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排序方式: 共有94条查询结果,搜索用时 15 毫秒
1.
Maria-Dolores Miñana Vicente Felipo Ruth Wallace Santiago Grisolía 《Journal of neurochemistry》1988,51(6):1839-1842
Ingestion of large amounts of ammonium increases markedly the content of tubulin in brain. The effect on tubulin induction of ammonium ingestion for up to 100 days was investigated. Brain tubulin content showed a rapid initial increase (28%) at 2 days and reached 50% after 100 days on the diet. To discern if ammonia, the increase in urea synthesis, or both was responsible for tubulin induction, rats were maintained at several levels of uremia (by administering diets containing 0 to 80% protein) or in hyperammonemia (by urease treatment). Only ammonium administration in the diet and urease injection induced tubulin in brain. Tubulin was quantified in three different brain regions. There was a regional selectivity of tubulin induction by ammonia in rat brain. Whereas the cerebellum remained unaltered, the paleencephalon showed the highest increase, and the cerebral cortex exhibited only a modest increase. 相似文献
2.
Rats were fed a diet containing ammonium for up to 6 months. High ammonia levels were attained in brain. The amount of polymerized tubulin in microtubules increased, while the amount of free tubulin remained unchanged. Polymerization of tubulin from brain of ammonium fed rats (30 min, 37°C) was approximately 60% of control. Depolymerization of the microtubules was also affected and took approximately 3 times longer than in controls. These results indicate that both assembly and disassembly of tubulin in brain are impaired by high ammonia levels. Interestingly, the amount of microtubule-associated proteins was not affected. 相似文献
3.
Synaptosomes were isolated from cerebrums of rats fed standard (20% protein) or protein-free diets for 30 days. Arrhenius plots of their (Na+/K+)ATPase activities revealed a transition temperature of 25.5°C for control rats and 23.4°C for rats on protein-free diet, indicating that the latter increases synaptosomal membrane fluidity. The only change observed in the composition of the synaptosomal membranes was a 26% decrease of sialic acid. In synaptosomes from rats on protein-free diet the uptake of tyrosine was slightly reduced while that of glutamate was not affected. However, the exit of glutamate was reduced. 相似文献
4.
Carlos Hermenegildo Goizane Marcaida Carmina Montoliu Santiago Grisolía María-Dolores Miñana Vicente Felipo 《Neurochemical research》1996,21(10):1237-1244
We proposed that acute ammonia toxicity is mediated by activation of NMDA receptors. To confirm this hypothesis we have tested
whether different NMDA receptor antagonists, acting on different sites of NMDA receptors, prevent death of mice induced by
injection of 14 mmol/Kg of ammonium acetate, a dose that induces death of 95% of mice. MK-801, phencyclidine and ketamine,
which block the ion channel of NMDA receptors, prevent death of at least 75% of mice. CPP, AP-5, CGS 19755, and CGP 40116,
competitive antagonists acting on the binding site for NMDA, also prevent death of at least 75% of mice. Butanol, ethanol
and methanol which block NMDA receptors, also prevent death of mice. There is an excellent correlation between the EC50 for preventing ammonia-induced death and the IC50 for inhibiting NMDA-induced currents. Acute ammonia toxicity is not prevented by antagonists of kainate/AMPA receptors, of
muscarinic or nicotinic acetylcholine receptors or of GABA receptors. Inhibitors of nitric oxide synthase afford partial protection
against ammonia toxicity while inhibitors of calcineurin, of glutamine synthetase or antioxidants did not prevent ammonia-induced
death of mice. These results strongly support the idea that acute ammonia toxicity is mediated by activation of NMDA receptors. 相似文献
5.
Elena Kosenko Yuri Kaminsky Eugenio Grau María-Dolores Miñana Goizane Marcaida Santiago Grisolía Vicente Felipo 《Journal of neurochemistry》1994,63(6):2172-2178
Abstract: Injection of large doses of ammonia into rats leads to depletion of brain ATP. However, the molecular mechanism leading to ATP depletion is not clear. The aim of the present work was to assess whether ammonium-induced depletion of ATP is mediated by activation of the NMDA receptor. It is shown that injection of MK-801, an antagonist of the NMDA receptor, prevented ammonia-induced ATP depletion but did not prevent changes in glutamine, glutamate, glycogen, glucose, and ketone bodies. Ammonia injection increased Na+ ,K+ -ATPase activity by 76%. This increase was also prevented by previous injection of MK-801. The molecular mechanism leading to activation of the ATPase was further studied. Na+ ,K+ -ATPase activity in samples from ammonia-injected rats was normalized by "in vitro" incubation with phorbol 12-myristate 13-acetate, an activator of protein kinase C. The results obtained suggest that ammonia-induced ATP depletion is mediated by activation of the NMDA receptor, which results in decreased protein kinase C-mediated phosphorylation of Na+ ,K+ -ATPase and, therefore, increased activity of the ATPase and increased consumption of ATP. 相似文献
6.
Ammonium Injection Induces an N-Methyl-d-Aspartate Receptor-Mediated Proteolysis of the Microtubule-Associated Protein MAP-2 总被引:1,自引:0,他引:1
Vicente Felipo Eugenio Grau María-Dolores Miñana Santiago Grisolía 《Journal of neurochemistry》1993,60(5):1626-1630
Abstract: We have shown previously that chronic hyperammonemia increases, in brain, the polymerization of microtubules that is regulated mainly by the level and state of phosphorylation of microtubule-associated protein 2 (MAP-2). Activation of the N -methyl- d -aspartate (NMDA) receptor dephosphorylates MAP-2. Because we have found that acute ammonia toxicity is mediated by the NMDA receptor, we have tested the effect of high ammonia levels on MAP-2 in brain. Microtubules isolated from rats injected intraperitoneally with 6 mmol/kg ammonium acetate showed a marked decrease of MAP-2. Also, the amount of MAP-2 in brain homogenates, determined by immunoblotting. was markedly reduced, presumably by proteolysis. The content of MAP-2 was decreased by ∼75% 1-2 h after ammonium injection and returned to normal values after 4 h. Proteolysis of MAP-2 was prevented completely by injection of 2 mg/kg MK-801, a specific antagonist of the NMDA receptor, suggesting that proteolysis is mediated by activation of this receptor. l -Carnitine, which protects rats against ammonia toxicity, also prevented MAP-2 degradation. Because activation of the NMDA receptor increases [Ca2+ ]i , we determined whether rat brain contains a Ca2+ -dependent protease that selectively degrades MAP-2. We show that there is a cytosolic Ca2+ -dependent protease that degrades MAP-2, but no other brain proteins. The protease has been identified tentatively as calpain I, for it is inhibited by a specific inhibitor of this protease. Our results suggest that ammonium injection activates the NMDA receptor, leading to an increase in [Ca2+ ]i , which activates calpain I. This, in turn, selectively degrades MAP-2. Possible implications in chronic hyperammonemic states and in the mechanism of ammonia toxicity are discussed. 相似文献
7.
Ammonium ingestion prevents depletion of hepatic energy metabolites induced by acute ammonium intoxication 总被引:1,自引:0,他引:1
E Kosenko V Felipo M D Mi?ana E Grau S Grisolía 《Archives of biochemistry and biophysics》1991,290(2):484-488
Ingestion of an ammonium containing diet produces hyperammonemia and protects rats against acute ammonium intoxication. Acute ammonium toxicity has been attributed to the depletion of energy metabolite intermediates. We show here that hyperammonemia affords considerable protection against depletion of hepatic energy metabolites evoked by ammonium acetate injection. In control rats there were marked decreases in the content of acetoacetate, beta-hydroxybutyrate, ATP, 2-oxoglutarate, lactate, and pyruvate while phosphoenolpyruvate increased markedly. In hyperammonemic rats beta-hydroxybutyrate, ATP, 2-oxoglutarate, and lactate were not significantly affected while pyruvate increased markedly and phosphoenolpyruvate slightly. These results suggest that in controls the activity of pyruvate kinase is inhibited after ammonium injection while in hyperammonemic rats it is not inhibited. The content of alanine (an inhibitor of pyruvate kinase) reached 2.8 mumol/g in controls and 1.6 mumol/g in hyperammonemic rats, 15 min after ammonium injection. This could explain the different effects of ammonium injection on control and hyperammonemic rats. 相似文献
8.
Corbalán R Hernández-Viadel M Llansola M Montoliu C Felipo V 《Neurochemistry international》2002,41(2-3):103-108
There is substantial evidence that hyperammonemia is one of the main factors contributing to the neurological alterations found in hepatic encephalopathy. The mechanisms by which chronic moderate hyperammonemia affects brain function involves alterations in neurotransmission at different steps. This article reviews the effects of hyperammonemia on phosphorylation of key brain proteins involved in neurotransmission (the microtubule-associated protein (MAP-2), Na+/K+-ATPase and NMDA receptors). The physiological function of these proteins is modulated by phosphorylation and its altered phosphorylation in hyperammonemia may contribute to impairment of neurotransmission. The effects of chronic hyperammonemia on signal transduction pathways associated to glutamate receptors, such as the glutamate-nitric oxide (NO)-cGMP pathway, are also reviewed. The possible contribution of the impairment of this pathway in brain in vivo to the neurological alterations present in patients with hepatic encephalopathy is discussed. 相似文献
9.
Magnetic resonance analysis of the effects of acute ammonia intoxication on rat brain. Role of NMDA receptors 总被引:2,自引:0,他引:2
Cauli O López-Larrubia P Rodrigues TB Cerdán S Felipo V 《Journal of neurochemistry》2007,103(4):1334-1343
Acute ammonia intoxication leads to rapid death, which is prevented by blocking N -methyl- d -aspartate (NMDA) receptors. The subsequent mechanisms leading to death remain unclear. Brain edema seems an important step. The aim of this work was to study the effects of acute ammonia intoxication on different cerebral parameters in vivo using magnetic resonance and to assess which effects are mediated by NMDA receptors activation. To assess edema induction, we injected rats with ammonium acetate and measured apparent diffusion coefficient (ADC) in 16 brain areas. We also analyzed the effects on T1, T2, and T2* maps and whether these effects are prevented by blocking NMDA receptors. The effects of acute ammonia intoxication are different in different brain areas. T1 relaxation time is reduced in eight areas. T2 relaxation time is reduced only in ventral thalamus and globus pallidus. ADC values increased in hippocampus, caudate-putamen, substantia nigra and cerebellar cortex, reflecting vasogenic edema. ADC decreased in hypothalamus, reflecting cytotoxic edema. Myo-inositol increased in cerebellum and substantia nigra, reflecting vasogenic edema. N -acetyl-aspartate decreased in cerebellum, reflecting neuronal damage. Changes in N -acetyl-aspartate, T1 and T2 are prevented by blocking NMDA receptors with MK-801 while changes in ADC or myo-inositol (induction of edema) are not. 相似文献
10.
Sancho-Alonso María Taoro-Gonzalez Lucas Cabrera-Pastor Andrea Felipo Vicente Teruel-Martí Vicent 《Neurochemical research》2022,47(7):2016-2031
Neurochemical Research - Chronic hyperammonemia alters membrane expression of AMPA and NMDA receptors subunits in hippocampus leading to impaired memory and learning. Increasing extracellular cGMP... 相似文献