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R N Glebov

Publications and source records attributed to R N Glebov.

At least 73 records · Page 4Linked to original sources
PubMed1978

[Activity of Na, K-ATPase and the enzymes of intermediate metabolism in the brains of rats exposed to electroshock].

Activity of Na, K -ATPase, acetylcholinesterase (AChE) and glutamic acid decarboxylase (GAD) in the fractions of the rat brain and spinal cord tissue were studied in rats during a single electroshock (ES) and 5 and 30 minutes after it. GAD activity of the synaptosome fraction was shown to decrease insignificantly, but activity of AChE, Na, K -ATPase and possibly of proteolytic enzymes increased 5 minutes after electroshock and became normal in 30 minutes. It is supposed that the revealed inhibition of Na, K -ATPase activity in the "synaptosomes" of the rat brain cortex could be of pathogenetic significance in the origination of the convulsive process.

Acetylcholinesterase↗
PubMed1977

[Effect of tetanus toxin and colchicine on synaptic membranes of rat cerebral cortex].

It was shown that purified tetanus toxin did not influence the activity of the Na, K-ATP-ase fractions of the synaptic membranes of the rat cerebral cortex, it had no effect on the inhibition of Na, K,-ATP-ase under electrical stimulation of the synaptic membrane suspension, or the GABA--3H binding by the synaptosomes in vitro. Tetanus toxin (400--4000 DLM) and colchicine (1 mM) induced a decrease of osmotic sensitivity of the nerve endings. Colchicine in low concentrations (10(-5)-10(-3) M) failed to influence Mg-and Na, K-ATP-ases, but considerably inhibited both ATP-ases at higher concentrations.

Adenosine Triphosphatases↗
PubMed1977

[Isolation and properties of an actomyosin-like protein from bovine brain glial cells].

Actomyosine-like protein (AMLP) was isolated from the enriched glial fraction of the bovine brain cortex. The AMLP yield constitutes 0.05% of protein in the glial cells. The AMLP contained nucleotides; there were reversible association-dissociation reactions under the effect of Mg2+ ions and ATP characteristic of AMLP. ATP-ase of glial AMLP, activated with Ca2+ ions more than with Mg2+ ions, differed from AMLP of neuronal origin.

Adenosine Triphosphate↗
PubMed1976

[The effect of psychotropic substances on synaptosomal uptake of gamma-aminobutyric H3-acid and the activity of Na,K-ATPase].

The centrally acting drugs belonging to different groups--fluphenazine, trifluperidol, phthoracyzine, imipramine, diazepam, apomorphine, fentanyl, diphneylhydantoin, nonachlazine displayed in vitro an inhibitory effect on the uptake of gamma-aminobutyric acid by rat brain synaptosomes. A decrease in the activity of synaptosomal Na,K-ATPase was found in most cases. Drugs that failed to alter GABA uptake were as a rule found to be ineffective in relation to the enzyme activity (carbidine, morphine). GABA uptake was not affected by certain drugs inhibiting the Na,K-ATPase activity (azabuperon, tetrabenazine). It is supposed that the drugs used had at least two possible sites of action - Na,K-ATPase itself and hypothetic GABA transmembrane carrier.

Adenosine Triphosphatases↗
PubMed1976

[Na, K-ATP-ase and acetylcholinesterase activity of the membrane structures of the rat brain and spinal cord during the seizure process].

The activity of ATP-ase and acetylcholinesterase (AChE) in crude mitochondrial fraction (CMF) and microsomal fraction of rat brain cortex and the spinal cord was studied in clonic seizures evoked by electroshock and 5 min after them. Inhibition of the Na, K-ATP-ase activity of the CMF of the brain at the clonic phase of convulsions and an increase in the activity of this enzyme in all the fractions of the tissues under study at the postconvulsive period were revealed. The activity of Ca-ATP-ase in the CMF of the brain increased during the convulsions and decreased at the postconfulsive period. The activity of Mg-ATP-ase remained unchanged. The AChE activity, as a rule increased during the convulsions, and grew even more during the postconvulsive period; the spinal cord tissue displayed a reduction of the activation effect. A possibility of structural reconstructions in the excitable neuron membranes during the convulsive activity is discussed.

Acetylcholinesterase↗
PubMed1976

[Effect of parathyroid hormone and thyrocalcitonin on the cell membrane Na, K-ATP-ase of rat brain and kidney].

The influence of parathyroid hormone (PH) and thyrocalcitonine (TCT) on the enzymatic activity of ATP-ase systems of the membrane specimens of the cerebral cortex and renal cortex was investigated in experiments on rats. It was found that parathyroid hormone increased the activity of Na, K-ATP-ase and Ca-activated ATP-ase transport of the membranes in the brain and the kidneys both in vivo and in vitro. TCT caused analogous, but less expressed changes of the ATP-ase activity. Both hormones showed no influence on the Mg-ATP-ase activity of the both organs. It is supposed that the PH hormone influenced the membrane structures with the ATP-ase activity directly, while the action of TCT on them was mediated.

Adenosine Triphosphatases↗
PubMed1976

[Structural-functional changes in the synaptic membranes of the cerebral cortex of rats during electric stimulation in vitro].

Electric stimulation (EC) of a suspension of native synaptic membranes of rat brain cortex in the Krebs-Ringer-glucose medium revealed Ca-dependent inhibition of Na+, K+-ATPase and inhibition of transport Ca-activated, Mg-dependent ATPase. The effects observed are not induced by a change in the SH-groups of the membrane proteins and are removed by an addition of total lipids of the brain (membrane protein: lipid = 5:1) or 0.35 mM novocaine. Cyclic 3',5'-AMP in concentrations of 0.1--1.0 mM causes an inhibition (up to 50%) of Na+, K+-ATPase of native synaptic membranes. The Na+, K+-ATPase activity of purified membrane preparations is not changed either by the cyclic nucleotide, or by EC. It is assumed that depolarization of excitable membranes results in structural changes, mediated by the activation of protein kinase, and manifesting themselves as labilization of protein-lipid ratios.

Adenosine Triphosphatases↗
PubMed1976

[Molecular mechanisms of mediator secretion].

A review is presented discussing problems of transmitter localization in nerve endings, their replenishment in synaptic vesicles (SV), reuptake of transmitters and their degradation products from the synaptic cleft, the structural variations in the presynaptic membrane (pre-SM) during rest and excitation and the role of contractile proteins in the mechanism underlying transmitter secretion. A hypothesis is proposed about the universality of the mechanisms involved in transmitter release and utilization and the key role of the membrane ATP-ase system in these processes. During depolarization of the pre-SM the increase in membrane permeability is ascribed to the loosening of protein-lipid bonds and inhibition of ATP-ase activity involved in transport mechanisms. During depolarization the number of complementary contacts between SV and the pre-SM increase probably through the action of myosin-like and actin-like proteins localized on the SV and pre-SM, respectively. The release of transmitters and polypeptides is thought to be initiated by an increased concentration of Ca2+ in the synaptoplasm which induces contraction of the actomyosin-like complex. Changes in the Na-gradient brought about by the activity of Na, K-ATP-ase, are involved in the active reuptake of transmitters from the synaptic cleft. The newly-synthesized transmitters and those taken up from the synaptic cleft are stored in the SV by a Mg-ATP-ase dependent mechanism. Transmitters are stored in SV bound to acid polypeptides containing nucleotides. The presynaptic action of different neurotoxins is also discussed.

Acetylcholine↗
PubMed1975

[Changes in the protein composition of the synaptic structures of the brain of rats in tetanus intoxication].

As shown by the method of electrophoresis on polyacrylamide gel, the number of proteins with low electrophoretic mobility proved to be increased in the triton extract fractions of synaptic structures isolated from spinal cord of rats with local tetanus; no changes in the protein spectrum were revealed in the dodecyl-sulphate extract. In vitro tetanus toxin stimulated the lysin-H3 incorporation into the total proteins of synaptosomes of rat brain cortex.

Animals↗