Number of correlates of membrane metabolism and long-term potentiation in rat brain slices.

Long-term potentiation was elicited in living slices of rat olfactory cortex by stimulation of the lateral olfactory tract. A group of interdependent parameters of membrane metabolism was studied, i.e., the kinetics of 45Ca metabolism, lipid peroxidation, and antioxidant defense; cytochemical measurements were made of Na+, K(+)-ATPase activity in neurons and glial cells; the functional (GTPase) activity of G-proteins was also studied. All parameters were compared with the bioelectrical activity of slices at three time points after tetanization, i.e., 3-5, 15, and 30 min. In most cases, regular phasic changes in metabolic parameters occurred, and their functional significance is discussed.

Peroxidative oxidation of lipids in slices of olfactory cortex of the rat brain during long-term potentiation.

The content of the products of the peroxidative oxidation of lipids (POL) in slices of olfactory cortex of the rat brain during long-term potentiation was investigated. The phasic character of the changes in the level of POL as a function of the duration of potentiation was demonstrated. The initial stages of potentiation (5 min) is characterized by an increase in POL; the stationary phase (15 min) is accompanied by inhibition of free-radical oxidation of lipids; the concluding phase of long-term potentiation (30 min) leads to the normalization of POL. The dynamics of the change in POL reflect the adaptive character of the development of potentiation in the slices.

[Lipid peroxidation in slices of rat olfactory cortex under long-term potentiation]. / Perekisnoe okislenie lipidov v srezakh oboniatel'noi kory golovnogo mozga krys pri dlitel'noi potentsiatsii.

Long-term potentiation (LTP) was shown to be accompanied by an increase in the lipid peroxidation at the initial stage. Stationary phase resulted in inhibition of the free radical lipid peroxidation. A decline of the LTP is accompanied by normalising of the lipid peroxidation level. The latter's dynamics seems to express the adaptive character of the LTP development in the rat brain slices.

[Lipid peroxidation in the rat brain under neurotization conditions]. / Perekisnoe okislenie lipidov golovnogo mozga krys v usloviiakh nevrotizatsii.

Neurotization provoked a stable activation of lipid peroxidation in homogenates and synaptosomes of the rat brain cortex. The activation persisted for 8 days after cessation of the neurotization. A single short-term emotional-pain stress produced but a transient increase of the lipid peroxidation level.

[Rat brain lipid peroxidation system under conditions of emotional-pain stress of varying duration]. / Sistema perekisnogo okisleniia lipidov golovnogo mozga krys v usloviiakh émotsional'no-bolevogo stressa razlichnoi dlitel'nosti.

Neurotization of rats, developed after long-term emotional-painful stress, resulted in activation of lipid peroxidation in brain both within 2 days and 8 days of stress interruption. Compensative activation of the antioxidative protective system in response to increase in lipid peroxidation rate was not observed especially in synaptosomes. Activation of glutathione peroxidase, which is involved in adaptation, was accompanied by inhibition of superoxide dismutase and glutathione transferase. Thus, the balance was impaired between the rate of lipid peroxidation and the mechanisms of antioxidative protection.

[Lipid peroxidation by rat brain synaptosomes in sleep disorders]. / Perekisnoe okislenie lipidov sinaptosom golovnogo mozgakrys pri narusheniisna.

Paradoxical sleep deprivation for 24 hrs reduced lipid peroxidation in synaptosomes from the rat brain cortex. Production of conjugated dienes was shown to decrease by 30% and fluorescent products--by 18%, the level of thiobarbituric acid reactive products being unchanged. The sleep disturbance resulted in a 25% activation of superoxide dismutase.

[Sorption of sulfophthaleinic dyes by the brain synaptosomes of rats deprived of parodoxical sleep]. / Sorbtsiia sul'foftaleinovykh krasitelei sinaptosomami golovnogo mozga krys, lishennykh paradoksal'noi fazy sna.

The influence of paradoxical sleep deprivation on sorption of bromphenol blue, bromcresol green and bromthymol blue by rat's brain synaptosomes was studied. Effect of sleep disturbance (increase in the number of dye bindings) was shown to augment with the increase in hydrophobicity of the sulfophtaleinic dye.

[Effect of glutamine on synaptosome respiration of the rat brain in depolarization and sleep disturbance]. / Vliianie glutamina na dykhanie sinaptosom golovnogo mozga krys v usloviiakh depoliarizatsii i narusheniia sna.

Depolarization induced by the increase in potassium content in the medium results in the augmented oxygen consumption by the rat brain synaptosomes, when glucose and pyruvate were used as substrates; with glutamate as substrates no such effect of potassium occurred. No effect of depolarization is present in the case of synaptosomes from animals with a paradoxical sleep deprivation; the addition of glutamine (0.5 mM) restores the capability in synaptosomes of metabolic response to depolarization. No effect of glutamine is observed with synaptosomes from brain hemispheres of rats with disturbed sleep.

[Effect of Ca2+ on ruthenium red sorption by the brain synaptosomes of rats deprived of the paradoxical sleep phase]. / Vliianie Ca2+ na sorbtsiiu rutenievogo krasnogo sinaptosomami golovnogo mozga krys, lishennykh paradoksal'noi fazy sna.

A sorption of ruthenium red by the rat's brain synaptosomes under condition of a paradoxical sleep deprivation: the number of dye binding sites decreased, whereas the affinity for the dye increased. If synaptosomes were cultivated in the Ca2+-containing medium (0.5 mM), the synaptosomal dye sorption registered in rats with paradoxal sleep deprivation did not differ from that in the control rats.

[Effect of Ca2+ and gamma-aminobutyric acid on glutamate and glutamine oxidation by rat brain synaptosomes]. / Vliianie Ca2+ i gamma-aminomaslianoi kisloty na okislenie glutamata i glutamina sinaptosomami golovnogo mozga krys.

It was shown in vitro that Ca2+ addition induced inhibition of the synaptosomal respiration with glutamate and glutamine. The presence of GABA in the medium increased the inhibitory effect of Ca2+ on glutamine oxidation, but not on glutamate. GABA, by itself, had no influence on both glutamate and glutamine oxidation.

[Effect of sodium and calcium ions on glutamate and glutamine oxidation by rat brain synaptosomes]. / Vliianie ionov natriia i kal'tsiia na okislenie glutamata i glutamina sinaptosomami golovnogo mozga krys.

5 mM oxidative substrates and 0.15 mM Ca(2+) being used, different effects of Ca(2+) on the oxidation are possible, such as an additional inhibition of glutamine oxidation and an additional activation of glutamate oxidation. A decreased Na+-ion concentration in the medium inhibited synaptosomal respiration with glutamate as a substrate. With glutamine as a substrate oxygen consumption does not change.

[Glutamate deamination and transamination in the presence of dinitrophenol]. / Dezaminirovanie i pereaminirovanie glutamata v prisutstvii dinitrofenola.

Oxidation of glutamate by the brain mitrochondrial fraction was studied in the in vitro experiments in the presence of 2,4-DNP in concentrations of 5.10(-6) and 1.10(-3) M. 5.10(-6) M DNP is shown to stimulate ammonia and aspartate formation when glutamate in a concentration of 10 mM was used. Under these conditions an increase in O2 consumption occurred. When 1.10(-3) DNP was used, O2 consumption was inhbited. In this case ammonia formation was more intensive and simultaneously aspartate production was decreased. An increase in the glutamate concentration up to 20 mM diminished 2,4-DNP effects on ammonia and aspartate production.

[Effect of monovalent cations on glutamate metabolism in rat brain]. / Vliianie odnovalentnykh kationov na metabolizm glutamata v golovnom mozge krys

Glutamate oxidation in vitro via deamination and transamination during gramicidin C-induced transport of K+ and Na+ in rat nervous tissue mitochondria was studied. An increase in ammonium production, i.e. in glutamate oxidation due to deamination, was shown to occur with maximal increase of oxygen consumption in the presence of cations. It was found that 1.5 mM Na+ activate oxygen consumption by 15% and accelerate ammonium production from glutamate (by 17%). No changes in aspartate production were observed. 15 mM K+ increase oxygen consumption by 29% and ammonium production by 11% during a decrease in aspartate production as compared to glutamate oxidation in the presence of a lower (10 mM) concentration of K+ in the samples.