[K](e), was dependent on the frequency and duration of stimulation and its time course correlated with the dissipation of Delta[K](e) when stimulation was discontinued.9. It is suggested that the extracellular K(+) accumulation could, under physiological conditions, contribute to the modulation of spinal cord transmission, acting both pre-and post-synaptically. Low levels of increased [K](e) were associated with facilitation of impulse transmission while higher increases could result in its inhibition.

Animals↗
PubMed1981

K+ changes in the extracellular space of the spinal cord and their physiological role.

K+ accumulates in the intercellular space as a result of neuronal activity. The changes in extracellular K+ concentration, delta[K]e (estimated by K+-selective microelectrodes), depends on neuronal activity, on the density of discharging neurones and the removal of the accumulated K+ by diffusion, active transport and current flow through cells. In the mammalian as well as the amphibian spinal cord a single volley in a peripheral nerve increases [K]e by 0.2-0.5 mmol . 1-1, while tetanic stimulation (100 Hz) by 7-8 m-mol . 1-1, with a maximum in the lower dorsal horn. Increased [K]e was also found in lumbar segments when the somatosensory cortex of the cat and medulla of the frog were stimulated. In the frog spinal cord, the tactile stimulation of the hindlimb evoked delta[K]e by about 0.1 mumol . 1-1, nociceptive stimulation by 0.2-1.0 mmol . 1-1. Spontaneous delta[K]e and dorsal root potentials (DRPs) were observed at various intervals after stimulation, associated with the decay phase of delta[K]e. It was shown that primary afferent depolarization (PAD) consists of two components: the 'early' component (mediated by GABA and depressed by picrotoxin or bicuculline) and the 'late' K+ component (potentiated by picrotoxin and bicuculline). Even when increased [K]e produces PAD, this does not mean that it also results in presynaptic inhibition. It was found that the delta[K]e produced depolarization of motoneurones and neuroglia and there is every reason to believe that this also applies to the interneurones. Evidence is available that an increase of [K]e up to 6 mmol . 1-1 facilitates impulse transmission in the spinal cord while higher levels result in its inhibition.

Afferent Pathways↗
PubMed1980

Potassium accumulation in the frog spinal cord induced by nociceptive stimulation of the skin.

Changes of extracellular K+ concentration (delta[K]e) were studied in the frog spinal cord in response to noxious skin stimulation by hot water (55-65 degrees C). The magnitude of delta[K]e was dependent on the duration and the extent of the skin area heated. The maximum of delta[K]e (0.2-1.0 mmol X 1(-1)) occurred in the dorsal horn at about the same location where the highest increase of [K]e was observed in response to electrical stimulation of the skin. The nociceptive as well as electrical stimulation of contralateral hindlimb resulted in delta[K]e, which was about 50% of that observed during ipsilateral stimulation.

Afferent Pathways↗
PubMed1980

Neurones activated from nociceptors in the spinal cord of the frog.

Neurones in the dorsal horns of the frog spinal cord were activated by innocuous (touch) and nociceptive stimuli (heat, pressure, pinch). Forty neurones which were found at depths between 300-700 microns reacted differentially, but not selectively, to various kinds of natural stimuli. The number and frequency of spikes induced by nociceptive stimuli exceeded that produced by innocuous stimuli from twice to many times. Some of the neurones were more sensitive to mechanical stimuli and others to heat. All the neurones tested could thus be classified as polymodal neurones.

Animals↗
PubMed1975

Extracellular potassium changes in the spinal cord of the cat and their relation to slow potentials, active transport and impulse transmission.

1. By means of K-specific double-barrelled micro-electrodes the time course of changes in K+ concentration in the extracellular space of the lumbar spinal cord was examined after peripheral tetanic stimulation and after a single volley in a mixed peripheral nerve in non-anaesthetized, intercollicularly decerebrated and spinalized cats. 2. Tetanic stimulation (100 Hz) which increases the [K]e from 3 to 9 mM is followed by a phase of reduced [K]e during which [K]e decreases by 0.5 mM below resting level, lasting 1-2 minutes before returning to its original resting level. Evidence is presented that this subnormal phase of [K]e reflects active processes redistributing accumulated K+ from extracellular space. 3. The subnormal phase of [K]e can be registered only when the microelectrode is located in very close vicinity of discharging neurones and is not primarily dependent on the absolute level of increased [K]e. This can be considered as evidence that the neurones and not the glial cells are responsible for active reabsorption of K+ from the extracellular space. 4. Increased E1K]e is reflected in focally recorded potentials as a negativity and decreased [K]e as a positivity. The latency of focally recorded positivity is, however, shorter than the latency of reduced [K]e. This makes it likely that the positivity reflects not only passive hyperpolarization of glial elements, but also an active, electrogenic ion transport across neuronal membrane. 5. The shortest latency of increased [K]e induced by a single volley in a mixed peripheral nerve was found to be 9 msec; the peak, representing 0.5 mM, was attained after 40 msec and the total duration was 200 msec. A theoretical consideration is put forward that the time course of transient increase in [K]e is consistent with the suggestion that K+ which accumulates in the spinal cord after neuronal discharge is responsible for primary afferent depolarization. 6. Evidence is presented that increased [K]e, induced by a long lasting peripheral stimulation, is accompanied by decreased efficacy of impulse transmission.

Animals↗