Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Slices of mouse or rat cerebral cortex were incubated with [3H]adenine or [3H]adenosine, and [14C]GABA. Purines and GABA could subsequently be released by ouabain. The release of purines previously shown to occur on restoring elevated K+ levels to normal was not mimicked by noradrenaline at concentrations which activate (Na+,K+)-ATPase. Potassium-free solutions evoked no release of purine during the test period, but resulted in a large release when K+ was restored to normal. K+-free solutions evoked an immediate release of GABA. It is concluded that (Na+,K+)-ATPase is not involved in purine release.
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PMID:Neuronal (Na+,K+)-ATPase and the release of purines from mouse and rat cerebral cortex. 625 76

The uptake of radiolabelled neurotransmitters: glutamate (GLU), GABA, and dopamine (DA) and the activity of the vacuolar type H(+)-pumping ATPase (H(+)-ATPase), were measured in crude synaptic vesicles treated in vitro with a neurotoxic (3 mM) dose of NH4+ (acetate or chloride), or isolated from rats with a moderate increase of brain ammonia (to approximately 0.6 mM) induced by i.p. administration of ammonium acetate (HA rats) or a hepatotoxin-thioacetamide (HE rats). In vitro treatment with ammonium salts increased the sodium-independent, chloride-dependent uptake of GLU but did not stimulate the uptake of GABA or DA. The in vitro treatment also stimulated the H(+)-ATPase activity. Since H(+)-ATPase generates the electrochemical gradient driving synaptic vesicular neurotransmitter transport, its stimulation by ammonia may have facilitated GLU uptake. However the GLU specificity of the effect must be related to other factors differentially affecting GLU uptake and the uptake of other neurotransmitters. Enhanced GLU accumulation in the synaptic vesicles may contribute to the increase of synaptic GLU exocytosis previously reported to accompany acute increases of brain ammonia to toxic levels. However, GLU uptake and H(+)-ATPase activity, but also the uptake of GABA and DA, were unchanged in synaptic vesicles prepared from rats with HA or HE. This indicates that changes in GLU and/or GABA release reported for moderate hyperammonemic conditions must be elicited by factors unrelated to the synaptic vesicular transport of the amino acids.
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PMID:Ammonia added in vitro, but not moderate hyperammonemia in vivo, stimulates glutamate uptake and H(+)-ATPase activity in synaptic vesicles of the rat brain. 783 67

Although disulfiram used as a pharmacological agent in the treatment of alcoholism is reported to act on both peripheral and central nervous systems with several adverse effects, the neurotoxic property of the drug has not been properly elucidated. We observed that the chronic administration of the drug to rats significantly inhibited synaptosomal (Na+,K+)-ATPase and basal Mg(2+)-ATPase activities. Further, the uptake of gamma-aminobutyric acid and L-glutamate which rely on the energy provided by this system was depleted following chronic drug administration. Similar findings were observed when the isolated synaptosomes were treated with the drug in an in vitro system. Further, treatment of synaptosomes with ouabain, a known inhibitor of (Na+, K+)-ATPase resulted in significant depletion of 3H-GABA and L-[3H]glutamate uptake into synaptosomes indicating the importance of the enzyme in the uptake mechanism. However, diethyldithiocarbamate, a major metabolite of disulfiram did not elicit any change in either the enzyme activity or the uptake of these neurotransmitters. On the basis of these evidences, we suggest that the chronic disulfiram administration attenuated the neurotransmitter uptake mechanism and resulted in higher extracellular concentration of glutamate that could lead to glutamate-induced neurotoxicity.
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PMID:Effect of disulfiram administration on glutamate uptake by synaptosomes in the rat brain. 786 94

1. Endosulfan insecticide is a polychlorinated compound used for controlling a variety of insects; it is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its mode of action involves repetitive nerve-discharges positively correlated to increase in temperature. This compound is extremely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood Ca(2+) and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain). 2. Bioaccumulation of endosulfan is reported for marine animals; however, freshwater animals (e.g., crayfish) accumulate it to some extent, but they lose the compound rapidly during depuration. Endosulfan is generally less toxic to aquatic invertebrates than fish. However, it causes decreases in adenylate energy charge, oxygen consumption, hemolymph amino acids, succinate dehydrogenase, heart-beat (mussel) and altered osmoregulation. 3. Generally, mammals are less susceptible to endosulfan's toxicity than aquatic animals. The majority of studies conducted on laboratory mammals can be summarized. (a) Neurotoxicity: male rats are more sensitive than females to endosulfan, which decreases brain and plasma acetylcholinesterase activity. Endosulfan I (a metabolite) causes a significant change in norepinephrine, 5-HT and GABA. (b) Renal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis of the tubular epithelium. (c) Hepatotoxicity: chemically-induced aminopyrine N-demethylase and aniline hydrolase were found in rat liver, and reduction in the glycogen level occurred. (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the level occurred. (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythrocyte glutathione reductase, hemoglobin amount, RBC number and mean corpuscular volume. 4. Respiratory toxicity: involved dyspnea, acute emphysema, cyanosis and hemorrhages in teh interalveolar portions of rat's lungs. 5. Biochemical: in rats, endosulfan caused increased glucose-6-phosphate dehydrogenase activity, blood glucose level, phospholipid contents of the microsomal and surfactant system, and profoundly induced the activity of alcohol dehydrogenase and cytosolic glutathione S-transferases. It also decreased significantly Na+, K+ and Mg(2+) ATPases, plasma calcium level and alkaline phosphatase in the intestinal epithelium. 6. Immunologic toxicity: rat serum antibody titer to tetanus toxin, IgG, IgM and gammaglobulins were significantly reduced. 7. Reproductive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting enzyme in testosterone production (3beta-hydroxysteroid transferase and 17 beta-hydroxysteroid transferase), histological changes in reproductive organs, testicular atrophy and the occurrence of ovarian cysts were noticed in rat. Reduction in the weight of secondary sex organ was also observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Bioaccumulative potential and toxicity of endosulfan insecticide to non-target animals. 790 Sep 59

The activity of specific ouabain-sensitive Na+,K(+)-ATPase was studied in crude membrane fraction of the brain of 1- to 3-day-old chicks after the administration of a chemical aversant methylanthranilate (MeA), shown in previous behavioral studies to induce avoidance of pecking of an otherwise attractive stimulus. Enzyme activity was dramatically decreased (by 40-50%) in the time interval between 10 min-2 h after MeA administration onto the tongue of awake chicks. It was possible to localize these changes in Na+,K(+)-ATPase activity into forebrain structures contained within the dorsal ventricular ridge comprising the hyperstriatum accessorium (HA), hyperstriatum ventrale (HV), hyperstriatum dorsale (HD), and parts of neostriatum (N). In contrast, Na+,K(+)-ATPase activity in the ectostriatum (E), the medial neostriatum (NM), and the paleostriatal complex were unaffected. Results from experiments involving preincubation of membrane fractions and with partial purification using detergents, suggest that some substances with inhibitory effects were produced under the effect of MeA and bound to membrane fractions in their respective areas. A similar decrease of Na+,K(+)-ATPase activity as after MeA administration in vivo was observed when inhibitory mediators (GABA, glycine) were added to membrane fractions in vitro. These findings may have implications for memory processing in chicks following aversive learning using MeA as the aversant.
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PMID:Na+,K(+)-ATPase activity in young chicks after taste stimulation. 790 3

Neuropeptide Y (NPY) or closely related peptides are present in the retina of certain vertebrates, but their actions are not known. We have therefore studied the NPY-induced release of [3H]-GABA, [3H]-glycine, [3H]-dopamine, [3H]-5-hydroxytryptamine, and [3H]-choline chloride-derived radioactivity in the rabbit and chicken retina. NPY affected the release of [3H]-glycine, [3H]-dopamine, [3H]-5-hydroxytryptamine, and [3H]-choline chloride-derived radioactivity in rabbit retina and of [3H]-GABA, [3H]-5-hydroxytryptamine and [3H]-choline chloride-derived radioactivity in chicken retina in an energy requiring, NA+K(+)-ATPase dependent and calcium dependent manner. Certain related peptides, APP (= avian pancreatic polypeptide), BPP (= bovine pancreatic polypeptide), and PYY (= peptide YY), had variable and less pronounced effects. The results suggest a neurophysiological role in both chicken and rabbit retina for NPY or some related peptide.
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PMID:NPY-induced neurotransmitter release from the rabbit and chicken retina. 790 71

The main aim of the present study was to investigate the effects of local perfusion with the tridecapeptide neurotensin on extracellular GABA and dopamine levels in the nucleus accumbens of the halothane-anaesthetized rat, using in vivo microdialysis. In an initial set of characterization studies we examined the Na+ dependence of neurotransmitter release by local perfusion with ouabain, veratridine and tetrodotoxin. Local perfusion with the Na+ ATPase inhibitor ouabain (10 microM) or the Na+ channel agonist veratridine (20 microM) perfused into the nucleus accumbens increased both extracellular GABA and dopamine levels. The Na+ channel antagonist tetrodotoxin (1 microM) consistently decreased (24% of basal) dopamine levels, while even at 10 microM it did not affect GABA. However, tetrodotoxin (10 microM) abolished the veratridine-induced increase in both GABA and dopamine, demonstrating that Na(+)-dependent neuronal activity is involved in this release mechanism. In a second set of experiments a hypothesis for a functional link between neurotensin, dopamine and GABA in the medial nucleus accumbens was tested. Towards this aim, the effects of local perfusion with a high 1 microM concentration of neurotensin into the nucleus accumbens increased both GABA (210% of basal value) and dopamine (145% of basal) release. However, a low (10 nM) concentration of neurotensin again increased GABA release (160% of basal), but decreased that of dopamine (75% of basal value). Furthermore, the local perfusion with the GABAA receptor antagonist bicuculline abolished the neurotensin (10 nM) induced inhibition of dopamine release without affecting the increase in GABA release. These findings suggest that neurotensin modulates both GABA and dopamine neurotransmission in the nucleus accumbens.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Facilitation of GABA release by neurotensin is associated with a reduction of dopamine release in rat nucleus accumbens. 793 92

The effect of an aqueous extract obtained from the roots of Valeriana officinalis was investigated on the uptake and release of GABA in synaptosomes isolated from rat brain cortex. Aqueous extract of valerian inhibited the uptake and stimulated the release of [3H]GABA, either in the absence or in the presence of K+ depolarization. The release was Na(+)-dependent and independent of the presence of Ca2+ in the external medium. It is concluded that valerian extract releases [3H]GABA by reversal of the GABA carrier, which is Na(+)-dependent and Ca(2+)-independent. This increase in [3H]GABA release appears to be independent from Na(+)-K(+)-ATPase activity and the membrane potential.
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PMID:Synaptosomal GABA release as influenced by valerian root extract--involvement of the GABA carrier. 797 30

Extract of the ichthyotoxic marine alga Prymnesium patelliferum has been shown to have several different effects on the transport of neurotransmitters across nerve membranes. It inhibits the sodium dependent uptake of L-glutamate and GABA and enhances the calcium-dependent release of acetylcholine. We have therefore investigated the effects of a purified toxic extract of P. patelliferum on some membrane properties using rat brain synaptosomes. We found that under conditions where the algal extract inhibited the uptake of L-glutamate, it increased the intracellular concentrations of Na+ and Ca2+, stimulated efflux of K+ determined as 86Rb efflux, and depolarized the synaptosomal membrane. There was no effect on Na+/K(+)-ATPase or ouabain-insensitive ATPase activities. Further, there was no leakage of the cytosolic marker LDH, indicating that the various effects of the algal extract were not due to nonspecific leakage or lysis of the synaptosomes. The rise in the cytosolic concentration of free Ca2+ induced by the algal extract was dependent on extracellular Ca2+, and was inhibited by flunarizine (1-100 microM) but not by the Ca2+ channel blockers omega-conotoxin GVIA (1 microM), diltiazem (100 microM), nifedipine (100 microM) or verapamil (100-500 microM). The increase in Na+ influx induced by the algal extract was insensitive to tetrodotoxin (3 microM) and procaine (100 microM), whereas both the Na+ influx and the membrane depolarization were inhibited by flunarizine (1-100 microM). The increase in K+ efflux was insensitive to flunarizine (5-100 microM). From these results it appears that the toxic extract of P. patelliferum increases the permeability of synaptosomes to Ca2+, Na+ and K+ and that these effects may be responsible for the plasma membrane depolarization and the disturbance of the neurotransmitter transport processes.
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PMID:The effects of a purified toxic extract of Prymnesium patelliferum on transport of ions through the plasma membrane of synaptosomes. 853 41

Transient changes in extracellular potassium concentration ([K+]o) and field potentials were evoked by 4-aminopyridine (4-AP; 50-100 microM) and recorded with ion-selective microelectrodes in CA1b, CA3b and dentate sectors of adult rat hippocampal slices. Long-lasting field potentials recurred at a frequency of approximately 1/60 s (0.016 +/- 0.003 Hz) in association with increases in [K+]o which were largest and most sustained in the dendritic regions where afferent fibers terminate (dentate > CA1 > CA3) and in the hilus. In stratum radiatum of CA1 or stratum moleculare of the dentate these fields had a peak amplitude of 1.4 +/- 0.29 mV, duration 8.3 +/- 1.6 s, and were accompanied by increases in [K+]o of 1.8 +/- 0.22 mM that lasted 32 +/- 5.5 s (n = 17 slices). Interictal epilentiform potentials, which were brief (< 0.2 s) and more frequent at approximately 1/3 s (0.30 +/- 0.02Hz) were also present in CA1, CA3 and the hilus and associated with small increases in [K+]o (< or = 0.5 mM, duration < or = 2 s). Interictal activity was blocked by 6-cyano-7-nitroquinoxalone-2,3-dione (CNQX; 5-20 microM); the slow, less frequent potentials were resistant to both CNQX and DL-2-amino-5-phosphonovaleric acid (APV; 50 microM) and reversibly blocked (or attenuated by approximately 80%) by bicuculline methiodide (BMI) (25-100 microM). The BMI-sensitive potentials were also abolished by baclofen (100 microM), an effect which was reversed by 2-OH-saclofen (100 microM). Focal application of KCI or GABA in the absence of 4-AP evoked long-lasting field and [K+]o potentials which were similar to those evoked by 4-AP but more sustained. The proportional relationship between the amplitudes of field and K+ potentials with GABA closely resembled that observed for 4-AP; in contrast the slope of KC1-evoked responses was lower. Our results demonstrate that in the adult rat hippocampus 4-AP induces in many different regions accumulations of [K+]o in synchrony with the long-lasting field potentials, which are known to correspond to an intracellular long-lasting depolarization of the pyramidal cells. These changes are smaller than those which occur in the immature rat hippocampus--which may be related to differences in Na-K-ATPase and susceptibility to seizures. These events involve the activation of GABAA receptors, are under the modulatory control of GABAB receptors, and likely arise from the activity of GABAergic interneuron and/or afferent terminals. The long-lasting field potentials appear to reflect mainly the direct depolarizing actions of GABA and to much more limited extent the associated accumulation of [K+]o.
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PMID:Extracellular K+ accumulations and synchronous GABA-mediated potentials evoked by 4-aminopyridine in the adult rat hippocampus. 874 Feb 10


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