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)

1. We have used in situ hybridization techniques to determine the mRNA for (Na + K)ATPase in 20 brain regions from control rats and rats treated with high doses of deoxycorticosterone (DOC). 2. DOC-treated rats developed a salt appetite following the second hormone administration on alternate days and were used after the fourth DOC administration. 3. DOC treatment did not change the number of silver grains/cell deposited in cells from Ca1, CA2, CA3, and CA4 hippocampal subfields, dentate gyrus, cerebral cortex, medial preoptic area (POA), substantia nigra, and periventricular gray matter. 4. Nonsignificant reductions were detected in lateral POA, medial and lateral septum, caudate-putamen, and three amygdaloid nuclei (cortical, basolateral, and central) from DOC-treated rats. 5. Significant reductions were obtained, after DOC administration, in arcuate and ventromedial hypothalamic nuclei and medial and lateral amygdala. 6. The results suggested that regulation of the beta-subunit mRNA of (Na + K)-ATPase may be related to the central actions of mineralocorticoids in the control of salt intake.
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PMID:Effects of deoxycorticosterone treatment on beta-subunit mRNA for (Na + K)ATPase in brain regions determined by in situ hybridization. 165 Nov 64

Intrahippocampal injection of 1 nmol ouabain, a sodium/potassium (Na+,K(+)-)ATPase inhibitor, produced a necrotic lesion within 4 days, characterised by a massive invasion by foaming macrophages. A lower dose of ouabain (0.1 nmol) produced a more discrete lesion of all groups of neuronal perikarya in the hippocampus, with only a minimal degree of glial infiltration. The neuronal perikaryal death produced in the subicular, CA1 and CA2 regions was only partially decreased by intraperitoneal injections of the anticonvulsants diazepam and MK-801; these drugs were without effect in the CA3 or hilar interneuronal regions. At neither dose of ouabain was there any indication of neuronal loss in brain regions outside the hippocampus, typically produced by prolonged seizure activity. It is suggested that ouabain has a two-fold action, a release of toxic acidic amino acids and a prolonged depolarization of neurons leading to osmolysis or calcium necrosis.
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PMID:The neurotoxicity of ouabain, a sodium-potassium ATPase inhibitor, in the rat hippocampus. 170 75

The adult rat hippocampus was investigated by light microscopic immunocytochemistry for (Na+ + K+)-ATPase. In the CA1, CA2 and CA3 hippocampal regions, dense immunostaining for (Na+ + K+)-ATPase, exhibiting a punctate appearance, was demonstrated along the soma plasmalemma of hippocampal pyramidal cells in the stratum pyramidale, thus outlining these cells distinctly, and along dendrites extending into the stratum radiatum. (Na+ + K+)-ATPase immunostaining was dense in the neuropil of the strata oriens and radiatum of the rat hippocampus, but much lighter in the corpus callosum. Immunostaining at the periphery of pyramidal cell soma may be associated with the plexus formed by axon terminals of hippocampal basket cells.
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PMID:Immunocytochemical localization of (Na+ + K+)-ATPase in the rat hippocampus. 253 78

Slices from rat CA3 hippocampal area show a 30% decrement in ATPase activity after 35 min of 'in vitro' incubation. Such a drop is accompanied by an alteration of mitochondrial ultrastructure. However, if rats are treated daily with GM1 ganglioside (10 mg/kg during 3 days) both phenomena are fully prevented. These results would suggest a protective effect of gangliosides onto membrane structures under stress conditions.
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PMID:In vivo treatment with GM1 prevents the rapid decay of ATPase activities and mitochondrial damage in hippocampal slices. 293 28

Regional differences in Na,K-ATPase activity, and development of Na,K-ATPase activity were examined in rabbit hippocampus using a histochemical marker of enzyme activity. Stratum lucidum of CA3/CA2, corresponding to the mossy fiber terminal field, showed high Na,K-ATPase activity compared to stratum radiatum of CA1. A significant increase in Na,K-ATPase activity was found between 8 and 15 days postnatal. Tissues with limited Na,K-ATPase activity (immature hippocampus, the mature CA1 region) appear particularly prone to seizure-like abnormalities, perhaps reflecting an inability to regulate extracellular potassium.
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PMID:Developmental and regional differences in the localization of Na,K-ATPase activity in the rabbit hippocampus. 299 29

Using the in vitro hippocampal slice preparation, we studied the electrophysiological properties of pyramidal cells in tissue that was 'preincubated' (2-6 h in a large, static volume of oxygenated bathing medium) before being placed in an interface chamber for study. Striking differences were found in 'preincubated' vs 'non-preincubated' CA3 cells. The preincubated cells had more negative resting potentials, higher input resistance, lower threshold for stimulus-evoked burst discharge and larger hyperpolarizing afterpotentials. Cells in the preincubated CA3 region were also more likely to show spontaneous synchronized burst discharge, but were relatively resistant to hypoxia-induced spreading depression. CA1 cells were less dramatically affected by preincubation, showing little difference from their non-preincubated counterparts. Possible mechanisms involved in the CA3 preincubation effect, including glial buffering alterations and changes in Na+, K+-ATPase activity, are discussed.
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PMID:Effects of tissue preincubation and hypoxia on CA3 hippocampal neurons in the in vitro slice preparation. 301 Nov 93

Ca2+ transport mediated by the plasma membrane Ca(2+)-ATPase (PMCA) serves an important role in regulation of cytosolic-free Ca2+ in a variety of cells. Isoform PMCA4 mRNA distribution in rat brain was studied by in situ hybridization using 33P-labeled antisense oligodeoxynucleotide probes. Very high levels of hybridization were found in piriform cortex with high levels in amygdaloid nucleus and laminae 2 and 6 of cerebral cortex. Significantly lower levels were found in hypothalamic nuclei and very low or undetectable levels were found in cerebellum, habenula, olfactory bulb, thalamus, choroid plexus of the third and fourth ventricles and in CA1 and CA3 cells of the hippocampus. These results suggest that PMCA4 is not a housekeeping form of the Ca(2+)-ATPase.
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PMID:The plasma membrane Ca(2+)-ATPase mRNA isoform PMCA 4 is expressed at high levels in neurons of rat piriform cortex and neocortex. 782 8

The axon initial segment of cortical principal neurones contains an organelle consisting of two to four stacks of flat, membrane-delineated cisternae alternating with electron-dense, fibrillar material. These cisternal organelles are situated predominantly close to the synaptic junctions of GABAergic axo-axonic cell terminals. To examine the possibility that the cisternal organelle is involved in Ca2+ sequestration, we tested for the presence of Ca(2+)-ATPase in the cisternal organelles of pyramidal cell axons in the CA1 and CA3 regions of the hippocampus. Electron microscopic immunocytochemistry using antibodies to muscle sarcoplasmic reticulum ATPase revealed immunoreactivity associated with cisternal organelle membranes. The localisation of Ca(2+)-ATPase in cisternal organelles was also confirmed by enzyme cytochemistry, which produced reaction product in the lumen of the cisternae. These experiments provide evidence for the presence of a Ca2+ pump in the cisternal organelle membrane, which may play a role in the sequestration and release of Ca2+. Cisternal organelles are very closely aligned to the axolemma and the outermost cisternal membrane is connected to the plasma membrane by periodic electron-dense bridges as detected in electron micrographs. It is suggested that the interface acts as a voltage sensor, releasing Ca2+ from cisternal organelles upon depolarisation of the axon initial segment, in a manner similar to the sarcoplasmic reticulum of skeletal muscle. The increase in intra-axonal Ca2+ may regulate the GABAA receptors associated with the axo-axonic cell synapses, and could affect the excitability of pyramidal cells.
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PMID:The cisternal organelle as a Ca(2+)-storing compartment associated with GABAergic synapses in the axon initial segment of hippocampal pyramidal neurones. 784 10

The effects of intraventricular injection of kainic acid on the Na,K-ATPase (Na,K pump) were examined in discrete pyramidal cell regions of rat hippocampus. [3H]Ouabain binding was used to quantitate Na,K-ATPase catalytic subunits and in situ hybridization was used to determine Na,K-ATPase mRNA levels. Large decreases were found in both [3H]ouabain binding and alpha 3 isoform mRNA in hippocampus areas, especially in the CA3 pyramidal cell layer, which sustains heavy cell losses as a result of bilateral, intraventricular injection of kainic acid. Substantial decreases in the high affinity component of ouabain binding and in the alpha 3 isoform mRNA (but not isoforms for other Na,K-ATPase subunits) were also observed in the CA1 region of hippocampus, an area preserved in this model. High affinity [3H]ouabain binding was decreased 25-33% in the stratum pyramidale and stratum radiatum after treatment with kainic acid, and alpha 3 mRNA was decreased by 26-50%. To further characterize the decrease in alpha 3 mRNA, animals were killed at 1, 2, and 3 weeks after injection of kainate and results show a large decrease in alpha 3 mRNA only at 2 weeks recovery time. While the pathology underlying temporal lobe epilepsy is unclear, changes in the Na,K-ATPase may be involved in abnormal firing characteristics of cells in epileptic tissue.
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PMID:Na,K-ATPase is decreased in hippocampus of kainate-lesioned rats. 801 44

In the brain, corticosteroids bind to intracellular glucocorticoid (GR) and mineralocorticoid (MR) receptors, affecting target gene transcription, and thereby altering neuronal function, including electrophysiological activity. The hippocampus very highly expresses both MR and GR; however, MR-regulated hippocampal transcripts have not yet been described. We investigated the effects of adrenalectomy +/- glucocorticoid or mineralocorticoid replacement on expression of mRNAs encoding alpha-subunit isoforms of Na(+)-K(+)-adenosinetriphosphatase, a critical transmembrane ion gradient-regulating enzyme. Aldosterone significantly increased alpha 3-subunit mRNA expression in dentate gyrus granule cells (62% increase compared with adrenalectomy) and in CA1 and CA4 hippocampal neurons (37 and 38%), but not in CA2, CA3, parietal cortex neurons, or glia. This effect was not reproduced by dexamethasone, and none of the corticosteroid manipulations altered alpha 1- or alpha 2-subunit mRNA expression at any site examined. Aldosterone-mediated upregulation of hippocampal alpha 3-subunit mRNA expression may underlie, at least in part, the specific actions of MR ligands on hippocampal function. The observation that aldosterone differentially affects alpha 3-isoform mRNA expression in distinct neuronal populations, associated with the established aldosterone modulations of alpha 1-isoform mRNA in epithelial cells, supports the presence of cell-specific factors that regulate MR-mediated transcriptional activity.
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PMID:Aldosterone selectively increases Na(+)-K(+)-ATPase alpha 3-subunit mRNA expression in rat hippocampus. 814 Dec 56


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