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Biomedical subjects

L V Baĭdan

Publications and source records attributed to L V Baĭdan.

16 recordsLinked to original sources
PubMed1988

[Apamin--a highly specific and effective blockader of calcium-dependent potassium conductance].

Apamin is a toxic polypeptide extracted from bee venom. It has been considered as a neurotoxin with central action, but its low concentrations (10(-8)-10(-7) M) were shown to reversibly block the nonadrenergic inhibition and effects of externally applied ATP, noradrenaline and caffeine in smooth muscles of the gastrointestinal tract. All these processes are related to the activation of Ca-dependent potassium permeability. Current-clamp, voltage-clamp and patch-clamp experiments have also shown that apamin blocks specifically some types of these conductances in other tissues: skeletal muscles, mammalian neurons and neuroblastoma, hepatocytes. Nowadays apamin is the most specific but not a universal blocker of the Ca-activated potassium conductance.

Animals↗
PubMed1983

[Properties of synaptic currents during non-adrenergic inhibition of the smooth muscle cells of the large intestine in the guinea pig].

Inhibitory junctional currents (IJCs) were recorded under voltage clamp conditions in response to brief transmural stimulation of the circular muscle of the guinea pig colon using the double sucrose gap method in the presence of atropine. The time course of IJC decay was approximately exponential 100-150 ms after the peak value. The IJC amplitude depended linearly on the membrane potential with the reversal potential (-70 mV) near the potassium equilibrium potential. The time constant (tau) of the IJC decay depended exponentially on the membrane potential and became e-fold decreased when the membrane was hyperpolarized approximately by 120 mV. Varying the quantal content of IJC caused an increase of tau upon rising the amount or transmitter released and its decrease with the depression of IJC. Application of ATP (10(-3)M) caused a decrease of tau and IJC amplitude, while apamine reduced the amplitude of IJC without any changes in their time course. The results are discussed in terms of a buffered diffusion hypothesis supposing a cooperative action of transmitter released on junctional receptors.

Adenosine Triphosphate↗
PubMed1976

[The influence of several surface-active substances on neuromuscular transmission of excitation].

Microelectrode method was applied to the study of the influence of sodium bile salts (BS), saponin and between-80 on the end-plate potentials (EPP) of m. sartorius of Rana ridibunda. Bile salts in a concentration of 10(-5) g/ml did not change these potentials significantly. With increase of the BS concentration up to 10(-4) g/ml the amplitude of EPP increased 1.5- 3 times. The action of these substances in a concentration up to 10(-3) g/ml caused similar, but more rapid, increase in the EPP amplitude, and then the amplitude decreased. Saponin and tween-80 were less efffective in their action on EPP, but evoked muscle contraction. It is suggested that an increase in the EPP amplitude as a result of the action of the mentioned agents was chiefly connected with stimulation of the acetylcholine release by the nerve terminals.

Acetylcholine↗
PubMed1976

[The effect of several surface-active substances on neuromuscular transmission in frogs].

The action of bile salts, saponin and tween-80 on miniature end-plate potentials (MEPP) and electrotonic potentials (ETP) of the muscle fibre membrane was studied in frog Rana ridibunda. Bile salts in a concentration of 10(-4) g/ml increased the frequency and amplitude of MEPP. The input resistance of the muscle fibre membrane decreased under the action of these substances. At higher concentrations (to 10(-3) g/ml) the frequency of the MEPP initially increased, then these potentials were depressed and finally they completely disappeared. Tween-80 did not change noticeably spontaneous synaptic activity, and saponin inhibited it. In Ca-free solutions bile salt were less effective. It is suggested that bile salts change the structure of the presynaptic membrane and at the same time stimulate the release of acetylcholine form the nerve terminals.

Animals↗