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Biomedical subjects

A V Romanenko

Publications and source records attributed to A V Romanenko.

At least 19 recordsLinked to original sources
PubMed1993

The effect of alpha-latrotoxin on a synaptic connection between identified neurons in the brain of the mollusc Helix pomatia L.

The effect of alpha-latrotoxin on identified monosynaptic peptidergic contacts between identified neurons from the brain of the snail Helix pomatia L. was studied. It was found that, after extracellular application, toxin evoked an increase in the amplitude of the postsynaptic response. Neither amplitude nor duration of the action potential in a presynaptic neuron was affected. Intracellular injection of toxin into the soma of a presynaptic neuron led to a decrease in the postsynaptic current amplitude. The current induced by intracellular injection of cAMP into a postsynaptic neuron was also inhibited by extracellular or intracellular application of toxin. These data indicate that toxin evokes both an increase of transmitter release from a presynaptic neuron and a decrease in amplitude of the postsynaptic response.

Action Potentials↗
PubMed1992

[Effect of alpha-latrotoxin on synaptic transmission between identified neurons in Helix central nervous system].

An identified monosynaptic peptidergic contact between identified neurons from the brain of snail Helix pomatia L. has been used to study the effect of alpha-latrotoxin. It was found that being applied extracellularly the toxin evoked an increase of the postsynaptic response amplitude. Intracellular injection of the toxin into the soma of the presynaptic neuron led to a decrease of the postsynaptic current amplitude. Current induced by intracellular injection of cAMP into postsynaptic neuron was also inhibited either by extra- or intracellular application of the toxin. According to previous data which demonstrate similarity between the postsynaptic response and the current which was induced by intracellular injection of cAMP into postsynaptic neuron it has been proposed that the toxin evokes both an increase of the transmitter release from the presynaptic neuron and a decrease of the postsynaptic response amplitude.

Action Potentials↗
PubMed1986

[Effect of thiamine on various types of synaptic junctions].

Thiamine (1.10(-14) -- 1.10(-4) mol/l) reversibly increased the frequency of miniature excitatory postsynaptic potentials, amplitude and quantal content of excitatory postsynaptic potentials in crayfish glutaminergic synapse. Thiamine also increased spontaneous electrical activity and amplitude of synaptic potentials in guinea-pig taenia coli. In synaptosomes from the rat brain thiamine produced depolarization of nerve endings. The role of thiamine in the regulation of synaptic transmission and mechanism of its action are discussed.

Animals↗
PubMed1986

[Effect of thiamine on auditory evoked potentials of the guinea pig].

Application of thiamine (1 X 10(-11)-1 X 10(-3) mol/l) on the membrane of cochlear round window increased the amplitude and decreased the latency of the auditory nerve action potential, waves I and II of brainstem auditory-evoked electrical potentials in response to acoustic clicks of different intensity. The mechanism of thiamine action on auditory-evoked electric potentials is discussed.

Animals↗
PubMed1985

[Effect of thiamine on neuromuscular transmission in the frog].

The action of thiamine on frog m. sartorius neuromuscular junction was investigated. Thiamine (1 X 10(-14)-1 X 10(-4) mol/l) reversibly increased miniature end-plate potential frequency, amplitude and quantal content of end-plate potentials, probability of quantal release. The role of thiamine in the regulation of synaptic transmission and mechanism of its action are discussed.

Acetylcholine↗
PubMedDate not supplied

[Activity of thiamine in skeletal muscles od rats].

Thiamine participates in neuromuscular transmission. This transmission is depressed when thiamine level in organism decreases and it is normalized in animals after thiamine injection.

Action Potentials↗
PubMedDate not supplied

[The thiazole derivative reduces transmembrane currents via ionic channels formed by alpha-latrotoxin and sea anemone toxin in the bilayer lipid membranes].

It was shown that the thiazole derivative 3-decyloxycarbonylmethyl-4-methyl- 5-(2-hydroxyethyl)thiazole chloride (DMHT) (0.1 mM) reversibly reduced the transmembrane current in solutions of 10 mM CaCl2 and 100 mM KCl via ionic channels produced by alpha-latrotoxin from black widow spider (alpha-LT) and sea anemone toxin (RTX) in the bilayer lipid membranes (BLM). Introduction of DMHT from the cis-side of BLM inhibited transmembrane current by 31.6 +/- 3% and by 61.8 +/- 3% from the trans-side of BLM for alpha-LT channels. Application of DMHT to the cis-side BLM decreased the inward current through the RTX channels by 50 +/- 5%. Addition of Cd(2+) (0.1 mM) to the cis- or trans-side of a membrane after the DMHT induced depression of transmembrane current across the alpha-LT channels caused its further decrease by 85 +/- 5% that coincides completely with the intensity of Cd(2+)-inhibition in the control experiments without DMHT. These data suggest that DMHT may exert its inhibitory action on alpha-LT channels without considerable influence on the ionogenic groups inside the channel cavity. The comparative analysis of effective radii measured for alpha-LT and RTX channels on the cis- (0.9 nm and 0.55 nm, respectively) and the trans-side of BLM (< 0.467 nm for alpha-LT) allowed to propose the blocking action of DMHT for alpha-LT and RTX channels to result from direct penetration into the channel, achieved due to similar hydrodynamic size of blocking molecules and the size of toxin pores.

Animals↗
PubMedDate not supplied

[Effect of different levels of carbonic acid on activity of dehydrogenases].

A dependence is established for the activity of NADP-dependent isocytrate dehydrogenase and malate dehydrogenase as well as of NAD-malate dehydrogenase on the carbonic acid level. When the biocarbonate concentration in rabbit blood and tissues rise, the activity of cytoplasmic NADP-isocytrate dehydrogenase and NADP-malate dehydrogenase of the liver lowers. The analogous regularity is observed in the in vitro experiments when the bicarbonate concentrations in the medium rises up to 40 mM (within the physiological limits). The activity of NAD-malate dehydrogenase in the soluble fraction of the rabbit liver and kidney increases with the bicarbonate level within the same limits. The found dependence was confirmed in experiments with the enzyme crystalline preparations.

Animals↗
PubMedDate not supplied

[Effect of carbon dioxide on the initial rate of the isocitrate and malate dehydrogenase reactions in rat liver].

The rate of reactions catalyzed by the NADP-dependent isocytrate dehydrogenase and malate dehydrogenase soluble fraction of the rat liver was studied as affected by carbonic acid. The reaction initial rate for both enzymes was determined under normal conditions and at physiological concentrations of carbonic acid. The initial rate of the direct isocytrate dehydrogenase reaction is established to decrease by 20, 35 and 57% at the carbonic acid concentrations 20, 40 and 60 mM. At the same time the initial rate of the malate dehydrogenase reactions increases by 51, 86 and 104% at the same levels of carbonic acid.

Animals↗