[Cerebral peptides and epileptic activity (review)].
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Animals↗
Biomedical subjects
R N Glebov
Publications and source records attributed to R N Glebov.
[Effect of neurotropic compounds on the transmembrane potential of synaptosomes].
Using the potential-sensitive dye (3,3-dipropylthiodicarbocyanine) [dis-C3-(5)] it has been shown that synaptosomes isolated from the rat brain cortex by the method of Hajôs retain their transmembrane potential (TMP) close to the K+-diffusional one. In the Krebs-Ringer medium containing 5 mM KCl the TMP of the synaptosomes was equal to 70-80 mV. The cytostatics cytochalazine B and colchicine and the peptides leu- and met-enkephalins and tuftcin in concentrations up to 10(-3) and 10(-4) M did not affect the TMP of the synaptosomes. Cytochalazine B in a concentration of 4 X 10(-4) M and over caused synaptosomal aggregation. The neuroleptics aminazine, trifluoroperazine, haloperidol, the antidepressant imipramine in concentrations about 10(-4) M as well as the tranquilizers diazepam and phenazepam in concentrations about 10(-3) M completely depolarized synaptosomal membranes.
Animals↗
[Calmodulin--a new universal protein and Ca-regulation of cell metabolism].
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Amino Acid Sequence↗
[Ratio between uptake and secretion of noradrenaline by nerve endings of the cerebral cortex during elaboration of conditioned reflexes in the rat].
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Animals↗
[Regulation of the superprecipitation of an actomyosin-like protein from the brain by glycolipids].
The optimal conditions (ionic strength, pH, Mg2+ and ATP concentrations) for nephelometric determination of the superprecipitation reaction of the actomyosin-like protein (AMLP) from ox brain cortex are described. At low ionic strength (0.1 M KCl, 200 micrograms of protein, pH 6.8, 37 degrees) MgATP (1 mM) first causes a fast (1--2 min) dissociation of AMLP with a decrease in the optical density (A620) at 620 nm and then a slow (15--20 min) true superprecipitation associated with a substantial rise of A620. EGTA (0.1 mM) moderately, i. e. by 20%, inhibits the reaction. The effects of glycolipids (total gangliosides and cerebrosides from ox brain) and phosphatidyl choline from chicken egg yolk on aggregation (without Mg-ATP), dissociation and superprecipitation of AMLP were examined. It was found that gangliosides (40 micrograms) and cerebrosides (2--80 micrograms) cause aggregation of AMLP; phosphatidylcholine (4--160 micrograms) has no effect on protein aggregation. Gangliosides within the concentration range of 0.8--4.0 micrograms do not cause AMLP aggregation but strongly inhibit superprecipitation of the protein, whereas phosphatidylcholine (40--80 micrograms) has practically no effect on the reaction intensity. A hypothesis on regulation by glycolipids on contractile proteins from brain presynaptic membranes under varying rest--excitation conditions is postulated.
Actomyosin↗
[Status of active and passive cation transport through cerebral synaptic membranes during seizures].
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Animals↗
[Technic for simultaneous recording of the uptake and secretion of 14C-noradrenaline by rat brain synaptosomes].
A procedure has been suggested for simultaneous recording of 14C-noradrenaline active uptake and induced secretion by rat brain synaptosomes. Active noradrenaline uptake was shown to depend on the presence in the incubation medium of Ca2+. Removal of Ca2+ from the incubation medium considerably reduces the intensity of noradrenaline uptake by the synaptosomes. Unlike the induced secretion in potassium depolarization of synaptosomal membranes, spontaneous release of noradrenaline does not depend on the presence of Ca2+ in the incubation medium.
Animals↗
[Ultrastructural and functional changes in the synaptosomes of the rat brain on in vitro electrostimulation].
Electrostimulation of suspension of the rat brain synaptosomes causes Ca(2)+-dependent endogenous norepinephrine release and at the same time Ca(2)-dependent increase of the mediator content in the synaptosomes. The activity of cAMP declines under the same conditions. Electrostimulation does not alter the ultrastructure of the synaptosomes but raises the content of high electron density synaptosomes.
Animals↗
[Effect of tetanus toxin on noradrenaline release from rat brain synaptosomes].
Purified tetanus toxin (TT) (80-800 Dlm/mg protein) releases both endogenous and exogenous (14)C-norepinephrine from the isolated nerve endings (synaptosomes) of the rat brain. Within the investigated range of concentrations TT does not suppress norepinephrine release induced by different ways of depolarizing the synaptosomes in vitro.
Animals↗
[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↗
[Use of the fluorescent probe 1-anilinonaphthalene-8-sulfonate to study the transmembrane potential of synaptosomes].
The properties of the transmembrane potential (TMP) of synaptosomes (Sin) from the rat brain cortex were studied by means of the fluorescent probe I-anilinonaphthalene-8-sulfonate (ANS). The fluorescent emission that increased at 464 nm (lambda ex = 365 nm) after addition of valinomycin to synaptosomes was considered as the reflection of Sin hyperpolarization. The reduction of K+-gradient across Sin membrane (decrease in TMP) induced by Sin preincubation with ouabain (1 mM) or by K+ increase from 5 to 20 mM noticeably decreased the effect of valinomycin. Valinomycin exerted no effect on Sin subjected to osmotic shock. It is suggested that valinomycin-induced changes in ANS fluorescence may be made use of for testing the ability of Sin obtained to retain K+-gradient (TMP presence), that is for testing the Sin nativity.
Anilino Naphthalenesulfonates↗
[Contractile proteins of nerve endings as a possible target of the presynaptic action of tetanus toxin].
Tetanus toxin (TT) in a dose of 0.25--250 DLM/ml inhibits the superprecipitation reaction of actomyosin-like protein (AMLP) of the bovine brain in response to Mg-ATP addition. Gangliosides of the bovine brain exert a similar action. Combined action of gangliosides (0.25 g/ml) and TT (0.25 DLM/ml) results in additivity of their effects. TT in a dose of 1600 DLM/ml blocks the formation of a complex of isolated synaptic vesicles (SV) of the rat brain. This effect was assessed from light scattering in response to MgCl2 and ATP addition. Under these conditions TT also inhibits release of the endogenous mediator noradrenaline from SV of bovine hypothalamus, with antitetanus serum reversing the effect of toxin. It is postulated that ALP associated with the synaptic membrane may be a potential TT target in the nerve endings.
Adenosine Triphosphate↗
[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↗
[Na, K-ATPase activity of the meninges in electroshock and the action of the anticonvulsant agent, diazepam].
It was shown that the phenomenon of inactivation of Na, K-ATPase of the non-purified fraction of the rat cortical synaptosomes under electroshock may be related to "modification" of the potassium active center of the enzyme. The anticonvulsant diazepam injected intramuscularly also inhibits Na, K-ATPase of the cerebral membranes. However, in subsequent electrical stimulation of the brain the drug activates Na, K-ATPase as compared to controls. Diazepam also abolishes clonic convulsions induced by electrical stimulation of the brain. At the same time it does not eliminate compensatory shifts in the activity of acetyl-cholinesterase of the rat cerebral and spinal synaptosomes, characteristic of electroshock. The results are discussed from the standpoint that inhibition of the activity of Na, K-ATPase of the nerve endings membranes may underlie the pathogenetic mechanism of the convulsive activity.
Acetylcholinesterase↗
[Changes in the Na, K-ATPase of neuronal membranes in penicillin-induced epileptic foci in the cerebral cortex of the rat].
The relationship between electrophysiological changes and Na, K-ATPase activity of neuronal membranes in sodium penicillin-induced epileptic foci was studied. Na,K-ATPase activity is inhibited both in the primary focus and in homotopic contralateral area during latent period and in the stage of forming epileptic activity. In the stage of marked convulsive activity Na, K-ATPase is inhibited only in the primary focus. It is shown that penicillin at a concentration range of 2 x 10(-6)--2 x 10(-3) M does not influence Na,K-ATPase activity of crude synaptosomes of the rat brain cortex. It is suggested that Na,K-ATPase inactivation may serve as a pathogenetic factor in the development of convulsive process.
Action Potentials↗
[Effect of diazepam on the Na, K-ATPase state in a penicillin--induced hyperactivity focus in the cerebral cortex].
Intramuscular injection of diazepam to rats at doses of 0.01 and 2 mg/kg 25-30 min after penicillin application to the rat brain cortex leads to alteration of periodic appearance of epileptic seizures (ES), to changes in the seizure pattern, and to emergence of periodic acceleration of epileptiform discharges (ED). Injection of diazepam at a dose of 2 mg/kg 20 min before penicillin application results in the reduction of ED latency in the epileptogenic focus and in a decrease in their frequency before seizures as compared to the control animals without diazepam injection. ES appear irregularly, their quantity is markedly reduced while duration is increased. Diazepam injection leads to disappearance of the rat moving reaction during ER and ES. In vivo experiments diazepam (2 mg/kg) does not influence brain cortex Na, K-ATPase of crude synaptosomes. However, diazepam leads to an increase in Na, K-ATPase activity both in the primary and dependent secondary epileptogenic foci. It is suggested that the anticonvulsant action of diazepam may be underlain by its activating effect on Na, K-ATPase of neuronal membranes in the epileptogenic focus.
Animals↗
[Changes in active 14C-noradrenaline uptake by cerebral synaptosomes during elaboration of a conditioned reflex].
It was shown that active noradrenaline-14C (NA) uptake by the rat brain synaptosomes is inhibited by ouabain (0.1 M) and K-depolarization. Acquisition of the defensive conditioned reflex leads to inhibition of active NA uptake by the synaptosomes. This effect may be connected both with changes in the presynaptic membrane state and possible enhancement of the postsynaptic adrenoreceptor function.
Absorption↗
[Effects of anticonvulsive substances on Na,K-ATPase from the synaptic membranes of animal brain].
The distribution pattern of marker enzymes (Na, K-ATPase, acetylcholinesterase) in three fractions of synaptic membranes (SM) of rat brain were studied. The effects of three anticonvulsive agents on Na, K-ATPase from the total fraction of rat brain SM and purified membrane preparation from ox brain were estimated by different methods. Under optimal conditions (Na/K = 5) diphenylhydantoin (DPH) at a concentration of 0,1 mM activates Na, K-ATPase from the total SM fraction only in the absence of ouabain, whereas carbamazepine and pyrroxane taken at the same concentrations have no effect on Na, K-ATPase, irrespective of the type of the enzyme assay. DPH seems to compete with ouabain. Under non-optimal ionic conditions (Na/K = 250) all the anticonvulsive substances studied inhibit Na, K-ATPase of the total SM fraction. The mixture of hydrophobic agents (propylene glycol and ethanol) used to dissolve carbamazepine inhibits Na, K-ATPase from the total SM fraction only under non-optimal conditions. The inhibiting effect of the anticonvulsive substances under study on Na, K-ATPase from the purified membrane preparations is maximal at the concentration of 10(-6) M; at higher concentrations the effect is less pronounced.
Adenosine Triphosphatases↗