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)

Potassium-stimulated p-nitrophenylphosphatase (K+-pNPPase) activity was investigated in rat somatosensory cortex where 64-88% of enzymatic activity survived 5-10 min of fixation with 3% formaldehyde in 0.1 M cacodylate buffer, pH 7.4. Potassium-stimulated activity was inhibited by 1-10 mM ouabain. Levamisole (1.7 mM) inhibited brain alkaline phosphatase activity, facilitating the detection of K+-pNPPase activity. Strontium (10-20 mM) inhibited enzymatic activity by 38-75%. In parallel histochemical studies reaction product was found in strata, with cortical layers 2, 3, 4 and the outer portion of 5 containing the heaviest deposits. Highly reactive, vertically oriented, large diameter fibers were seen as groups between the outer portion of layer 5 and the pail surface. These fibers apparently arborize in the superficial layers. Smaller fibers were also positive and were oriented in various planes. The highest density of smaller, positive fibers occurred in layers 2 through 5. All positive fibers appeared to be axons or dendrites. Reaction product was not heavily concentrated in neuron perikarya or in glial elements. Sections did not contain reaction product when incubated in media lacking K+ or containing ouabain. The convergence of data from parallel histochemical and biochemical approaches supports the conclusion that the reactivity localized in the cerebral cortex represented the site of K+-pNPPase, a known component of the Na+,K+-adenosine triphosphatase complex. Neuronal processes demonstrated the highest enzymatic activity and may be most important in the active transport of Na+ and K+ in somatosensory cortex.
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PMID:Histochemical localization of potassium-stimulated P-nitrophenylphosphatase activity in the somatosensory cortex of the rat. 18 89

The vasoactive peptide endothelin-1 (ET-1) which is present in high concentrations in the colon, causes concentration-dependent electrogenic Cl- secretion in rabbit descending colon. This effect is half-maximal at 0.11 mumol/l. Like other secretagogues, ET-1 also stimulates K+ secretion. The secretory effect of ET-1 is associated with increased release of prostaglandin E2 from the serosal surface of the mucosa. ET-1-induced Cl- secretion is completely inhibited by the loop diuretic bumetanide and by indomethacin and quinacrine, inhibitors of prostaglandin synthesis. Neuronal mechanisms do not seem to be involved, as tetrodotoxin did not affect the secretory response to ET-1 significantly. On the other hand, neither the catalytic activity nor the transport function of the Na+/K(+)-ATPase of rabbit colon epithelium is affected by endothelin-1 (ET-1) in concentrations up to 10 mumol/l. It is concluded that ET-1 causes Cl- and K+ secretion by stimulating phospholipase A2 and release of prostaglandins, whereas Na+ transport is not altered.
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PMID:Endothelin-1 stimulates chloride and potassium secretion in rabbit descending colon. 132 45

Vanadium in the 4+ (vanadyl-ion) and 5+ (vanadate-ion) oxidation state stimulates furosemide-sensitive electrogenic Cl- secretion in isolated epithelia of rabbit descending colon. This effect is associated with an increased release of prostaglandin E2 from the tissue. Inhibitors of phospholipase A2 or cyclooxygenase abolish both vanadium-induced release of prostaglandin E2 and Cl- secretion. Neuronal mechanisms are not likely to be involved, as tetrodotoxin does not affect the vanadate induced Cl- secretion. Although vanadate is known to inhibit Na+,K(+)-ATPase activity, no inhibition of active Na+ transport was observed in intact colonic epithelia suggesting a rapid intracellular reduction of vanadate ions to vanadyl ions which have no inhibitory effect on the Na+,K(+)-ATPase. The present findings therefore indicate that vanadate stimulated colonic Cl- secretion involves intracellular conversion of vanadate to vanadyl and release of prostaglandin E2.
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PMID:Vanadium-induced Cl(-)-secretion in rabbit descending colon is mediated by prostaglandins. 161 17

Neuronal death generally involves, directly or indirectly, free radical attack and peroxidation. Targets are nucleic acids, proteins, the cytoskeleton, the extracellular matrix and especially membrane polyunsaturated fatty acids. a) One example for the fundamental role of fatty acids. Dietary fatty acids, and more particularly essential polyunsaturated fatty acids, have a direct influence on the composition of cerebral membranes, and hence on their functioning. Each of the two series of polyunsaturated fatty acids plays a particular role. In animals, a deficiency in linolenic acid causes serious perturbations in the nervous system. In fact, feeding animals with oils that have a low n-3 content leads to severe abnormalities in the composition of membranes, both of the brain and other organs. The rate of recovery from these anomalies is extremely slow in the brain, but rapid in the liver. Compared to certain other organs, the nervous system is neither protected against deficiency nor has it priority in the satisfaction if its needs. A decrease in acids of the linolenic series in the membranes results in a 40% reduction of Na-K-ATPase in nerve endings and a 20% reduction in 5'-nucleotidase. It also leads to anomalies in the electroretinogram which disappear with age. This deficiency in linolenic acid has little effect on motor function and disturbes activity and emotivity only slightly, but it seriously affects learning tasks. The presence of linolenic acid in the diet confers greater resistance to certain neurotoxic substances (triethyl lead, for example). Fatty acids essential for the brain could be those with very long chains. They are probably synthesized in the liver from linolenic and linoleic acids. They can also be supplied directly by food. However, if the diet contains a large proportion of very long chain fatty acids (fish oils), the lipid composition of all organs, including the brain, is altered. During the period of brain development there is a linear relation between the polyunsaturated fatty acid content of the brain and that of the diet. The requirement in linolenic acid is 200 mg/100 g of diet (0.4% of calories). That of linoleic acid is 1,200 mg/100 g of diet (2.4% of calories). b) Peroxidation of polyunsaturated fatty acids. Arachidonic acid is released by lysis of phospholipids (it is directly toxic), its peroxidized derivatives are extremely toxic. Peroxidation of membrane lipids alters enzymatic activity, the relationship between receptor and ligand, transport, and the symmetry of the lipid bilayer.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Free radicals, polyunsaturated fatty acids, cell death, brain aging]. 284 29

Neuronal membrane enzyme activities were determined in naive and ethanol-treated (30 min after 2 g/kg) male and female rats of lines developed for more (ANT) and less (AT) ethanol-induced motor impairment. Ethanol did not affect acetylcholinesterase, (Na+K)-ATPase or 5'-nucleotidase activities, but adenylate cyclase activities were lowered in both cerebellum and cerebrum. Cerebral acetylcholinesterase activities were higher in ANT than AT rats. No consistent line difference was observed regarding (Na+K)-ATPase activities. Slightly higher cerebellar 5'-nucleotidase activities were found in the ANT line. Cerebellar adenylate cyclase levels were substantially higher in the AT line. No line differences were displayed in the activation of adenylate cyclase activity by dopamine or norepinephrine. It is concluded that ethanol in vivo may inhibit neuronal adenylate cyclase activity and that cerebellar phosphorylation may be a regulator of motor impairment. Cholinergic mechanisms may also be connected to the ethanol-induced motor impairment.
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PMID:Neuronal membrane enzymes in rat lines selected for differential motor impairment by ethanol. 301 92

Studies were performed to identify the response characteristics of nucleus of the solitary tract neurons receiving afferent projections from the hepatic branch of the vagus nerve. Thirty Sprague-Dawley rats under pentobarbital anesthesia had catheters placed in the ileocolic vein and the inferior vena cava. Neuronal recordings were made in the left medial nucleus of the solitary tract (NST), in the area where hepatic vagal fibers terminate. Sixteen NST cells were identified that responded selectively to the portal infusion of water or hypertonic saline. Two patterns of response were seen: 1) 12 neurons were persistently stimulated by portal hypertonic saline and persistently inhibited by portal water, and 2) four neurons were either transiently excited (n = 3) or transiently inhibited (n = 1) by portal hypertonic saline with no water effect. All units recorded responded to changes of 1% or less in portal blood sodium concentration. Hypertonic mannitol was an ineffective stimulus but choline chloride was as effective as sodium chloride. This suggests that the hepatic receptors utilize an Na+-K+-ATPase electrogenic pump in the transduction process.
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PMID:Rat brainstem neurons responsive to changes in portal blood sodium concentration. 609 3

Injection of ouabain, a potent and selective inhibitor of Na+/K+ ATPase, into the rat striatum and substantia nigra caused a selective neuronal loss in up to 70% of the lesioned area. However, there was a glial cell/macrophage proliferation in the core of the lesion. Neuronal loss was demonstrated by staining in vivo with Trypan Blue, a marker for dead cells. Cholinesterase staining was also lost, but in the striatum this was revealed only after pre-existing enzyme was irreversibly inhibited in vivo.
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PMID:The sodium-potassium ATPase inhibitor ouabain is neurotoxic in the rat substantia nigra and striatum. 754 Jul 38

The amyloid beta-peptide (A beta) that accumulates as insoluble plaques in the brain in Alzheimer's disease can be directly neurotoxic and can increase neuronal vulnerability to excitotoxic insults. The mechanism of A beta toxicity is unclear but is believed to involve generation of reactive oxygen species (ROS) and loss of calcium homeostasis. We now report that exposure of cultured rat hippocampal neurons to A beta 1-40 or A beta 25-35 causes a selective reduction in Na+/K(+)-ATPase activity which precedes loss of calcium homeostasis and cell degeneration. Na+/K(+)-ATPase activity was reduced within 30 min of exposure to A beta 25-35 and declined to less than 40% of basal level by 3 hr. A beta did not impair other Mg(2+)-dependent ATPase activities or Na+/Ca2+ exchange. Experiments with ouabain, a specific inhibitor of the Na+/K(+)-ATPase, demonstrated that impairment of this enzyme was sufficient to induce an elevation of [Ca2+]i and neuronal injury. Impairment of Na+/K(+)-ATPase activity appeared to be causally involved in the elevation of [Ca2+]i and neurotoxicity since suppression of Na+ influx significantly reduced A beta- and ouabain-induced [Ca2+]i elevation and neuronal death. Neuronal degeneration induced by ouabain appeared to be of an apoptotic form as indicated by nuclear condensation and DNA fragmentation. The antioxidant free radical scavengers vitamin E and propylgallate significantly attenuated A beta-induced impairment of Na+/K(+)-ATPase activity, elevation of [Ca2+]i and neurotoxicity, suggesting a role for ROS. Finally, exposure of synaptosomes from postmortem human hippocampus to A beta resulted in a significant and specific reduction in Na+/K(+)-ATPase and Ca(2+)-ATPase activities, without affecting other Mg(2+)-dependent ATPase activities or Na+/Ca2+ exchange. These data suggest that impairment of ion-motive ATPases may play a role in the pathogenesis of neuronal injury in Alzheimer's disease.
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PMID:Amyloid beta-peptide impairs ion-motive ATPase activities: evidence for a role in loss of neuronal Ca2+ homeostasis and cell death. 766 6

Intracerebral microdialysis combined with a sensitive and specific radioimmunoassay was used to monitor the neuronal release of somatostatin (somatostatin-like immunoreactivity, SLI) in the dorsal hippocampus of freely moving rats. The sensitivity of the radioimmunoassay was optimized to detect < 1 fmol/ml. The basal concentration of SLI in 20-min dialysate fractions (5 microliters/min) collected 24 h after probe implantation was stable over at least 200 min. The spontaneous efflux dropped by 54 +/- 6.4% (p < 0.05) when Ca2+ was omitted and 1 mM EGTA added to the Krebs-Ringer solution and by 65.5 +/- 3.2% (p < 0.05) in the presence of 1 microM tetrodotoxin. Depolarizing concentrations of the Na+ channel opener veratridine (6.25, 25, 100 microM) induced 11 +/- 2 (p < 0.05), 17 +/- 2 (p < 0.05), and 21 +/- 5 (p < 0.01) fold increase in SLI concentration, respectively, during the first 20 min of perfusion. The effect of 100 microM veratridine was blocked by coperfusion with 5 microM tetrodotoxin (p < 0.01) and reduced by 79% (p < 0.01) in the virtual absence of Ca2+. Neuronal depolarization by 20 min of perfusion with Krebs-Ringer solution containing 25 and 50 mM KCl and proportionally lowered Na+ increased the dialysate SLI 4.4 +/- 1 (p < 0.05) and 17 +/- 3 (p < 0.01) fold baseline, respectively. Ten micromolar ouabain, a blocker of Na+,K(+)-ATPase, increased the dialysate SLI 15-fold baseline, on average (p < 0.05), during 80 min of perfusion. The results demonstrate the suitability of brain microdialysis for monitoring the neuronal release of SLI and for studying its role in synaptic transmission.
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PMID:Extracellular somatostatin measured by microdialysis in the hippocampus of freely moving rats: evidence for neuronal release. 809 81

Neuronal ATPases comprise a wide variety of enzymes which are not uniformly distributed in different membrane preparations. Since purified vesicle fractions have Mg2+/Ca(2+)-ATPase, the purpose of the present study was to know whether such enzyme activities have a preferential concentration in a synaptic vesicle fraction in order to be used as markers for these organelles. Resorting to a procedure developed in this Institute, we fractionated the rat cerebral cortex by differential centrifugation following osmotic shock of a crude mitochondrial fraction and separated a purified synaptic vesicle fraction over discontinuous sucrose gradients. Mg2+/Ca(2+)-ATPase activities and ultrastructural studies of isolated fractions were carried out. It was observed that similar specific activities for Mg2+/Ca(2+)-ATPases were found in all fractions studied which contain synaptic vesicles and/or membranes. Although the present results confirm the presence of Mg2+ and Ca(2+)-ATPase activities in synaptic vesicles preparations, they do not favor the contention that Mg2+/Ca(2+)-ATPase is a good marker for synaptic vesicles.
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PMID:Mg2+/Ca(2+)-ATPase activity is not enriched in synaptic vesicles isolated from rat cerebral cortex. 905 64


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