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Biomedical subjects

G N Kryzhanovskii

Publications and source records attributed to G N Kryzhanovskii.

At least 19 recordsLinked to original sources
PubMed2006

Effect of complex phytoadaptogen on MPTP-induced Parkinson's syndrome in mice.

Oral administration of 10% solution of Phytomix-40 (multicomponent plant phytoadaptogen) to C57Bl/6 mice with MPTP-induced Parkinson's syndrome alleviated symptoms (oligokinesia and muscle rigidity), compensated for the deficiency of dopamine and its metabolites (DOPAC and homovanillic acid), and reduced the level of lipid peroxides in the striatum. In vitro Phytomix-40 in a concentration of 3.3 x 10(-2) g/liter exhibited a pronounced antioxidant effect (5-fold decreased MDA level in mouse brain homogenate in Fe(2+)-ascorbate-dependent LPO).

3,4-Dihydroxyphenylacetic Acid↗
PubMed2004

Immunization of rats with conjugates of dopamine and serotonin with bovine serum albumin prevents the development of experimental MPTP-induced depressive syndrome (electrophysiological parameters).

Electrophysiological experiments on Wistar rats demonstrated that prior immunization of animals with conjugates of dopamine and serotonin with bovine serum albumin, as well as with bovine serum albumin alone, played a partial protective role in relation to the subsequent development in these animals of experimental MPTP-induced depressive syndrome: immunized animals showed no signs of the depressive state such as decreases in the latency of onset of REM sleep and the development of epileptiform activity in the caudate-putamen complex, though the increase in the proportion of REM sleep in the overall structure of sleep persisted. Changes in the spectral characteristics of brain electrical activity and sleep structure during the development of experimental MPTP-induced syndrome in animals immunized with conjugates of dopamine and serotonin with bovine serum albumin and with bovine serum albumin alone were antigen-specific and reflected functional shifts in the activity of those neurotransmitter systems targeted by immunization, as well as others sensitive to changes in the body's immunological status.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2002

Experimental depressive-pain syndrome in rats with initial various anxiety-phobic levels: a behavioral study.

Modeling of neurogenic pain syndrome by sciatic nerve transection in rats with pronounced dopamine-deficiency-dependent 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine-induced experimental depressive syndrome forms a stable state of combined pain and depression, which can be considered as a model of the pain-depressive syndrome. The neurogenic pain syndrome prolongs the state of behavioral depression in rats irrespective of their initial anxiety level. The depressive symptoms can potentiate the severity of pain syndrome. By a number of indices, more pronounced behavioral changes during the development of pain-depressive syndrome occur in initially nonanxious rats.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2002

Contribution of protein synthesis to mechanisms of antiepileptic system activity in kindling.

We studied changes in protein composition and their effects on convulsive activity in drug-induced and electrical kindling. Injection of protein fraction of brain extract from animals subjected to metronidazole-induced kindling to intact recipients reduced their sensitivity to the convulsant (i. e. increased the dose of metronidazole inducing clonic convulsions and lethal seizures). Incorporation of labeled amino acids in proteins in different brain structures after appearance of stable afterdischarges in the zone of synaptic stimulation significantly decrease compared to the control. Label incorporation decreased also in the frontal and occipital cortex. Kindling-associated changes in the protein spectrum were studied by electrophoresis.

Animals↗
PubMed2000

Effect of glutamate and antagonists of N-methyl-D-aspartate receptors on experimental parkinsonian syndrome in rats.

Intranigral administration of glutamate to rats with parkinsonian syndrome induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine augmented the development of parkinsonian symptoms (oligokinesia and muscular rigidity), but did not affect motor activity of intact animals. Memantine administered intraperitoneally in parallel with induction of parkinsonian syndrome weakened the development of oligokinesia and muscular rigidity in a dose-dependent manner starting from 5 mg/kg and abolished toxic effect of glutamate. Ketamine (15 mg/kg) under the same conditions less potently prevented the development of oligokinesia, did not prevent the development of muscular rigidity, and did not antagonize glutamate toxicity. The data attest to an important role of glutamate and activation of N-methyl-D-aspartate receptors in the induction and development of parkinsonian syndrome.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2000

Count and phagocytic activity of leukocytes in rats with experimental depressive syndrome caused by systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

Leukocyte count decreased, relative content of neutrophils and monocytes increased, and their phagocytic activity was suppressed in rats with 1-methyl-4-phenyl-1,2,3,4-tetrahydropyridine-induced depressive syndrome at the stage of acute behavioral depression. The severity of behavioral depression inversely correlated with changes in the absolute neutrophil and monocyte counts.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1980

[Lipoperoxidation in the hyperactive focus of rat cerebral cortex].

The possibility of participation of lipoperoxidation (LPO) in the mechanisms of development of epileptic activity in rat cerebral cortex has been shown. The appearance of epileptic activity after penicillin application to the sensorimotor cortex induced a considerable increase in the concentration of LPO products in the crude synaptosomal fraction from the hyperactive focus. Preliminary injection to rats of the antioxidant alpha-tocopherol abolished the effect of LPO activation and decreased the number of seizures recorded on the electrocorticogram in the course of the focus existence.

Animals↗
PubMed1979

[Interaction between actin like protein of the brain and isolated synaptic vesicles].

It was shown that Mg-ATP increased light diffusion in the suspension of synaptic vesicles (SV) of the rat brain in the presence of actinolike protein (ALP) of the bovine brain (the superprecipitation test). ALP enhanced the activity of the SV Mg-ATPase and increased endogenic moradrenaline release from the bovine hypothalamus SV, eliminated by cutochalazine B. Glycolipids (gengliosides and cerebrosides) inhibited the superprecipitation test. The results are considered from the standpoint of a contractile hypothesis on the mediator secretion.

Actins↗
PubMed1979

[Problem of focal pathology in "genuine" epilepsy].

Chronic experiments on rats permitted one to obtain an experimental model of photogenic epilepsy. This was accomplished by creating in the external geniculate body (EGB) a generator of pathologically intensified excitation (GPIE) with the aid of tetanus toxin (TT). According to some clinical and electrographic characteristics this form of epilepsy may be alloted to the type of primarily generalized or "genuine" epilepsy. The existance of focal pathology in the respective EGB was detected only by special electrophysiological and pharmacological methods. The studied model demonstrates a necessity of using special methods of detecting brain focal pathology (GPIE) in order to determine the focus of neuron hyperactivity in those cases where the clinical picture is characterized by signs of the so-called genuine epilepsy. Experimental photogenic epilepsy attained by creating GPIE in the EGB with the aid of TT, is proposed as a model for studying the mechanism of epileptogenesis and testing the efficacy of anticonvulsive drugs.

Animals↗
PubMed1979

[Analysis of analgesia induced by the generator of excitation in the dorsal raphe nucleus].

In experiments on white rats the generator of excitation was created in the dorsal raphe nucleus by microinjection of tetanus toxin. After formation of the excitation generator electrical activity in this nucleus was changed as the following: the first negative component (N1) was strongly increased, general EP configuration changed and the spontaneous paroxysmal activity became more frequent. The time of the generator formation correlated with the appearance of intense and prolonged analgesia. Naloxone did not reverse the effects of analgesia described.

Analgesia↗
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↗
PubMed1975

Investigation of a pain syndrome of spinal origin (on the concept of the generator mechanism of the pain syndrome).

A pain syndrome was induced in rats by means of a microinjection of purified tetanus toxin into the posterior horns of gray matter of the lumbosacral segments of the spinal cord. The toxin was used as a means of disturbing inhibitory mechanisms. Investigation showed that a pain syndrome can be reproduced if afferent stimulation from the periphery is blocked (by division of the nerves of the hind limbs or division of the dorsal lumbosacral roots on the side of injection of the toxin). Under these conditions the latent period of onset of the syndrome was lengthened and the degree of its development weakened a little in the initial stages by comparison with animals with intact afferentation. In many animals with blocked afferentation from the hind limb general manifestations (restlessness, aggressiveness, crying, etc.) were accompanied by a localized response in the form of increased licking, biting, or even chewing the tissues of the deafferented limb at the site of projection of the pain (the phantom syndrome). In some animals only the general reaction was observed without localization of the pain (protopathic pain). In all cases the attacks of pain arose paroxysmally. In animals with intact limb innervation the zones of licking were trigger zones of facilitated induction of an attack of pain. Injection of glycine into the affected posterior horns of the spinal cord abolished the pain syndrome during the time of action of the glycine. It is concluded that the pain syndrome is based on the formation of a generator of pathologically intensified excitation, as a result of disturbance of inhibitory processes, in the system of neurons connected with pain sensation. These mechanisms are evidently those principally concerned in the pathogenesis of all pain syndromes.

Animals↗