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Biomedical subjects

A A Andreev

Publications and source records attributed to A A Andreev.

At least 19 recordsLinked to original sources
PubMed1998

[Long-term morphofunctional preservation of guinea pig hippocampal slices following short-term treatment with cyclooxygenase inhibitors].

Hippocampal slices treated with cyclooxygenase inhibitor indomethacin for three min during the sectioning (45 min) or aspirin (0.5 min) in long term (up to 5 days) preservation in periodic nocturnal hypothermia were studied morphofunctionally using light microscopy and electrophysiological registration of induced population responses of area CAI to stimulation of Schaffers collaterals. Structural disorders were revealed in control slices as early as the third hour of incubation and they were destroyed following the first hypothermal challenge (24 hrs following preparation). The structure in slices treated with blockers remained more stable as compared to control ones and the activity was registered until d 3 (aspirin) and 5 (indomethacin). Morphological changes were not immediately, followed by electric activity decline. On the whole it may be suggested that essential viability increase occurred due to destructive processes inhibition mediated by short living cyclooxygenase metabolites.

Animals↗
PubMed1997

Functional stability of hippocampal slices after treatment with cyclooxygenase inhibitors.

The influence of cyclooxygenase inhibitors on functional stability of hippocampal slices, determined by electrophysiological criteria of recovery after slicing and long-term maintainence of population activity, was studied. Transient (3 min) treatment of slices during slicing with indomethacin (45 microM) or aspirin (0.5 mM) allowed registration of the population responses from the second minute. The activity reached 100% after 15 min incubation and could be registrated for 3 days under conditions of overnight hypothermia. The presence of the same drugs for the entire incubation period had the same effect. The present findings suggest that slicing is a crucial point for triggering of pathological events mediated by cyclooxygenase products and that blockade of cyclooxygenase provides for the further high longterm functional stability of brain slices.

Animals↗
PubMed1988

[Use of enzyme-antibody immune complexes in serological analysis].

In model experiments with simulation of rabbit immune response to mouse IgG and antibody production in echinococcosis patients the indirect enzyme-linked immunosorbent assay has been several times more sensitive with peroxidase-antiperoxidase and catalase-anticatalase complexes than with enzyme-antiglobulin chemical conjugates. The immune complexes have been found to retain their activity for 6 months and longer.

Animals↗
PubMed1986

Depression of neuron responses to acetylcholine by combined application of norepinephrine and substrates of the tricarboxylic acid cycle.

The possible relationship between the function of nicotinic acetylcholine receptors in Lymnaea stagnalis neurons and energy metabolism was studied. Oxidative phosphorylation was activated by treatment of neurons with substrates of the tricarboxylic acid cycle and norepinephrine. Transmembrane currents induced by acetylcholine in isolated neurons were measured by voltage clamp. Succinate dehydrogenase activity was determined histochemically in the same neurons. Cyclic adenosine monophosphate concentration in ganglia were assayed by the protein saturation method of Gilman (1970). When used alone, succinate depressed the responses of about 50% of neurons to acetylcholine. Norepinephrine did not affect the acetylcholine-induced currents but almost doubled the inhibitory action of succinate. The mixture of norepinephrine and isocitrate also diminished the responses to acetylcholine but to a lesser extent than norepinephrine with succinate. A short-term exposure of the ganglia to succinate with norepinephrine led to the activation of succinate dehydrogenase in neurons and a threefold increase in cyclic adenosine monophosphate concentrations in ganglia. When used alone, norepinephrine doubled the cyclic adenosine monophosphate concentration. The results obtained suggest energy-dependent regulation of acetylcholine receptors.

Acetylcholine↗
PubMed1984

Two-component desensitization of nicotinic receptors induced by acetylcholine agonists in Lymnaea stagnalis neurones.

The kinetics of desensitization induced by different agonists of acetylcholine (ACh) as well as the kinetics of recovery from densensitization, have been studied using the voltage-clamp technique in isolated, identified Lymnaea stagnalis neurones. Desensitization follows the sum of two exponentials: one fast and one slow. The time constant of the fast desensitization component (tau Ids) under ACh application is in the range of seconds at room temperature (18-23 degrees C). It increases upon cooling (Q10 = 2.8 +/- 0.9), decreases with increasing ACh concentration and is independent of membrane voltage. The time constant of the slow component of densensitization (tau Ids) is in the range of tens of seconds. It decreases with increasing drug concentration and is weakly dependent upon temperature (Q10 = 1.3 +/- 0.4). The relative amplitude of the fast component, estimated by back extrapolation to the position of the peak current, increases with agonist concentration and decreases upon cooling. Recovery from desensitization follows the sum of two exponentials with time constants (tau Ir and tau IIr) of the order of seconds and minutes, respectively. Cooling prolongs the slow component (Q10 of tau IIr is approx. 3) and reduces its contribution during recovery. A comparison of the desensitization induced by various agonists indicates that for the small monoquaternary agonists the onset and recovery of desensitization resemble the onset and recovery observed with ACh. For more bulky agonists, like ethoxysebacylcholine, sebacylcholine and suberylcholine, the decay of the response during prolonged application of the agonist may involve an additional blocking process.

Acetylcholine↗