[The regulation of the Na, K-ATPase system by neurotransmitters]. / Reguliatsiiia Na, K-ATFaznoi sistemy neirotransmitterami.

Factors regulating the activity of synaptosomal Na, K-ATPase have been found in the cytosol of nerve endings. The activatory effect of the factor increases in the presence of neurotransmitters regardless of their direct action on Na, K-ATPase. Synaptosomal Na, K-ATPase is not sensitive to the factor obtained from the cytosol of kidney tissue, or the cytosolic fraction obtained after sedimentation of microsomes. The effect of inhibiting low molecular ET(S) fraction on Na, K-ATPase activity is not mediated through noradrenaline, dopamine and serotonin as well by the system of secondary messengers. Factor stimulated by neurotransmitters activates the Na, K-ATPase system affecting the phosphorylating intermediates of the enzyme and putting the Na, K-ATPase system in the mode of simultaneous transport of Na and K ions.

[A kinetic analysis of the action of a synaptosomal factor on Na, K-ATPase]. / Kineticheskii analiz deistviia sinaptosomal'nogo faktora na Na, K-ATFazu.

A synaptosomal factor stimulated by neurotransmitters activates the Na, K-ATPase system effecting the phosphorylating intermediates moving the Na, K-ATPase system in the mode of simultaneous transport of Na+ and K+. This conclusion has been made during the analysis of kinetics of the effect of MgATP complex, free Mg2+ ions and ATP on Na, K-ATPase activity. Unlike the EGTA, the factor under study does not change the number of essential activators (ions of Na+ and K+) of the Na, K-ATPase system at the equimolar ATP and Mg2+ correlation.

[Synaptosomal factors, regulating the activity of Na,K-ATPase and its sensitivity to neurotransmitters]. / Sinaptosomal'nye faktory, reguliruiushchie aktivnost'Na,K-ATPase i ee chuvstvitel'nost' k neirotransmitteram.

The factors regulating the activity of synaptosomal Na,K-ATPase have been found in nerve endings cytosol. One of these (Mr 10,000) essentially inhibits, whereas the other one (Mr 60,000) in the presence of norepinephrine, 5-hydroxytryptamine and dopamine activates the Na,K-ATPase of synaptosomes. Regardless of their direct action on Na,K-ATPase, the effect of the activating factor increases in the presence of neurotransmitters. In cell ksap obtained by microsome precipitation the activating factor is absent.

[Regulation of Na,K-ATPase by synaptosomal factors and neurotransmitters]. / Reguliatsiia Na, K-ATFazy sinaptosomal'nymi faktorami i neirotransmitterami.

The identical increase of Na, K-ATPase activity is caused by oxidated and reduced forms of noradrenaline, serotonin and dopamine through the synaptosomal activating factors. The synaptosomal inhibiting factor, orthovanadate and calcium ions independently inhibit Na, K-ATPase activity. The inhibition constant (Ki) for vanadate does not change in the presence of EDTA, whereas in the presence of synaptosomal factors regulating the Na, K-ATPase factors, noradrenaline causes drastic increase of Ki for vanadate. It has been concluded, that the data point to the existence of special regulating system of brain synaptosomal Na, K-ATPase.

Functional significance of the effects of neurotransmitters on the Na+,K+-ATPase system.

The aim of the present experiments was to study the effects of the neurotransmitters acetylcholine, noradrenaline, 5-hydroxytryptamine, and dopamine on the Na+,K+-ATPase of rat brain synaptosomal fractions. It is shown that dopamine at low concentrations specifically inhibits the Na+,K+-ATPase of synaptic membranes from the brain regions rich in dopaminergic endings, but has no effect on the synaptosomal Na+,K+-ATPase from the other parts of brain. Acetylcholine and noradrenaline have similar specific effects on Na+,K+-ATPase from cholinergic and adrenergic synaptosomes. The Na+,K+-ATPase of synaptic membranes from the different brain regions, characterised by different distributions of cholinergic, adrenergic, and 5-hydroxytryptaminergic endings, show different reactions with neurotransmitters. These data indicate a functional significance of the effects of the neurotransmitters on the synaptosomal Na+,K+-ATPase.

[Some properties of glial membrane Na, K-ATPase]. / Nekotorye svoistva Na,K-ATPazy glial'nykh membran.

Na,K-ATPase activity in glial membranes is rather low that in the nerve ending membranes, but is characterized by the same kind of Na+/K+-dependence. Glial Na,K-ATPase is insensitive to acetylcholine (ACh), 5-hydroxytryptamine (5-HT) and gamma-aminobutyric acid (GABA) while norepinephrine activates Na,K-ATPase at low concentrations and inhibits it at high concentrations. Participation of Na,K-ATPase in the regulatory mechanisms of the neuron-neuroglia relations is discussed.

[Effect of acetylcholine on Na, K-ATPase of synaptasomes]. / Deistvie atsetilkholina na Na, K-ATRazy sinaptasom

Effect of acetylcholine (ACh) on Na, K-ATPase system has a complex character. ACh concentration, as well as the type of membrane are responsible for the increase or decrease of Na, K-ATPase activity. The inhibition and activation capacity is not constant in different subcellular fractions. The maximal effect is observed in subcellular fractions rich in junctional complexes, whereas minimal effect is in microsomes. There is no effect in mitochondria and myelin at all. EGTA and EDTA removes the inhibition, but the activation remains unchanged. ACh is supposed to release from membrane structure Ca2+, which subsequently inhibits Na, K-ATPase. On the other hand, activation by ACh is the result of its direct effect. The inhibition prevails over the activation at high (2-10 mM) concentration of ACh, whereas at low (2mM) concentration it might be vice versa. Thus the effect of ACh on Na K-ATPase is the result of two different processes having opposite effects.