Search results for "hyperammonemia"

showing 10 items of 19 documents

Differential role of interleukin-1β in neuroinflammation-induced impairment of spatial and nonspatial memory in hyperammonemic rats.

2019

Activated microglia and increased brain IL-1β play a main role in cognitive impairment in much pathology. We studied the role of IL-1β in neuroinflammation-induced impairment of the following different types of learning and memory: novel object recognition (NOR), novel object location (NOL), spatial learning, reference memory (RM), and working memory (WM). All these processes are impaired in hyperammonemic rats. We assessed which of these types of learning and memory are restored by blocking the IL-1 receptor in vivo in hyperammonemic rats and the possible mechanisms involved. Blocking the IL-1 receptor reversed microglial activation in the hippocampus, perirhinal cortex, and prefrontal cor…

0301 basic medicineMaleInterleukin-1betaPostrhinal cortexHippocampusBiochemistryHippocampusReceptors N-Methyl-D-Aspartate03 medical and health sciences0302 clinical medicineReceptors GABAAmmoniaMemoryPerirhinal cortexGeneticsmedicineMemory impairmentAnimalsHyperammonemiaReceptors AMPARats WistarPrefrontal cortexMolecular BiologyNeuroinflammationCerebral CortexInflammationMicrogliabusiness.industryWorking memoryAnimal FeedRatsInterleukin 1 Receptor Antagonist ProteinProtein Subunits030104 developmental biologymedicine.anatomical_structureGene Expression RegulationReceptors GlutamateMicrogliabusinessNeuroscience030217 neurology & neurosurgeryBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Hyperammonemia alters the mismatch negativity in the auditory evoked potential by altering functional connectivity and neurotransmission

2020

Minimal hepatic encephalopathy (MHE) is a neuropsychiatric syndrome produced by central nervous system dysfunction subsequent to liver disease. Hyperammonemia and inflammation act synergistically to alter neurotransmission, leading to the cognitive and motor alterations in MHE, which are reproduced in rat models of chronic hyperammonemia. Patients with MHE show altered functional connectivity in different neural networks and a reduced response in the cognitive potential mismatch negativity (MMN), which correlates with attention deficits. The mechanisms by which MMN is altered in MHE remain unknown. The objectives of this work are as follows: To assess if rats with chronic hyperammonemia rep…

0301 basic medicineMalehippocampusPopulationMismatch negativityNeurotransmissionStimulus (physiology)Auditory cortexBiochemistrySynaptic Transmissionbehavioral disciplines and activitiesmetabolic diseases03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineNeural PathwaysmedicineAnimalsHyperammonemiaEvoked potentialRats Wistareducationeducation.field_of_studybusiness.industryGlutamate receptorBrainHyperammonemiamedicine.diseaseencephalopathyRats030104 developmental biologyHepatic EncephalopathyEvoked Potentials AuditorybusinessNeuroscience030217 neurology & neurosurgerypsychological phenomena and processes
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Chronic hyperammonemia alters extracellular glutamate, glutamine and GABA and membrane expression of their transporters in rat cerebellum. Modulation…

2018

Trafficking of glutamate, glutamine and GABA between astrocytes and neurons is essential to maintain proper neurotransmission. Chronic hyperammonemia alters neurotransmission and cognitive function. The aims of this work were to analyze in cerebellum of rats the effects of chronic hyperammonemia on: a) extracellular glutamate, glutamine and GABA concentrations; b) membrane expression of glutamate, glutamine and GABA transporters; c) how they are modulated by extracellular cGMP. Hyperammonemic rats show increased levels of extracellular glutamate, glutamine, GABA and citrulline in cerebellum in vivo. Hyperammonemic rats show: a) increased membrane expression of the astrocytic glutamine trans…

0301 basic medicineNeurotransmitter transporterMaleGlutamineGlutamate-glutamine cycleGlutamic AcidNeurotransmissionSynaptic Transmission03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineCerebellumNeurotransmitter Transport ProteinsmedicineExtracellularGABA transporterAnimalsHyperammonemiaRats WistarCyclic GMPgamma-Aminobutyric AcidPharmacologybiologyChemistryCell MembraneGlutamate receptorHyperammonemiamedicine.diseaseCell biologyRatsGlutamine030104 developmental biologynervous systembiology.proteinCitrullineExtracellular Space030217 neurology & neurosurgeryNeuropharmacology
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Modulation of GABAA receptors by neurosteroids. A new concept to improve cognitive and motor alterations in hepatic encephalopathy

2016

Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome affecting patients with liver diseases, mainly those with liver cirrhosis. The mildest form of HE is minimal HE (MHE), with mild cognitive impairment, attention deficit, psychomotor slowing and impaired visuo-motor and bimanual coordination. MHE may progress to clinical HE with worsening of the neurological alterations which may lead to reduced consciousness and, in the worse cases, may progress to coma and death. HE affects several million people in the world and is a serious health, social and economic problem. There are no specific treatments for the neurological alterations in HE. The mechanisms underlying the cognitive …

0301 basic medicinemedicine.medical_specialtyNeuroactive steroidCirrhosisEndocrinology Diabetes and MetabolismClinical BiochemistryBiochemistry03 medical and health sciences0302 clinical medicineEndocrinologyCognitionMedicineAnimalsHumansHyperammonemiaPsychiatryMolecular BiologyHepatic encephalopathyHepatic encephalopathyPsychomotor learningComaNeurotransmitter Agentsbusiness.industryGABAA receptorsBrainCognitionHyperammonemiaCell Biologymedicine.diseaseReceptors GABA-AMotor coordination030104 developmental biologyHepatic EncephalopathyMolecular MedicineNeuroteroidsMotor coordinationCognitive functionmedicine.symptombusinessNeuroscience030217 neurology & neurosurgeryLocomotionPsychomotor Performance
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Minimal hepatic encephalopathy is associated with expansion and activation of CD4+CD28−, Th22 and Tfh and B lymphocytes

2017

AbstractPeripheral inflammation acts synergistically with hyperammonemia in inducing neurological alterations in cirrhotic patients with minimal hepatic encephalopathy (MHE). We hypothesized that appearance of MHE would be associated to some specific qualitative change in peripheral inflammation. The aim of this work was to characterize the changes in peripheral inflammation associated to appearance of MHE. We analyzed it by immunophenotyping and cytokine profile analysis, in cirrhotic patients without or with MHE and controls. The main alterations associated specifically with MHE are: 1) increased activation of all subtypes of CD4+ T-lymphocytes, with the increased expression of CD69; 2) i…

0301 basic medicinemedicine.medical_specialtyScienceInflammationArticleMonocytesImmunophenotyping03 medical and health sciencesImmune systemImmunophenotypingCD28 AntigensInternal medicinemedicineHumansCX3CL1Hepatic encephalopathyB-LymphocytesMultidisciplinarybusiness.industryCD69QRCD28HyperammonemiaT-Lymphocytes Helper-Inducermedicine.disease030104 developmental biologyEndocrinologyHepatic EncephalopathyImmunoglobulin GCD4 AntigensImmunologyMedicineCytokinesmedicine.symptombusinesshuman activitiesScientific Reports
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Urea cycle dysregulation in non-alcoholic fatty liver disease.

2018

Background & Aims: In non-alcoholic steatohepatitis (NASH), the function of urea cycle enzymes (UCEs) may be affected, resulting in hyperammonemia and the risk of disease progression. We aimed to determine whether the expression and function of UCEs are altered in an animal model of NASH and in patients with non-alcoholic fatty liver disease (NAFLD), and whether this process is reversible. Methods: Rats were first fed a high-fat, high-cholesterol diet for 10 months to induce NASH, before being switched onto a normal chow diet to recover. In humans, we obtained liver biopsies from 20 patients with steatosis and 15 with NASH. Primary rat hepatocytes were isolated and cultured with free fatty …

AdultMale0301 basic medicinemedicine.medical_specialtyCarbamoyl-Phosphate Synthase (Ammonia)Ornithine transcarbamylase03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAmmoniaGlutamate-Ammonia LigaseNon-alcoholic Fatty Liver DiseaseInternal medicineGene expressionmedicineAnimalsHumansUreaRats WistarPromoter Regions GeneticCells CulturedOrnithine CarbamoyltransferaseAgedHepatologyChemistryFatty liverHyperammonemiaDNA MethylationMiddle Agedmedicine.diseaseRats030104 developmental biologyEndocrinologyLiverUrea cycleHepatocytesUreaFemale030211 gastroenterology & hepatologySteatohepatitisSteatosis
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Interplay between glutamatergic and GABAergic neurotransmission alterations in cognitive and motor impairment in minimal hepatic encephalopathy.

2015

The cognitive and motor alterations in hepatic encephalopathy (HE) are the final result of altered neurotransmission and communication between neurons in neuronal networks and circuits. Different neurotransmitter systems cooperate to modulate cognitive and motor function, with a main role for glutamatergic and GABAergic neurotransmission in different brain areas and neuronal circuits. There is an interplay between glutamatergic and GABAergic neurotransmission alterations in cognitive and motor impairment in HE. This interplay may occur: (a) in different brain areas involved in specific neuronal circuits; (b) in the same brain area through cross-modulation of glutamatergic and GABAergic neur…

CerebellumMinimal hepatic encephalopathyGlutamic AcidNeurotransmissionSynaptic TransmissionCellular and Molecular NeuroscienceGlutamatergicmedicineHyperammonemiaAnimalsHumansGlutamatergic neurotransmissionGABAergic neurotransmissionHepatic encephalopathygamma-Aminobutyric AcidHepatic encephalopathyGABAA receptorbusiness.industryGlutamate receptorHyperammonemiaCognitionCell Biologymedicine.diseaseMotor Skills Disordersmedicine.anatomical_structureHepatic EncephalopathyCognitive functionCognition DisordersbusinessNeuroscience
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The Study of Carbamoyl Phosphate Synthetase 1 Deficiency Sheds Light on the Mechanism for Switching On/Off the Urea Cycle

2015

12 páginas, 4 figuras, 2 tablas.

Conformational changeCarbamoyl-Phosphate Synthase I Deficiency DiseaseAllosteric regulationCarbamoyl-Phosphate Synthase (Ammonia)Urea cycle diseases610 Medicine & healthBiologyMolecular Dynamics Simulationurologic and male genital diseases03 medical and health sciences0302 clinical medicineGlutamates1311 GeneticsAmmoniaEnzyme StabilityGeneticsmedicine1312 Molecular BiologyHumansUreaHyperammonemiaSite-directed mutagenesisMolecular Biology030304 developmental biologychemistry.chemical_classification0303 health sciencesSite-directed mutagenesisurogenital systemMutagenesisCarbamoyl phosphate synthetase 1HyperammonemiaCarbamoyl phosphate synthetasemedicine.diseaseAllosteric regulation3. Good healthProtein Structure TertiaryRestrained molecular dynamicsKineticsEnzymeBiochemistrychemistry10036 Medical ClinicEnzymeUrea cycleMutationInborn errors030217 neurology & neurosurgerySignal Transduction
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Alteraciones de la neurotransmisión en hipocampo de ratas hiperamonémicas. papel de la neuroinflamación. modulación por GMPc extracelular

2021

La Encefalopatía Hepática (EH) es un síndrome neuropsiquiátrico complejo producido por un fallo hepático. Cuando el hígado falla se producen hiperamonemia (HA) e inflamación que actúan sinérgicamente produciendo neuroinflamación, lo que da lugar a alteraciones en la neurotransmisión y alteraciones cognitivas y motoras. Estudios anteriores del grupo han demostrado que el aumento de los niveles de GMPc extracelular disminuye la neuroinflamación y revierte las alteraciones cognitivas y motoras observadas en ratas hiperamonémicas. Sin embargo, los mecanismos responsables se desconocían. En la presente tesis doctoral hemos demostrado que la hiperamonemia crónica reduce la respuesta de los recept…

GABAextracellular cGMPnervous systemhyperammonemiaNMDAAMPAUNESCO::CIENCIAS DE LA VIDA:CIENCIAS DE LA VIDA [UNESCO]neuroinflammation
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Chronic exposure to ammonia induces isoform-selective alterations in the intracellular distribution and NMDA receptor-mediated translocation of prote…

2004

Hyperammonemia is responsible for most neurological alterations in patients with hepatic encephalopathy by mechanisms that remain unclear. Hyperammonemia alters phosphorylation of neuronal protein kinase C (PKC) substrates and impairs NMDA receptor-associated signal transduction. The aim of this work was to analyse the effects of hyperammonemia on the amount and intracellular distribution of PKC isoforms and on translocation of each isoform induced by NMDA receptor activation in cerebellar neurons. Chronic hyperammonemia alters differentially the intracellular distribution of PKC isoforms. The amount of all isoforms (except PKC zeta) was reduced (17-50%) in the particulate fraction. The con…

Intracellular Fluidmedicine.medical_specialtyN-MethylaspartateChromosomal translocationBiologyPKC alphaBiochemistryReceptors N-Methyl-D-AspartateCellular and Molecular NeuroscienceAmmoniaInternal medicineCerebellummedicineAnimalsHyperammonemiaRats WistarProtein kinase CCells CulturedProtein Kinase CDiacylglycerol kinaseNeuronsPhospholipase CDose-Response Relationship DrugHyperammonemiamedicine.diseaseCell biologyRatsIsoenzymesCytosolProtein TransportEndocrinologySignal transductionJournal of neurochemistry
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