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I E Katina

Publications and source records attributed to I E Katina.

At least 19 recordsLinked to original sources

Changes in the functioning of the electromechanical connection during tetanic contraction.

The functioning of the electromechanical connection during tetanic contraction in frog skeletal muscle was studied. Analysis using caffeine, calcium-free medium, the ryanodine receptor blocker dantrolene, and the Ca-ATPase inhibitor thapsigargin showed that the initial increase in tetanus, as in twitch contractions, did not require the presence of calcium ions in the surrounding medium, which is in agreement with published data. Contraction was accompanied by activation of potential-dependent release of calcium from the sarcoplasmic reticulum. In contrast, the secondary rise phase and/or the duration of the tetanus plateau were critically dependent on the present of Ca2+ in the surrounding medium. Given that contraction in this situation was inhibited by dantrolene, activation of prolonged contraction was also mediated by calcium released from the sarcoplasmic reticulum, though ryanodine receptors were now activated not by changes in the membrane potential but by the influx of external calcium. Thus, external calcium plays a significant role in the formation of prolonged contractile responses, providing for longer-lasting maintenance of power in contracted muscles.

Animals↗

Effect of clonidine on potential-dependent sodium currents in sensory neurons.

In experiments on rat pups we studied the effect of clonidine on potential-dependent Na+ currents in dorsal root ganglia by the voltage clamp method. Clonidine decreased the amplitude of tetrodotoxin-sensitive and tetrodotoxin-resistant sodium currents. The range of acting concentrations and the absence of modulatory effect of norepinephrine on the efficiency of clonidine-induced blockade of sodium currents suggest that this blockade results from a direct interaction of clonidine with sodium channels.

Analgesics↗

Inhibitory effect of clonidine on cholinergic transmission.

Equilibrium geometry and electronic structure of three local anesthetic molecules and clonidine were computed. It was shown that clonidine molecule could incorporate into local anesthetic binding centers in potential-operated Na+ channels and in ionic channels coupled to nicotinic cholinergic receptors. The modulatory effect of clonidine on contractile responses of skeletal muscle showed that blockade of Na+ channels and nicotinic cholinergic receptors is a part of its analgesic action.

Adrenergic alpha-Agonists↗

[Changes in the electromechanical activity in the course of tetanic contraction].

The functioning of excitation-contraction coupling during tetanic contraction was investigated on frog skeletal muscle. The effect of the calcium release blocker dantrolene was tested on electrically evoked twitches and tetanic contractions. It was shown that the first: developmental stage of tetanus is inhibited by dantrolene as well as a twitch contraction, and does not influenced by calcium-free medium. This substantiates it as based on "voltage dependent Ca-release" (VDCR) mechanism of activation, when depolarization directly opens the rhyanodin receptor calcium channels. The next stage: the long lasting plateau of tetanic contraction, is directly dependent on external Ca2+ entry and also inhibited by dantrolene, and therefore may be described as "calcium-induced Ca-release" (CICR) activation mechanism. It is proposed that such change in ECC mechanism taking place during tetanic contraction, can occur also in conditions of natural muscle activity, because of its rhythmical nature.

Animals↗

[Functioning of the electromechanical connection in the course of the contracture contraction].

The effects of calcium release blocker dantrolene was tested on electrically evoked twitches and on contractures induced by potassium depolarization, by acetylcholine or caffeine. It was shown that the first: developmental, stage of potassium or acetylcholine contracture is inhibited by dantrolene and is not influenced by calcium free medium, therefore we may interpret it as based on a "voltage-dependent Ca release" (VDCR) mechanism of activation, whereas depolarization directly opens the rhyanodin receptor calcium channels. On the contrary, the next stage: the long-lasting plateau of contracture, is directly dependent on external Ca2+ and inhibited by dantrolene, and therefore can be described as "calcium induced Ca-release" (CICR) activation mechanism. In this case stored calcium is also released by rhyanodine receptors, although by means of entering the extracellular Ca2+. Finally, the last stage of low amplitude is not influenced by dantrolene nor by calcium-free medium. Therefore the activation of contraction on this stage is not based on the Ca2+ release through the rhyanodin receptor calcium channels.

Acetylcholine↗

Development of muscle-specific features in cultured frog embryonic skeletal myocytes.

To study the development of muscle-specific features during myogenesis, we analysed the ultrastructure and voltage-dependent currents of frog embryonic skeletal myocytes maintained in culture for 10 days. The cells were maintained under culture conditions that prevented cell division, fusion and cell contacts with neuroblasts. The cell surface was estimated morphometrically and from cell capacity and the values obtained were used to calculate ion current densities. It was shown that the expression of all main types of voltage dependent ionic currents occurs during the first 3-5 days. Na+ maximum specific conductance at days 1-2 was low but by day 7 it showed a 20-fold increase. The magnitude of Na+ current densities increased 16-fold from day 1 (3.6 microA/cm) to the day 7 (58.1 microA/cm). The maximum specific K+ conductance increased almost 3-fold during the first 5 days. In contrast to the other types of currents, I(K) undergoes qualitative changes. Sodium action potentials, whose amplitude and time course depend on gNa/gK ratio, appeared from day 4 in culture, when myofibrils and the T-system also developed. The amplitude of DHP-sensitive slow I(Ca) increased in parallel with the development of the T-membrane. I(Ca,S) density per unit of T-membrane area reached an equilibrium of ca., 17 microA/cm2 on the day 4 and then remained stable until the end of the period of observation. These studies demonstrate that muscle-specific characteristics including morphology and excitatory properties begin to develop on the third day and resemble those of adult muscle cells by the sixth day in culture.

Actin Cytoskeleton↗

[Ethanol modifies the ion selectivity of sodium channels in the rat sensory neurons].

Ethanol was shown to decrease the reversal potential of tetrodotoxin-resistant (TTXr) and TTX-sensitive channels in short-term culture of the dorsal root ganglion cells. The ethanol led to alterations in ionic selectivity of the TTXr channels (its shifting from the X-th Eisenmann selectivity sequence to the XI-th one). The data obtained suggest that the findings were due to selectivity filter modification because of disturbed hydrogen bounds in the channel macromolecule.

Animals↗

[Inward rectifier potassium current in the frog embryonic skeletal myocytes].

Pharmacological and kinetic properties of the inward rectifier potassium current Iir the frog embryonic skeletal myocytes were found to be identical to those of adult frog skeletal muscle fibres. The data obtained suggest that the Iir plays the main role in maintaining the myocytes resting membrane potential (RMP) when chloride conductance is insignificant. Changes of the integral conductance Gir and the RMP values correlated with the T-system development. The inward rectifier K+ channels, from the early stages of the muscle seem to be located in the T-tubule membranes.

Animals↗

Voltage-insensitive Na channels of different selectivity in human leukemic cells.

Patch clamp method was used to search for, and characterize ion channel activity which may participate in cation influx in human myeloid K562 cells. In cell-attached, outside-out and whole-cell experiments two types of voltage-insensitive Na-permeable channels were identified with different selectivities for monovalent cations, referred to as channels of high (HS) and low (LS) selectivity. The unitary conductance was similar for both channel types being 12 pS (145 mmol/l Na, 23 degrees C). The relative permeability PNa/PK estimated from the extrapolated reversal potential values were 10 and 3 for HS and LS channels, respectively. Both HS and LS channels were found to be impermeable to bivalent cations (Ca2+ or Ba2+). The activity of HS and LS channels displayed a tendency to increase with depolarization. Both channel types were not blocked by tetrodotoxin and were insensitive to amiloride in the concentration range of up to 100 mumol/l. At higher concentrations (0.1-2 mmol/l), amiloride reversibly inhibited HS channels only. The results obtained lead us to conclude that, under physiological conditions, both types of Na-permeable channels may provide sodium influx in leukemic cells. Our data imply the existence of a novel family of Na channels in blood cells.

Amiloride↗

[The formation of electrical excitability in cultured frog embryonic myocytes].

Quantitative changes of sodium and potassium ionic currents were studied in the frog embryonic skeletal myocytes cultures under conditions preventing cell fusion and division. During 7 days of culturing the mean values of the sodium and potassium currents densities were 7- and 1.8-fold increased, resp. In currents clamp records the APs were observed only after 5 days of culturing, and in cells with proportion of sodium and potassium conductances above the critical level.

Animals↗

Beta-adrenergic regulation of voltage-dependent calcium currents in cultured skeletal myocytes of the frog Rana temporaria.

Effects of beta-agonists isoproterenol (Isp) and adrenaline (Adr) and beta-adrenoblocker obsidan (Obs) on the voltage-dependent calcium currents in cultured embryonic skeletal myocytes were studied at various stages of development ranging from day 2 to 10, using the whole-cell patch-clamp technique at 19-21 degrees C. Adr (or Isp) in concentrations 0.1-10 mumol/l increases the amplitude of both the slow dihydropyridine(DHP)-sensitive calcium current (ICa) and the fast-activated DHP-insensitive ICa. From day 2 to 6 after myoblast plating, Adr and Isp did not change the amplitude of ICa at all or slightly increased it. Obvious strong positive effects (an approximately twofold amplitude increase) on the calcium channels have been observed in 7-10-day-old myocytes only. beta-adrenoblocker obsidan known to abolish the positive beta-agonist effect, had a positive effect on membrane calcium currents. It may have been a result of the immaturity of the beta-adrenergic regulatory system of the myocytes. It is concluded that the beta-adrenergic regulatory complex can stimulate the activity of the fast and the slow voltage-dependent calcium channels of the frog skeletal myocytes, and that there is a distinct developmental stage at which a functioning beta-adrenergic regulatory complex appears in the membrane of skeletal myocytes.

Adrenergic beta-Agonists↗

Pharmacological analysis of voltage-dependent potassium currents in cultured skeletal myocytes of the frog Rana temporaria.

Previously, the existence of nine types of outward potassium current (IK) was shown. The whole family of IK may be divided into two groups: fast transient currents (f) with time to peak less than 70 ms (at test potential near 0 mV), and slow (s) components (Lukyanenko et al. 1993). The latter were completely blocked by 4-aminopyridine (4-AP) and the former were more sensitive to TEA than slow IK. In the present study we analyzed the effects of calcium blockers on different types of IK using the whole-cell patch-clamp technique. One to seven-day-old myocytes without slow calcium current and without contact with nerve cells were examined. Extracellullar application of 40-80 mumol/l dihydropyridine (DHP) antagonist nifedipine did not change maximal conductance of K-channels, but induced a parallel shift by 5-10 mV of chord conductance curve along the voltage axis in the direction of more negative potentials. Quinidine in concentrations 30-200 mumol/l caused a reversible block of the fast and the slow IK (C0.5 = 75 mumol/l), and enhanced the current decay (2-3-fold at 150 mumol/l). Verapamil (VP) in concentrations 100-700 mumol/l reduced IK with dose-dependent effect (C0.5 = 200 mumol/l) and changed its kinetic properties. VP 100 mumol/l caused a complete irreversible block of the slow IK. VP reduced the time inactivation constant of fast IK with a dose-dependent effect (8-10-fold at 300 mumol/l), and this effect was stronger during depolarizing pulses. The latter points to the possibility that the fast K-channels preferentially bind VP in open state. An analysis of the effects suggests that K-channels of the frog myocytes could be divided into 2 groups: 1) K-channels which irreversibly blocked by VP and 4-AP (slow), and 2) those reversibly inhibited by VP and 4-AP (fast potassium channels).

4-Aminopyridine↗

Voltage dependent fast calcium current in cultured skeletal myocytes of the frog Rana temporaria.

Voltage dependent calcium currents in cultured frog embryonic skeletal myocytes at stages of development ranging from 2 to 9 days were studied using the whole-cell patch clamp technique at 19-21 degrees C. Membrane currents were recorded in the presence of 2 mmol/l Ca2+ (outside), and 60 mmol/l CsCl and 50 mmol/l TEACl (inside). In the absence of sodium current two components of inward current were observed in response to depolarization already during the early stages of myogenesis: the well-known slow dihydropyridine (DHP)-sensitive calcium current (ICa,s), and a fast-activated current. Both components persisted in the presence of 2 mumol/l tetrodotoxin. The fast-activated component was enhanced upon addition of 6 mmol/l Ca2+ or Ba2+ to the external recording solution and was decreased when the standard external solution was replaced by Ca2+ free solution. Thus, the fast component of the inward current was also carried by Ca2+ (ICa,f). Unlike ICa,s, it was not blocked with 30-150 mumol/l DHP nifedipine. During 7 s depolarization ICa,f was detected at approximately -50 mV, 20 mV more negative than the membrane potentials at which ICa,s appeared. At various test potentials t0.5 for activation of ICa,f was 8-20 ms, and the current declined during depolarization with tau in of 500-800 ms. These results indicate the existence of two types of voltage-dependent Ca2+ channels in early stages of development of frog myocytes, both known in mature frog skeletal muscle fibres.

4-Aminopyridine↗

Voltage dependent ionic currents in frog cultured skeletal myocytes.

The voltage dependent ionic currents in cultured embryonic skeletal myocytes at stages of development ranging from 1 to 6 day were studied using the whole-cell patch clamp technique. Sodium (INa) and calcium (ICa) inward and potassium (IK) outward currents were observed at all stages. INa did not differ from that described in adult frog striated muscle fibres. Slow ICa was mediated by current through dihydropyridine sensitive Ca channels and it did not differ in its kinetics from corresponding slow ICa in frog adult twitch muscle fibres. In about 10% of cells examined for ICa, this current was significantly slower and similar to ICa described in frog tonic muscle fibres. In some cases two slow calcium currents with distinguishable kinetics were recorded in the same myocytes. Fast dihydropyridine-insensitive noninactivating ICa could also be observed. At least 6 types of IK were registered, with approximate time-to-peak (at test pulse of -10 mV) 5, 12, 20, 30, 50 ms (fast IK) and more than 7 s (slow IK). Three of them (5, 20 and 30 ms) predominated in 3-day cultures and disappeared in 6-day-old cultures. IK in myocytes did not correspond fully in the kinetics to IK reported in adult frog skeletal muscles. Channels associated with transient fast and noninactivating slow IK were shown to be highly sensitive to low temperature (+5 degrees C).

Animals↗