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V V Sherstnev

Publications and source records attributed to V V Sherstnev.

16 recordsLinked to original sources
PubMed1988

[Limited proteolysis of brain-specific protein S100. Isolation, physico-chemical and immunochemical characteristics of the neuropeptide AT-1-1].

Six peptides (presumably products of natural protein S100 catabolism) were isolated from bovine brain extracts by hydrophobic chromatography, affinity chromatography on immobilized antiprotein S100 antibodies, gel filtration and chromatography on TSK HW-40 columns in a methanol: water system. At 10(-12) M, peptide AT-I-I caused a 70% inhibition of the specific binding activity of endogenous benzodiazepine brain receptors. When used at higher concentrations (10(-9)-10(-5) M), AT-I-I inhibited the binding activity of central serotonin, dopamine and m-cholinoreceptors. Immunochemical analysis revealed the presence of identical material in rat brain glial cell nuclei (astrocytes). Using a solid phase immunoenzymatic assay, it was shown that peptide AT-I-I was not identical to any other of the 14 peptides tested (commercial preparations). Data from immunochemical analysis testified to the species non-specificity of AT-I-I. It was concluded that in brain tissue natural proteolysis of proteins S100 leads to the formation of biologically active oligopeptide products that are involved, in particular, in the modulation of the functional activity of central benzodiazepine receptors.

Animals↗
PubMed1987

[Effect of gamma globulins against brain-specific non-histone chromosomal proteins on the reproduction of a conditioned response in grape snails].

The effects of gamma-globulins to brain specific nonhistone chromatin proteins (BSNCP-3.5;-3.6) on conditioned food avoidance behaviour (carrot or apple) was studied in the garden snail. It was found that half an hour later the intracorporeal injection of BSNCP-3.5 inhibited conditioned carrot, but not apple avoidance reaction. Injection of BSNCP-3.6 was ineffective in avoidance behaviour induced by both conditioned stimuli. BSNCP-3.5 is suggested to be specifically involved in the process of information recollection.

Animals↗
PubMed1987

[Participation of brain-specific S-100-group proteins in the neurophysiological mechanisms of habituation].

The possible role of S-100 brain specific proteins and their participation in the neuronal mechanisms of habituation were studied on identified neurons of the snail Helix pomatia. Extracellular application and intracellular injection of antibodies to S-100 proteins caused a rapid and significant decrease of neuronal responses to repeated stimulation in comparison with the control. During the action of antibodies a significant decrease of the evoked EPSP amplitude, increase of the action prepotential latency and a decrease in discharge frequency were observed. At the same time the membrane potential, membrane input impedance, pacemaker potentials did not change. The obtained effect is supposed to be caused by interruption of the synaptic transmission. Possible involvement of S-100 protein in the functioning of synaptic structures as one of the integrating apparatus of the neuron is discussed.

Animals↗
PubMed1986

[Effect of antibodies to S-100 group proteins on the electrical activity and chemical sensitivity of the cerebral cortical neurons].

The influence of antibodies to proteins S-100 group on electrical activity and chemical sensitivity of rabbit cortical neurons has been investigated by means of extracellular recording and microiontophoresis. It has been found that anti-S-100 increase as a rule spontaneous discharge rate of the neurons, decrease, blockade or invert the neuronal responses to acetylcholine, noradrenaline and glutamate action. It is supposed that proteins S-100 group take part in regulation of eleitrogenic and postsynaptic (primarily glutamate- and GABA-ergic) processes of neural and glial cells in the brain.

Acetylcholine↗
PubMed1986

[Correlation between the in vivo dynamics of redox processes and neuronal electrical activity in response to angiotensin II and cyclic AMP].

The biologically active substances induced mostly similar changes of the restorative equivalents level whereas the pattern of equivalents varied in neuronal activity of the mammal brain cortex. The effects of angiotensin II and cAMP on neuronal activity were different. The data obtained suggest that the angiotensin II effect on neurons is actualized both through the cAMP system and through other molecular mechanisms.

Action Potentials↗
PubMed1979

[Bradykinin, morphine and naloxone interaction on the sensorimotor cortical neuron level].

In experiments on awake rabbits the effect of bradykinin, morphine and naloxone (applied by means of microiontophoresis) on sensomotor cortical neurons was studied. Bradykinin increased the discharge frequency in the majority of neurons. Morphine inhibited the neuronal activity. Bradykinin had no activating effect in the presence of morphine. Naloxone eliminated morphine depressing effect and restored the neuronal reaction to bradykinin. According to the data obtained it is suggested that bradykinin interacts with opiate receptors in the brain.

Action Potentials↗
PubMed1976

[Direct action of angiotensin II on the central neurons].

Reactions of the nervous cells in the somatosensory and visual regions of the brain cortex and the frontal hypothalamus in rabbits, as well as of the isolated nervous peripharyngeal ring of the Helix pomatia to the microionophoretic application of angiotensin II (A-II) was studied. Reactions of the neurons in the rabbit brain to A-II displayed an increase in the spike frequency depending on the quantity of the agent applied. Reactions of the frontal hypothalamus neurons showed a lower threshold than those of the brain cortex. A-II application to the some of the recorded cells of the mollusc evoked a marked reversible decrease in the membrane potential; as to the membrane resistance--it diminished 2--4 fold. These experimental data pointed to the direct A-II effect on the central neurons.

Angiotensin II↗
PubMedDate not supplied

Selective participation of brain-specific nonhistone Np-3.5 proteins of chromatin in the processes of the reproduction of a defensive habit in response to food in edible snails.

The role of brain-specific nonhistone Np-3.5 proteins of chromatin in the processes of the reproduction of a developed defense habit in response to food was studied in preliminarily trained edible snails. It was found that gamma globulins to Np-3.5 over the course of tens of minutes suppress behavioral and neuronal reactions elicited by a specific conditional stimulus, carrot juice, while not altering the reaction to a different conditional stimulus, apple juice. The gamma globulins to other nonhistone proteins of chromatin did not exert an influence on the reproduction of habits of food rejection. It is hypothesized that brain-specific nonhistone Np-3.5 proteins of chromatin are selectively involved in the molecular processes supporting the neurophysiological mechanisms of the extraction of information from long-term memory.

Animals↗
PubMedDate not supplied

[The selective participation of brain-specific non-histone proteins of chromatin Np-3,5 during the reproduction of a defensive habit to food in edible snails].

The role of brain-specific nonhistone proteins of chromatine Np-3.5 in the processes of reproduction of elaborated defensive habit to food was studied in previously learning snails. It was found, that gamma-globulines to Np-3.5 during tens of minutes inhibited behavioural and neuronal reactions elicited by a definite conditioned stimulus--carrot juice, without changing reactions to other conditioned stimulus--apple juice. gamma-globulines to other nonhistone proteins of chromatine did not influence the reproduction of food rejection habits. It was supposed that brain-specific nonhistone proteins of chromatine Np-3.5 were selectively involved in the molecular processes providing for neurophysiological mechanisms of information extraction from the long-term memory.

Animals↗
PubMedDate not supplied

[Predatory aggressiveness of the rat after intraventricular administration of individual brain-specific proteins of the S-100 group and their peptide fragments].

Intraventricular injections to rats of the basic fraction of the brain specific protein S-100 in a concentration of 3 mg/ml, significantly facilitates the formation of their predatory aggression induced by the alimentary deprivation and social isolation, expressed in mice killing. This effect is not produced by fragments of S-100 molecules obtained as a result of treatment of the basic protein fraction by proteolytic enzymes. Administration of the minor S-100 fraction, albumin and rats summate brain proteins did not influence animals predatory aggression.

Aggression↗