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Biomedical subjects

A F Semiokhina

Publications and source records attributed to A F Semiokhina.

At least 19 recordsLinked to original sources
PubMed1992

Increase of brain endogenous monoamine oxidase inhibitory activity (tribulin) in experimental audiogenic seizures in rats: evidence for a monoamine oxidase A inhibiting component of tribulin.

Brain tribulin activity in rats with an inherited predisposition to audiogenic epilepsy was studied after seizures of different intensity were induced by an electric bell. Weak seizures (from 0 to 2 arbitrary units) did not produce any changes in endogenous inhibitory activity towards either monoamine oxidase (MAO) A or B. Moderate seizures were characterized by increases in both MAO A and MAO B inhibitory activity (up to 1.9-fold). Complete tonic epileptiform seizures with total areflexia (4 arbitrary units) induced further augmentation (up to 2.5-fold) of MAO A but not of MAO B inhibitory activity. This dissociation between the two inhibitory activities points to the existence of a separate MAO A-inhibiting component of brain tribulin which is different from isatin.

Animals↗
PubMed1989

[DNA fingerprinting of Rattus norvegicus: a new approach in genetic analysis].

Recent finding in highly effective DNA probes for RFLP testing (of hypervariable minisatellite DNA type) has led to the invention of DNA fingerprinting--the new technique of great value for identification of individuals, establishing biological kinship and studies in population genetics. We anticipate that DNA fingerprinting procedure with M13 phage DNA as a probe which we have developed earlier, makes it possible to apply new approach in genetic analysis--establishing, whether or not a particular locus is associated with the inheritance of genetic disease, by comparing the whole restriction fragment data from affected and unaffected animals. In this work, using the method described we characterized the Kroushynsky-Molodkina rat strain with hereditary disposition for epileptic attacks and performed comparative fingerprint analysis of these defective and normal rat genomes. The data obtained may hold some promises for further seeking the particular defective gene.

Animals↗
PubMed1981

[Effect of hyperbaric oxygenation on animal deaths from acute circulatory disorders caused by intense cerebral excitation].

Sound exposure to 100--120 dB caused death of about 6--16% of white rats KM line from the blood circulation disturbances. The hyperbaric oxygenation (2 atm) decreased the death rate among rats of 4 to 15 months old while having no effect upon younger ones (2--4 months old). The rats who died in hyperbaric oxygenation suffered from O2 intoxication more often than those who survived. Administration of caffeine reduced the positive effect of hyperbaric oxygenation.

Acoustic Stimulation↗
PubMedDate not supplied

The role of lipid peroxidation in the possible involvement of membrane-bound monoamine oxidases in gamma-aminobutyric acid and glucosamine deamination in rat brain. Focus on chemical pathogenesis of experimental audiogenic epilepsy.

Incubation of rat brain synaptosomes and mitochondria with LPO inducers (Fe2+ and ascorbate) was accompanied by a decrease of deamination of serotonin (substrate of MAO-A) in mitochondria, but not in synaptosomes, with simultaneous stimulation of GABA and GLCA deamination, apparently owing to modification of catalytic properties of brain membrane-bound MAO. Oxidation of PEA (substrate of MAO-B) was insignificantly altered in both fractions. Reactions of deamination of serotonin, GABA, and GLCA (but not PEA), were highly sensitive to a selective inhibitor of MAO-A pyrazidol (pyrlindole). Isoniazid and hydrazides of quinoline carbonic acids (inhibitors of both modified MAO and copper-containing amine oxidases) strongly inhibited deamination of GABA and GLCA. During epileptiformic seizures in rats, genetically selected for high incidence of audiogenic epilepsia, stimulation in brain synaptosomes and mitochondria of LPO was observed. This was accompanied by a marked decrease in serotonin and PEA deamination, with a simultaneous increase in GABA and GLCA deamination in both fractions. The data obtained suggest that appearance of GABA-deaminating activity owing to modification of catalytic properties of MAO, might be an essential pathogenetic component in the development of epileptic seizures.

Acoustic Stimulation↗
PubMedDate not supplied

[Developmental changes in audiogenic epilepsy and myoclonus in KM rats].

The reaction to a single sound stimulation (a bell) applied daily and the time of the first appearance of myoclonus were recorded in Krushinsky-Molodkina (KM) rats of different ages (30, 60, and 150-200 days). The audiogenic seizures in adult animals were of short latency and always resulted in tonic convulsions, which were stable in their patten. In contrast, in young animals (in particular, in 30-day-old rats), the seizures were less pronounced and unstable. The daily sound stimulation produced a gradual development of myoclonic seizures in young and adult rats. In old rats, the stable myoclonus appeared on the 17th day of stimulation, and in 30-day-old animals the myoclonus was recorded on the 26th day. In 60-day-old rats the myoclonus appeared for the first time on the 20th day of stimulation. It is suggested that these age differences can be explained by the btain immaturity (in particular, of neurotransmitter system) in young animals.

Animals↗
PubMedDate not supplied

[Remote effects of early postnatal pituitary hormone melatonin injection on audiogenic seizures in Krushinsky-Molodkina rats].

Rats Krushinsky-Molodkina inbred strain (KM) genetically prone to audiogenic seizures were injected with pineal hormone melatonin (50 mg/kg, s.c.) within the period 7th to the 14th posnatal days (PND). The remote effects of this injection adult KM rats consisted in a decrease in the latency and increase in severity of myoclonic seizures produced by audiogenic kindling (20 sound stimuli, 100 dB and 12-15 kHz). As compared to the control, in the cortex and hippocampus of rats of melatonin group, we also found a significant reduction of both total and functional activity of Ca2+/calmodulin-dependent protein kinase II (CAMK II) after audiogenic kindling. On the contrary, melatonin administration within the 1st to 7th PND and the 14th to the 21st PND resulted in a decrease in seizure activity. In the first case, both the total (cortical) and functional (hippocampal) CAMK II activities in melatonin-injected rats were increased as compared to control, whereas in the second case, only a slight increase in Ca2+-independent CAMK II activity in the hippocampus of melatonin-injected rats was observed. Probably, the melatonin administration in the period of early postnatal development changes the features of expression and/or regulation of CAMK II activity, and this could be one of the mechanisms of audiogenic seizure modulation in KM rats.

Animals↗
PubMedDate not supplied

[Rats of Krushinsky-Molodkina strain: studies of audiogenic epilepsy, vascular pathology, and behavior].

Physiological, biochemical and genetic studies of audiogenic epilepsy in Krushinsky-Molodkina (KM) rat strain are analyzed. In brief, the history of KM strain selection and its current state are reviewed. Physiological mechanisms of the typical audiogenic seizure development and the audiogenic myoclonus (audiogenic kindling phenomena) are considered. The EEG correlates of these phenomena are presented. Biochemical features of the strain (neurotransmitter and neuronal membrane biochemistry) are described.

Acoustic Stimulation↗