Search PubMed⌕ Search

Biomedical subjects

R N Glebov

Publications and source records attributed to R N Glebov.

101 records · Page 6Linked to original sources
PubMedDate not supplied

[Na+, K+ -ATPase inactivation as a trigger coupling factor of mediator depolarization and secretion].

The paper deals with an analysis of ouabain-induced processes: a decrease in transmembrane potential of neurone, an increase in the intensity of passive Na+, K+ and Ca2+ transport, secretion of different mediators by nerve endings. A hypothesis on inactivation of Na+, K+-ATPase as a trigger coupling factor of depolarization and secretion of mediators (and hormones) is discussed. According to this hypothesis inhibition of the Na, K-pump "work" may induce an additional opening of ion-selective canals, cause Ca2+ outflow from synaptic mitochondria to synaptoplasm due to intracellular accumulation of Na+, promote penetration of Ca2+ into a cell through the Ca2+ and Na+ metabolism.

Animals↗
PubMedDate not supplied

[Specific proteins of synaptic structures].

The article deals with the data concerning localization, properties and functions of specific proteins of nerve endings, especially in the synaptic vesicles and synaptic membranes, as well as concerning their metabolism. In the fractions of the synaptic vesicles and synaptic membranes simple and conjugated proteins (glycoproteids) typical of these high-specialized structures only are localized. Acid polypeptides, contractile proteins and neurospecific proteins of S-100, 14-3-2 type and glycoproteids are such specific proteins of the studied structures. Their possible function in the mechaninsm of secretion and circulation of mediators in synapses is discussed.

Animals↗
PubMedDate not supplied

[The properties of the benzodiazepine receptors in the rat cerebellum after acute seizures and the development of korazol-induced kindling].

The acute korazol (pentylenetetrazol) injection (50 mg/kg) induced seizures which were accompanied by a long-lasting (from 30 minutes to 3 days) decrease in benzodiazepine receptor (BDR) density (Bmax) in rat cerebellum without change in affinity. The density of the BDR was normalized on the 7th day after seizure termination. There were no differences in the initial BDR characteristics between the animals more sensitive to korazol (a dose of 25 mg/kg was sufficient for seizure induction) and less sensitive (30 mg/kg were ineffective). The chronic daily (for 24 days) administration of korazol in a subconvulsive dose led to an increase in seizure readiness (kindling). In 30 min after the last korazol injection the BDR density was decreased to the same extent as after the acute 50 mg/kg korasol administration. The BDR density was normalized on the 7th day after kindling. It was demonstrated that the high-dose-induced and after-kindling seizures were underlain by the same mechanisms. The results suggest that the development of kindling depends on the state of the long-lasting receptors rather than the development of kindling forms the long-lasting reactions. The process of summation is at the basis of kindling development. The long-lasting decrease in activity of BDR receptors induced by a subconvulsive dose of korazol is summed with the following effect of the same dose.

Acute Disease↗
PubMedDate not supplied

[The properties of the benzodiazepine receptors of the rat cerebellum 6 months after korazol-induced kindling and recurrent seizures].

It was shown that the increased brain seizure readiness persisted within 6 months after termination of corazol kindling. Seizures of the same severity as during kindling (corazol injection in a dose of 20 mg/kg) were reproduced by corazol injection in a dose of 30 mg/kg. In contrast to the control rats, in this situation an autoenhancement of seizures was observed in the kindled animals. Acute corazol seizures induced a decrease in Bmax and Kd of 3H-diazepam binding with benzodiazepine receptors (BDR) in the cerebellum of the 10-months-old control rats white the young animals demonstrated only a decrease in Bmax of binding. In 6 months after kindling termination the BDR activity (Bmax) was reduced by one half. However, we think that the increase in Bmax is not responsible for persistence of the increased seizure readiness. It seems possible that down regulation of receptor activity develops independently of kindling but in response to long-lasting corazol application. Probably, Bmax spontaneously decreases after the termination of the long-term corazol application. The single dose of corazol (30 mg/kg) restores the changes in BDR density to the level when seizure readiness has been just fixed (6 months after kindling termination), independently of the primary receptor density.

Animals↗