Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurones in rat hippocampal cortex were exposed to hypoxia while their membrane properties and responses to different kinds of stimuli were recorded with an intracellular electrode. The initial changes consisted of a small depolarization followed by a hyperpolarization. Following these early events the neurones lost their membrane potential through a large depolarization. Similar changes were observed in neurones where the Na/K-ATPase was blocked by ouabain. Responses to direct application of the transmitters GABA and glutamate, which was lost at this point, were restored by passive reestablishment of the membrane potential with current through the intracellular electrode.
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PMID:Intracellular recordings from neurones in rat cerebral cortex during hypoxia. 290 75

The potassium potential EK, of rat brain slices was estimated by determining the uptake of 86Rb+. The ERb was the same for slices prepared from five rostral brain regions, the average value being 66.4 mV. The ERb values in the presence of 20 microM ouabain were only slightly lower than the resting values; increasing concentrations of ouabain above 20 microM resulted in a graded depolarization in all five brain regions. High concentrations (1 mM) of two other inhibitors of Na+,K+-ATPase, dihydro-ouabain and strophanthidin, produced no more depolarization than did 20 microM ouabain. Competitive binding studies indicated that the differential effects were due to the relative binding to brain slices. Erythrosin B, an inhibitor of Na+,K+-ATPase, had no measurable effect on ERb. Intermediate concentrations of the Na+/H+ ionophore monensin slightly hyperpolarized striatal slices, whereas the same monensin concentrations plus 20 microM ouabain, 1 mM strophanthidin or 70 microM erythrosin B resulted in marked depolarization. Measurement of the membrane potential via uptake of methyltriphenylphosphonium cation indicated that ERb was indeed a valid estimation of the membrane potential. EK was measured directly by monitoring 42K+ uptake in striatal slices and was found to be essentially identical to ERb. Uptake of 22Na+ was consistent with the values for ERb or EK. Several conditions that resulted in little or no measurable depolarization of striatal slices did induce efflux of exogenously loaded GABA and dopamine; these conditions included 20 microM ouabain, 1 mM dihydro-ouabain or strophanthidin, and 70 microM erythrosin B. Neurotransmitter efflux in the absence of general cell depolarization was not accompanied by altered rates of respiration or decreased ATP levels.
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PMID:Effects of inhibitors of Na+,K+-ATPase on the membrane potentials and neurotransmitter efflux in rat brain slices. 298 77

Na+/K+-ATPase activity and GABA uptake were measured in the bulk isolated astrocytes and synaptosomes from rats in which an early, metabolic phase of hepatogenic encephalopathy (HE) was induced by the treatment with thioacetamide (TAA). Both the enzyme activity and the amino acid neurotransmitter uptake were increased above control in the astroglial fraction but remained unaffected in synaptosomes. The results lend support to the earlier observations that the astrocytes are the primary target cells in HE. Furthermore, they may be interpreted as indicating that the early astroglial reaction to HE comprises stimulation of the astrocytes' function, especially concerning clearance of K+ ions and neurotransmitters from the extracellular space of CNS.
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PMID:Na+/K+-ATPase activity and GABA uptake in astroglial cell-enriched fractions and synaptosomes derived from rats in the early stage of experimental hepatogenic encephalopathy. 299 45

Ouabain-sensitive, K+-dependent p-nitrophenylphosphatase (K+-pNPPase) activity, which represents the second dephosphorylation step of Na+,K+-ATPase, was localized histochemically at the light and electron microscopical levels in the goldfish retina. K+-pNPPase staining was most intense in the outer and inner plexiform layers and less intense over the photoreceptor inner segments. K+-pNPPase staining was observed on the membranes of horizontal cell dendrites and presynaptic membrane of all cone pedicles but only rarely over rod spherules. Bipolar cell dendrites in the outer plexiform layer were not stained for K+-pNPPase. In the inner plexiform layer (IPL), K+-pNPPase staining was observed at 90% of the bipolar cell ribbon synapses but only at 40% of amacrine cell synapses. The proportion of K+-pNPPase staining at amacrine cell synapses increased from 26 to 49% as one progressed from the outer to inner layers of the IPL, while staining at bipolar cell synapses showed no such trend. Only 16% of the amacrine synapses onto mixed, rod-cone (mb) bipolar cell synaptic terminals were positive for K+-pNPPase. We suggest that the differential distribution of K+-pNPPase staining at retinal synapses can be explained, in part, by the ionic conductances gated at the postsynaptic sites. In addition, the presence of K+-pNPPase on lateral horizontal cell dendrites in cone pedicles is consistent with the hypothesis that the sodium pump is involved in the release of GABA at feedback synapses from horizontal cells to cone photoreceptors.
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PMID:Ultracytochemical distribution of ouabain-sensitive, K+-dependent, p-nitrophenylphosphatase in the synaptic layers of goldfish retina. 304 Aug 13

The neuronal activity in spinal cord in response to electrical or adequate stimulation of afferent fibres increases extracellular K+ activity. The increase during a stimulation can reach 9-10 mM (so-called ceiling level) and persists for some time even when a stimulation is discontinued. The activation of a neuronal Na-K pump is a limiting factor in stimulation-evoked increase in extracellular K+ activity and in the time course of its recovery to the resting level. Drugs that affect either the neuronal activity (picrotoxin, strychnine, GABA, 5-HT) or activity of Na-K ATPase (oubain, naloxone, morphine, enkephalins) substantially change the K+ transience. Repetitive electrical stimulation of low threshold cutaneous afferents at frequency 1-100 Hz induced transient shrinkage of extracellular space in spinal dorsal horns by 5-75%. The increase in extracellular K+ activity depolarizes the membranes of neurones, glial cells, and primary afferent fibres and may eventually lead to either facilitation or inhibition of synaptic transmission. It is also suggested that the transient poststimulation changes in extracellular volume may alter synaptic potency in spinal cord.
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PMID:Modulation of spinal cord transmission by changes in extracellular K+ activity and extracellular volume. 362 Oct 32

Effects of pantogam (calcium homopantotenate), piracetam, phenibut (beta-phenyl-GABA), sodium hydroxybutyrate and sodium valproate (depakine) at concentrations of 100 and 500 microM on the activities of glutamic acid decarboxylase, GABA-transaminase, Na, K- and Mg-ATPases, synaptosomal uptake and K+-stimulated release of 3H-GABA were studied in vitro. None of the compounds influenced the 3H-GABA uptake and activity of Mg-ATPase. Piracetam and phenibut stimulated slightly Na, K-ATPase. Phenibut and hydroxybutyrate exerted the inhibitory effect on GABA-transaminase activity. Hydroxybutyrate produced a moderate decrease of 3H-GABA release and suppressed the activity of glutamic acid decarboxylase.
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PMID:[Effects of pharmacological substances structurally close to gamma-aminobutyric acid on the synthesis, metabolism and membrane transport systems in the cerebral cortex of rats in vitro]. 375 22

Antibodies raised against synaptosomal plasma membranes of rat hippocampus (anti-HPC IgG) caused inhibition of [3H]noradrenaline, [3H]5-hydroxytryptamine, [3H]GABA and [3H]aspartate uptake into S1 fractions and slices of hippocampus and cerebral cortex, but not those of caudate nucleus and hypothalamus. Similar inhibition was not observed on using antibodies against synaptosomal membranes of rat caudate nucleus. Anti-HPC IgG raised against synaptosomal membranes of hippocampus failed to alter both spontaneous and K+-evoked release of [3H]noradrenaline. They did not interfere with the binding of [3H]desipramine (the potent noradrenaline-uptake inhibitor) and with the binding of [3H]dihydroalprenolol, thus excluding any interaction of the antibodies with drug receptors which are located on either the pre- or postsynaptic membrane. The anti-HPC IgG inhibit the enzymatic activity of [Na+-K+-]ATPase by 30% upon incubation of the antibodies with crude membrane preparations. A comparison of their inhibitory effects with those of the neurotoxin 6-hydroxydopamine suggests that the corresponding hippocampal specific antigens are located at a presynaptic site.
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PMID:The effect of anti-synaptosomal membrane antibodies of neurotransmitter uptake. 611 32

Isolated frog rod outer segments (ROS) with a leaky plasma membrane showed a bicarbonate-dependent, ATP-activated 45Ca accumulation. This calcium uptake requires magnesium and is specific for ATP; other nucleotides, ITP, GTP, UTP and the non-hydrolysable analogue of ATP beta-gamma-methylene ATP did not substitute for ATP. 45Ca accumulation was inhibited by mersalyl, ethylmaleimide, ruthenium red, oligomycin and dicyclohexylcarbodiimide and was unaffected by ouabain. Addiction of taurine to the incubation medium enhanced 45Ca uptake in a concentration-dependent manner; increases of more than 100% being produced by 25 mM taurine. The taurine-induced stimulation of 45Ca uptake was also sensitive to the tested inhibitors. The effect of taurine was only exerted on the bicarbonate-dependent, ATP-activated 45Ca uptake. Calcium accumulation observed in the absence of ATP or in a tris-buffered medium was unaffected by taurine. Other amino acids, glycine, GABA, beta-alanine, glutamic acid and the taurine analogue guanidinoethyl-sulfonate did not stimulate 45Ca uptake. These results suggest that taurine is affecting a Mg-ATPase activity responsible for calcium accumulation in frog ROS.
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PMID:Taurine activation of a bicarbonate-dependent, ATP-supported calcium uptake in frog rod outer segments. 612 3

A study was made of the changes in synaptosomal membranes and in some synaptic processes under the development of experimental neurosis in rats. Neurotic rats demonstrated changes in the protein/lipid correlation and in the interaction of the fluorescent ANS probe and synaptosomal membranes. This can be accounted for by an increase in the membrane water repellency. The activity of Na, K-ATPase remains unchanged. The rate of noradrenaline, serotonin, dopamine and GABA synaptosomal reverse uptake in neurotic rats was found to be increased.
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PMID:[Changes in the synaptosomal membranes in the chronic neurotization of rats]. 614 68

Using slices of mouse or rat cerebral cortex incubated with [3H]adenosine or [3H]adenine and/or [14C]GABA we have examined factors affecting the release of these compounds, and especially the influence of methylxanthines. Although release of purines and GABA could be induced by ouabain (10(-4) M), or p-hydroxymercuribenzoate (5 x 10(-4) M) no release was produced by ethacrynic acid (10(-3) or 10(-4) M) phenytoin (10(-3) M), noradrenaline or SC 13504. Release is probably not therefore related to (Na+, K+) ATPase or Mg2+-ATPase inhibition. At concentrations of 10(-3) and 10(-4) M, caffeine, theophylline, aminophylline and isobutyl-methylxanthine (IBMX) markedly depressed the release of purines evoked by ouabain. Non-xanthine inhibition of phosphodiesterase had much weaker though statistically significant effects. The methylxanthines had no significant effect on GABA release. It is suggested that the results can be explained on the basis of a positive feedback system in which released adenosine activates membranal adenylate cyclase, and the increased concentration of cyclic AMP which results form or origin of much of the adenosine released subsequently. However, we cannot exclude the existence of an intracellular receptor for methylxanthines which causes directly the inhibition of purine release.
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PMID:Methylxanthines modulate adenosine release from slices of cerebral cortex. 616 26


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