当前位置： SCI文献检索 > NEUROBIOLOGY OF DISEASE期刊下所有文献 > Neurons exposed to ammonia reproduce the differential alteration in nitric oxide modulation of guanylate cyclase in the cerebellum and cortex of patients with liver cirrhosis.

Neurons exposed to ammonia reproduce the differential alteration in nitric oxide modulation of guanylate cyclase in the cerebellum and cortex of patients with liver cirrhosis.

Abstract：

:The activation of soluble guanylate cyclase by nitric oxide is increased in the frontal cortex but is reduced in the cerebellum of patients who died with liver cirrhosis. The aims of this work were to assess whether hyperammonemia is responsible for the region-selective alterations in guanylate cyclase modulation in liver cirrhosis and to assess whether the alteration occurs in neurons or in astrocytes. The activation of guanylate cyclase by nitric oxide was lower in cerebellar neurons exposed to ammonia (1.5-fold) than in control neurons (3.3-fold). The activation of guanylate cyclase by nitric oxide was higher in cortical neurons exposed to ammonia (8.7-fold) than in control neurons (5.5-fold). The activation was not affected in cerebellar or cortical astrocytes. These findings indicate that hyperammonemia is responsible for the differential alterations in the modulation of soluble guanylate cyclase in cerebellum and cerebral cortex of cirrhotic patients. Moreover, the alterations occur specifically in neurons and not in astrocytes.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Rodrigo R,Erceg S,Felipo V

doi

10.1016/j.nbd.2004.12.001

keywords:

subject

Has Abstract

pub_date

2005-06-01 00:00:00

pages

150-61

issue

1-2

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(04)00288-8

journal_volume

19

pub_type

杂志文章

相关文献

NEUROBIOLOGY OF DISEASE文献大全
  • DLK-dependent signaling is important for somal but not axonal degeneration of retinal ganglion cells following axonal injury.

    abstract：:Injury to retinal ganglion cell (RGC) axons triggers rapid activation of Jun N-terminal kinase (JNK) signaling, a major prodeath pathway in injured RGCs. Of the multiple kinases that can activate JNK, dual leucine kinase (Dlk) is known to regulate both apoptosis and Wallerian degeneration triggered by axonal insult. H...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2014.05.015

    authors： Fernandes KA,Harder JM,John SW,Shrager P,Libby RT

    更新日期：2014-09-01 00:00:00

  • Restoring tactile and proprioceptive sensation through a brain interface.

    abstract：:Somatosensation plays a critical role in the dexterous manipulation of objects, in emotional communication, and in the embodiment of our limbs. For upper-limb neuroprostheses to be adopted by prospective users, prosthetic limbs will thus need to provide sensory information about the position of the limb in space and a...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2014.08.029

    authors： Tabot GA,Kim SS,Winberry JE,Bensmaia SJ

    更新日期：2015-11-01 00:00:00

  • Formoterol, a β2-adrenoreceptor agonist, induces mitochondrial biogenesis and promotes cognitive recovery after traumatic brain injury.

    abstract：:Traumatic brain injury (TBI) leads to acute necrosis at the site of injury followed by a sequence of secondary events lasting from hours to weeks and often years. Targeting mitochondrial impairment following TBI has shown improvements in brain mitochondrial bioenergetics and neuronal function. Recently formoterol, a h...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2020.104866

    authors： Vekaria HJ,Hubbard WB,Scholpa NE,Spry ML,Gooch JL,Prince SJ,Schnellmann RG,Sullivan PG

    更新日期：2020-07-01 00:00:00

  • Neuroprotective effects of the Sigma-1 receptor (S1R) agonist PRE-084, in a mouse model of motor neuron disease not linked to SOD1 mutation.

    abstract：:The identification of novel molecular targets crucially involved in motor neuron degeneration/survival is a necessary step for the development of hopefully more effective therapeutic strategies for amyotrophic lateral sclerosis (ALS) patients. In this view, S1R, an endoplasmic reticulum (ER)-resident receptor with cha...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2013.10.010

    authors： Peviani M,Salvaneschi E,Bontempi L,Petese A,Manzo A,Rossi D,Salmona M,Collina S,Bigini P,Curti D

    更新日期：2014-02-01 00:00:00

  • Characterisation of immune cell function in fragment and full-length Huntington's disease mouse models.

    abstract：:Inflammation is a growing area of research in neurodegeneration. In Huntington's disease (HD), a fatal inherited neurodegenerative disease caused by a CAG-repeat expansion in the gene encoding huntingtin, patients have increased plasma levels of inflammatory cytokines and circulating monocytes that are hyper-responsiv...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2014.10.012

    authors： Träger U,Andre R,Magnusson-Lind A,Miller JR,Connolly C,Weiss A,Grueninger S,Silajdžić E,Smith DL,Leavitt BR,Bates GP,Björkqvist M,Tabrizi SJ

    更新日期：2015-01-01 00:00:00

  • Quantitative ultrasound and apoptotic death in the neonatal primate brain.

    abstract：:Apoptosis is triggered in the developing mammalian brain by sedative, anesthetic or antiepileptic drugs during late gestation and early life. Whether human children are vulnerable to this toxicity mechanism remains unknown, as there are no imaging techniques to capture it. Apoptosis is characterized by distinct struct...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2019.03.032

    authors： Rosado-Mendez IM,Noguchi KK,Castañeda-Martinez L,Kirvassilis G,Wang SH,Manzella F,Swiney BS,Masuoka K,Capuano S III2,Brunner KG,Crosno K,Guerrero QW,Whitson H,Brambrink A,Simmons HS,Mejia AF,Zagzebski JA,Hall TJ,Ikono

    更新日期：2019-07-01 00:00:00

  • Cerebrospinal fluid beta-glucocerebrosidase activity is reduced in Dementia with Lewy Bodies.

    abstract：:The autophagy-lysosomal degradation pathway plays a role in the onset and progression of neurodegenerative diseases. Clinical and genetic studies indicate that mutations of beta-glucocerebrosidase represent genetic risk factors for synucleinopathies, including Parkinson's Disease (PD) and Dementia with Lewy Bodies (DL...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2009.03.002

    authors： Parnetti L,Balducci C,Pierguidi L,De Carlo C,Peducci M,D'Amore C,Padiglioni C,Mastrocola S,Persichetti E,Paciotti S,Bellomo G,Tambasco N,Rossi A,Beccari T,Calabresi P

    更新日期：2009-06-01 00:00:00

  • DJ-1 associates with synaptic membranes.

    abstract：:Parkinson's disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic neurons. Although many reports have suggested that genetic factors are implicated in the pathogenesis of PD, molecular mechanisms underlying selective dopaminergic neuronal degeneration remain unknown. DJ-1 is a causative gene for ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2011.05.014

    authors： Usami Y,Hatano T,Imai S,Kubo S,Sato S,Saiki S,Fujioka Y,Ohba Y,Sato F,Funayama M,Eguchi H,Shiba K,Ariga H,Shen J,Hattori N

    更新日期：2011-09-01 00:00:00

  • A WNT1-regulated developmental gene cascade prevents dopaminergic neurodegeneration in adult En1(+/-) mice.

    abstract：:The protracted and age-dependent degeneration of dopamine (DA)-producing neurons of the Substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) in the mammalian midbrain is a hallmark of human Parkinson's Disease (PD) and of certain genetic mouse models of PD, such as mice heterozygous for the homeodomai...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2015.05.015

    authors： Zhang J,Götz S,Vogt Weisenhorn DM,Simeone A,Wurst W,Prakash N

    更新日期：2015-10-01 00:00:00

  • Cln5-deficiency in mice leads to microglial activation, defective myelination and changes in lipid metabolism.

    abstract：:CLN5 disease, late infantile variant phenotype neuronal ceroid lipofuscinosis, is a severe neurodegenerative disease caused by mutations in the CLN5 gene, which encodes a lysosomal protein of unknown function. Cln5-deficiency in mice leads to loss of thalamocortical neurons, and glial activation, but the underlying me...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2011.12.009

    authors： Schmiedt ML,Blom T,Blom T,Kopra O,Wong A,von Schantz-Fant C,Ikonen E,Kuronen M,Jauhiainen M,Cooper JD,Jalanko A

    更新日期：2012-04-01 00:00:00

  • Interaction of ASK1 and the beta-amyloid precursor protein in a stress-signaling complex.

    abstract：:The amyloid precursor protein (APP) is a type I transmembrane protein translocated to neuronal terminals, whose function is still unknown. The C-terminus of APP mediates its interaction with cellular adaptor and signaling proteins, some of which signal to the stress-activated protein kinase (SAPK) pathway. Here we sho...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2007.06.017

    authors： Galvan V,Banwait S,Spilman P,Gorostiza OF,Peel A,Ataie M,Crippen D,Huang W,Sidhu G,Ichijo H,Bredesen DE

    更新日期：2007-10-01 00:00:00

  • Neuronal tissue-specific ribonucleoprotein complex formation on SOD1 mRNA: alterations by ALS SOD1 mutations.

    abstract：:Amyotrophic lateral sclerosis (ALS) is a fatal disease of unknown etiology. Mutations in copper/zinc superoxide dismutase (SOD1) are the most commonly associated genetic abnormality. Given that SOD1 is ubiquitously expressed, the exclusive vulnerability of motor neurons is one of the most puzzling issues in ALS resear...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2006.03.007

    authors： Ge WW,Leystra-Lantz C,Sanelli TR,McLean J,Wen W,Strong W,Strong MJ

    更新日期：2006-08-01 00:00:00

  • The glycoprotein GPNMB is selectively elevated in the substantia nigra of Parkinson's disease patients and increases after lysosomal stress.

    abstract：:GPNMB is a glycoprotein observed upon tissue damage and inflammation and is associated with astrocytes, microglia, and macrophages. Gene variations in GPNMB are linked with Parkinson's disease (PD) risk, and changes in protein levels of GPNMB have been found in lysosomal storage disorders, including Gaucher's disease ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2018.08.013

    authors： Moloney EB,Moskites A,Ferrari EJ,Isacson O,Hallett PJ

    更新日期：2018-12-01 00:00:00

  • Approaches to transport therapeutic drugs across the blood-brain barrier to treat brain diseases.

    abstract：:The central nervous system is protected by barriers which control the entry of compounds into the brain, thereby regulating brain homeostasis. The blood-brain barrier, formed by the endothelial cells of the brain capillaries, restricts access to brain cells of blood-borne compounds and facilitates nutrients essential ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2009.07.028

    authors： Gabathuler R

    更新日期：2010-01-01 00:00:00

  • Sequence of deposition of heterogeneous amyloid beta-peptides and APO E in Down syndrome: implications for initial events in amyloid plaque formation.

    abstract：:Patients with trisomy 21 [Down syndrome (DS)] progressively develop amyloid beta-protein (A beta) deposits and then other features of Alzheimer's disease (AD), apparently due to increased gene dosage and thus expression of the beta-amyloid precursor protein. Because the neuropathological phenotype in older DS subjects...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.1996.0003

    authors： Lemere CA,Blusztajn JK,Yamaguchi H,Wisniewski T,Saido TC,Selkoe DJ

    更新日期：1996-02-01 00:00:00

  • The IL-1beta system in epilepsy-associated malformations of cortical development.

    abstract：:Focal cortical dysplasia (FCD) and glioneuronal tumors (GNT) are recognized causes of chronic intractable epilepsy. The cellular mechanism(s) underlying their epileptogenicity remain largely unknown. Compelling evidence in experimental models of seizures indicates an important role of interleukin (IL)-1beta in the mec...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2006.06.003

    authors： Ravizza T,Boer K,Redeker S,Spliet WG,van Rijen PC,Troost D,Vezzani A,Aronica E

    更新日期：2006-10-01 00:00:00

  • Apolipoprotein E-low density lipoprotein receptor interaction affects spatial memory retention and brain ApoE levels in an isoform-dependent manner.

    abstract：:Human apolipoprotein E (apoE) exists in three isoforms: apoE2, apoE3 and apoE4. APOE ε4 is a major genetic risk factor for cardiovascular disease (CVD) and Alzheimer's disease (AD). ApoE mediates cholesterol metabolism by binding various receptors. The low-density lipoprotein receptor (LDLR) has a high affinity for ap...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2013.12.016

    authors： Johnson LA,Olsen RH,Merkens LS,DeBarber A,Steiner RD,Sullivan PM,Maeda N,Raber J

    更新日期：2014-04-01 00:00:00

  • Insights into Abeta and presenilin from a canine model of human brain aging.

    abstract：:In this review, we describe insights into beta-amyloid (Abeta) production using aged dogs as a model of human brain aging. The advantage of using dogs is that they naturally accumulate Abeta neuropathology with age. In parallel, dogs also develop age-associated learning and memory impairments. Thus, dogs can complemen...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1006/nbdi.2002.0476

    authors： Head E,Torp R

    更新日期：2002-02-01 00:00:00

  • Deep brain stimulation in the treatment of refractory epilepsy: update on current data and future directions.

    abstract：:Deep brain stimulation for epilepsy has garnered attention from epileptologists due to its well-documented success in treating movement disorders and the low morbidity associated with the implantation of electrodes. Given the large proportion of patients who fail medical therapy and are not candidates for surgical ame...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2009.07.007

    authors： Lega BC,Halpern CH,Jaggi JL,Baltuch GH

    更新日期：2010-06-01 00:00:00

  • Neuropeptide Y (NPY) as a therapeutic target for neurodegenerative diseases.

    abstract：:Neuropeptide Y (NPY) and NPY receptors are widely expressed in the mammalian central nervous system. Studies in both humans and rodent models revealed that brain NPY levels are altered in some neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, Huntington's disease and Machado-Joseph disease...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2016.07.022

    authors： Duarte-Neves J,Pereira de Almeida L,Cavadas C

    更新日期：2016-11-01 00:00:00

  • Gene therapy mediated seizure suppression in Genetic Generalised Epilepsy: Neuropeptide Y overexpression in a rat model.

    abstract：:Neuropeptide Y (NPY) is an important 36 amino acid peptide that is abundantly expressed in the mammalian CNS and is known to be an endogenous modulator of seizure activity, including in rat models of Genetic Generalised Epilepsy (GGE) with absence seizures. Studies have shown that viral-mediated "gene therapy" with ov...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2018.01.016

    authors： Powell KL,Fitzgerald X,Shallue C,Jovanovska V,Klugmann M,Von Jonquieres G,O'Brien TJ,Morris MJ

    更新日期：2018-05-01 00:00:00

  • Prodegenerative IκBα expression in oligodendroglial α-synuclein models of multiple system atrophy.

    abstract：:Multiple system atrophy is a progressive, neurodegenerative disease characterized by parkinsonism, ataxia, autonomic dysfunction, and accumulation of α-synuclein in oligodendrocytes. To understand how α-synuclein aggregates impact oligodendroglial homeostasis, we investigated an oligodendroglial cell model of α-synucl...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2013.12.002

    authors： Kragh CL,Gysbers AM,Rockenstein E,Murphy K,Halliday GM,Masliah E,Jensen PH

    更新日期：2014-03-01 00:00:00

  • Glial overexpression of Dube3a causes seizures and synaptic impairments in Drosophila concomitant with down regulation of the Na+/K+ pump ATPα.

    abstract：:Duplication 15q syndrome (Dup15q) is an autism-associated disorder co-incident with high rates of pediatric epilepsy. Additional copies of the E3 ubiquitin ligase UBE3A are thought to cause Dup15q phenotypes, yet models overexpressing UBE3A in neurons have not recapitulated the epilepsy phenotype. We show that Drosoph...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2017.09.003

    authors： Hope KA,LeDoux MS,Reiter LT

    更新日期：2017-12-01 00:00:00

  • Post-mortem assessment of the short and long-term effects of the trophic factor neurturin in patients with α-synucleinopathies.

    abstract：:Substantial interest persists for developing neurotrophic factors to treat neurodegenerative diseases. At the same time, significant progress has been made in implementing gene therapy as a means to provide long-term expression of bioactive neurotrophic factors to targeted sites in the brain. Nonetheless, to date, no ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2015.03.023

    authors： Bartus RT,Kordower JH,Johnson EM Jr,Brown L,Kruegel BR,Chu Y,Baumann TL,Lang AE,Olanow CW,Herzog CD

    更新日期：2015-06-01 00:00:00

  • N-Palmitoylethanolamine-oxazoline (PEA-OXA): A new therapeutic strategy to reduce neuroinflammation, oxidative stress associated to vascular dementia in an experimental model of repeated bilateral common carotid arteries occlusion.

    abstract：AIM:Recent studies revealed that pharmacological modulation of NAE-hydrolyzing acid amidase (NAAA) can be achieved with PEA oxazoline (PEA-OXA). Hence, the aim of the present work was to thoroughly evaluate the anti-inflammatory and neuroprotective effects of PEA-OXA in an experimental model of vascular dementia (VaD) ...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2019.01.007

    authors： Impellizzeri D,Siracusa R,Cordaro M,Crupi R,Peritore AF,Gugliandolo E,D'Amico R,Petrosino S,Evangelista M,Di Paola R,Cuzzocrea S

    更新日期：2019-05-01 00:00:00

  • Impaired glutamate uptake in the R6 Huntington's disease transgenic mice.

    abstract：:Huntington's disease (HD) is a late-onset neurodegenerative disease for which the mutation is CAG/polyglutamine repeat expansion. The R6 mouse lines expressing the HD mutation develop a movement disorder that is preceded by the formation of neuronal polyglutamine aggregates. The phenotype is likely caused by a widespr...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.2001.0430

    authors： Liévens JC,Woodman B,Mahal A,Spasic-Boscovic O,Samuel D,Kerkerian-Le Goff L,Bates GP

    更新日期：2001-10-01 00:00:00

  • Intermittent hypoxia induces time-dependent changes in the protein kinase B signaling pathway in the hippocampal CA1 region of the rat.

    abstract：:Intermittent hypoxia (IH) during sleep induces temporally defined increases in apoptosis within vulnerable brain regions such as the hippocampal CA1 region in rats. Protein kinase B (AKT) has emerged as major signal transduction protein underlying inhibition of apoptosis and consequent increases in cell survival. Spra...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2003.08.004

    authors： Goldbart A,Cheng ZJ,Brittian KR,Gozal D

    更新日期：2003-12-01 00:00:00

  • Erythropoietin promotes hippocampal neurogenesis in in vitro models of neonatal stroke.

    abstract：:The hippocampus is often injured in neonatal stroke. We have investigated the effect of erythropoietin (EPO) on oxygen-glucose deprived hippocampal slices and hypoxic progenitor cells. EPO improved survival of the organotypic hippocampal slices with significantly less cell death in the dentate gyrus and an increased n...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1016/j.nbd.2010.01.015

    authors： Osredkar D,Sall JW,Bickler PE,Ferriero DM

    更新日期：2010-05-01 00:00:00

  • Cellular distribution of NMDA glutamate receptor subunit mRNAs in the human cerebellum.

    abstract：:We have used a quantitative in situ hybridization method with human ribonucleotide probes to examine the regional and cellular distribution of N-methyl-D-aspartate receptor (NMDAR) subunit mRNAs in the human cerebellum. Purkinje cells showed very dense labeling for NMDAR1 mRNA, dense labeling for NMDAR2A mRNA, and mod...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章

    doi：10.1006/nbdi.1997.0136

    authors： Scherzer CR,Landwehrmeyer GB,Kerner JA,Standaert DG,Hollingsworth ZR,Daggett LP,Veliçelebi G,Penney JB Jr,Young AB

    更新日期：1997-01-01 00:00:00

  • Sex dimorphism in seizure-controlling networks.

    abstract：:Males and females show a different predisposition to certain types of seizures in clinical studies. Animal studies have provided growing evidence for sexual dimorphism of certain brain regions, including those that control seizures. Seizures are modulated by networks involving subcortical structures, including thalamu...

    journal_title：Neurobiology of disease

    pub_type： 杂志文章,评审

    doi：10.1016/j.nbd.2014.05.010

    authors： Giorgi FS,Galanopoulou AS,Moshé SL

    更新日期：2014-12-01 00:00:00