Search results for "Seizures"

showing 10 items of 152 documents

Metal complexes of phenobarbituric acid. Chelating behavior of the phenobarbiturate ring. Anticonvulsant properties of the K2[Cu(N-methylphenobarbitu…

1992

Abstract Na2Ni(phenobarbiturato)4·3H2O, Na2Ni3(phenobarbiturato)2(OH)6·4H2O, and NaZn(phenobarbiturato)2(OH)·H2O derivatives were prepared from Ni(II) and Zn(II) and phenobarbital. The Na2Ni(phenobarbiturato)4·3H2O complex is diamagnetic and isostructural with the complex previously reported, Na2Cu(phenobarbiturato)4, suggesting a square-planar environment around the Ni(II) ion. The DMF solutions of this complex show the existence of two species. The EPR spectra of the Cu(II) doped complex show the hyperfine and superhyperfine structures. The covalence parameters α2, β2, and δ2 show a strong bonding in the equatorial plane and suggests the formation of a [CuN4] chromophore. The anticonvulsa…

Magnetic Resonance SpectroscopyStereochemistryMephobarbitalBiochemistrylaw.inventionIonInorganic ChemistryMetalStructure-Activity RelationshiplawSeizuresAnimalsChelationIsostructuralElectron paramagnetic resonanceHyperfine structureChelating AgentsElectroshockMolecular StructureChemistryElectron Spin Resonance SpectroscopyChromophoreCrystallographyCovalent bondMetalsvisual_artPhenobarbitalvisual_art.visual_art_mediumAnticonvulsantsCopperJournal of inorganic biochemistry
researchProduct

Generalization of seizures parallels the formation of "dark" neurons in the hippocampus and pontine reticular formation after focal-cortical applicat…

2008

Abstract Distribution and time course of the occurrence of “dark” neurons were compared with the EEG activity and behavior of rats during 4-aminopyridine (4-AP) induced epileptic seizures. A crystal of the K + channel blocker 4-AP (0.5 mg/kg) was placed onto the exposed parieto-occipital cortex of Halothane-anesthetized rats for 40 min. Thereafter, the anesthesia was discontinued and the behavioral signs of the epileptic seizure activity were observed. The presence of “dark” neurons was demonstrated by the sensitive silver method of Gallyas in rats sacrificed at 0, 3 and 6 h after the end of the 4-AP crystal application. The EEG activity was recorded in the rats with longer survival times. …

Male* Dark neuronMicroinjections* Epilepsy; * Dark neuron; * Hippocampus; * Pontine reticular formation; * Cell injury; * Animal model; * Neurogliaform cell; * Astrocyte; * Status epilepticusHippocampus* Status epilepticusStatus epilepticusReticular formationHippocampusSettore BIO/09 - FisiologiaRats Sprague-DawleyEpilepsySeizuresPonsConvulsionmedicinePotassium Channel BlockersAnimals4-AminopyridineMolecular Biology* Animal modelNeurons* Pontine reticular formationBehavior AnimalChemistryGeneral NeuroscienceReticular Formation* Neurogliaform cellElectroencephalographyParamedian pontine reticular formation* Hippocampumedicine.disease* Cell injuryRats* Astrocyte* Epilepsymedicine.anatomical_structureMossy Fibers HippocampalNeurology (clinical)Epileptic seizureNeuronmedicine.symptomNeuroscienceDevelopmental Biology
researchProduct

High Rate of Recurrent De Novo Mutations in Developmental and Epileptic Encephalopathies

2017

Item does not contain fulltext Developmental and epileptic encephalopathy (DEE) is a group of conditions characterized by the co-occurrence of epilepsy and intellectual disability (ID), typically with developmental plateauing or regression associated with frequent epileptiform activity. The cause of DEE remains unknown in the majority of cases. We performed whole-genome sequencing (WGS) in 197 individuals with unexplained DEE and pharmaco-resistant seizures and in their unaffected parents. We focused our attention on de novo mutations (DNMs) and identified candidate genes containing such variants. We sought to identify additional subjects with DNMs in these genes by performing targeted sequ…

Male0301 basic medicineCandidate genemedicine.medical_specialtymedical geneticsglycosylationNonsense mutationGenome-wide association studyGene mutationBiologySensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Articlesevere intellectual disability03 medical and health sciencesEpilepsy0302 clinical medicinechildrenRecurrenceSeizuresGenetic linkageIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyJournal ArticleGeneticsmedicineHumansChilddisordersGenetics (clinical)Genetic associationGeneticsBrain DiseasesdiseaseEpilepsycis-prenyltransferaseGenome Humanstructural basismedicine.diseasediphosphate synthase030104 developmental biologyChild PreschoolMutationMedical geneticsFemalenogo-b receptor030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyGenome-Wide Association StudyMeta-Analysis
researchProduct

Pyridoxine dependent epilepsies: new therapeutical point of view

2017

Abstract Pyridoxine dependent epilepsies (PDEs) are rare autosomal recessive disorders with onset in neonatal period. Seizures are typically not responsive to conventional antiepileptic drugs, but they cease after parental pyridoxine administration. Atypical forms are characterized partly response to pyridoxine and a late onset of symptoms (up to the age of three years). Prevalence is variable and it has rarely been described. The genes involved in PDEs are the gene encoding for the Alpha-aminoadipic-semialdehyde dehydrogenase (ALDH7A1) and PROSC gene, which encodes a pyridoxal-5-phosphate binding protein. Mutations in the gene encoding for the pyridoxal-5′-phosphate oxidase enzyme (PNPO) a…

Male0301 basic medicineNew therapeutical approachTreatment outcomePNPOBioinformaticsSeverity of Illness IndexEpilepsy0302 clinical medicineLetter to the EditorAnticonvulsant drugsDrugs-resistant seizuresBrain Diseases MetabolicIncidencelcsh:RJ1-570PyridoxineElectroencephalographyPyridoxine dependent epilepsiesPrognosisPyridoxaminephosphate OxidaseTreatment OutcomeChild PreschoolHypoxia-Ischemia BrainConventional anticonvulsant drugAnticonvulsantsFemalemedicine.drugmedicine.medical_specialtyLate onsetRisk Assessment03 medical and health sciencesDrugs-resistant seizureSeizuresInternal medicinePyridoxine administrationmedicineHumansGenetic Predisposition to DiseaseGeneEpilepsyPyridoxaminephosphate Oxidasebusiness.industryInfantlcsh:PediatricsPyridoxinemedicine.disease030104 developmental biologyEndocrinologyConventional anticonvulsant drugsbusiness030217 neurology & neurosurgeryItalian Journal of Pediatrics
researchProduct

Pathology-selective antiepileptic effects in the focal freeze-lesion rat model of malformation of cortical development

2021

Malformations of cortical development (MCD) represent a group of rare diseases with severe clinical presentation as epileptic and pharmacoresistant encephalopathies. Morphological studies in tissue from MCD patients have revealed reduced GABAergic efficacy and increased intracellular chloride concentration in neuronal cells as important pathophysiological mechanisms in MCD. Also, in various animal models, alterations of GABAergic inhibition have been postulated as a predominant factor contributing to perilesional hyperexcitability. Along with this line, the NKCC1 inhibitor bumetanide has been postulated as a potential drug for treatment of epilepsy, mediating its antiepileptic effect by red…

Male0301 basic medicinePathologymedicine.medical_specialtyZonisamideInhibitory postsynaptic potentialCryosurgeryLesion03 medical and health sciencesEpilepsyOrgan Culture Techniques0302 clinical medicineSodium Potassium Chloride Symporter InhibitorsDevelopmental NeuroscienceSeizuresmedicineAnimals4-AminopyridineRats WistarBumetanideCerebral Cortexbusiness.industryCarbamazepinemedicine.diseaseRatsMicrogyrusMalformations of Cortical Development030104 developmental biologyNeurologyGABAergicAnticonvulsantsmedicine.symptombusiness030217 neurology & neurosurgeryBumetanidemedicine.drugExperimental Neurology
researchProduct

The landscape of epilepsy-related GATOR1 variants

2019

Purpose:\ud \ud To define the phenotypic and mutational spectrum of epilepsies related to DEPDC5, NPRL2 and NPRL3 genes encoding the GATOR1 complex, a negative regulator of the mTORC1 pathway.\ud \ud Methods:\ud \ud We analyzed clinical and genetic data of 73 novel probands (familial and sporadic) with epilepsy-related variants in GATOR1-encoding genes and proposed new guidelines for clinical interpretation of GATOR1 variants.\ud \ud Results:\ud \ud The GATOR1 seizure phenotype consisted mostly in focal seizures (e.g., hypermotor or frontal lobe seizures in 50%), with a mean age at onset of 4.4 years, often sleep-related and drug-resistant (54%), and associated with focal cortical dysplasia…

Male0301 basic medicineProbandDEPDC5SUDEP030105 genetics & heredityBioinformaticsLoss of Function Mutation/geneticsEpilepsyINDEL MutationLoss of Function MutationmTORC1 pathwayGenetics(clinical)ChildGenetics (clinical)Multiprotein Complexes/geneticsBrugada SyndromeDNA Copy Number VariationBrugada syndromeINDEL Mutation/geneticsGTPase-Activating ProteinsNPRL3SeizureDEPDC5PhenotypePedigree3. Good healthBrugada Syndrome/geneticsChild PreschoolFemaleHumanSignal TransductionDNA Copy Number VariationsAdolescentSeizures/complicationsMechanistic Target of Rapamycin Complex 1/geneticsDNA Copy Number Variations/geneticsMechanistic Target of Rapamycin Complex 1Tumor Suppressor Proteins/geneticsArticleFocal cortical dysplasia03 medical and health sciencesSeizuresGTPase-Activating Proteins/geneticsmedicineHumansGenetic Predisposition to DiseaseDEPDC5; Focal cortical dysplasia; Genetic focal epilepsy; mTORC1 pathway; SUDEPGenetic focal epilepsyEpilepsy/complicationsRepressor Proteins/geneticsEpilepsybusiness.industryGTPase-Activating ProteinTumor Suppressor ProteinsInfant NewbornCorrectionInfantRepressor ProteinCortical dysplasiamedicine.diseaseddc:616.8Repressor Proteins030104 developmental biologyFrontal lobe seizures[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMultiprotein ComplexesMultiprotein ComplexeSignal Transduction/geneticsHuman medicinebusiness
researchProduct

The FAAH inhibitor URB597 suppresses hippocampal maximal dentate afterdischarges and restores seizure-induced impairment of short and long-term synap…

2017

Synthetic cannabinoids and phytocannabinoids have been shown to suppress seizures both in humans and experimental models of epilepsy. However, they generally have a detrimental effect on memory and memory-related processes. Here we compared the effect of the inhibition of the endocannabinoid (eCB) degradation versus synthetic CB agonist on limbic seizures induced by maximal dentate activation (MDA) acute kindling. Moreover, we investigated the dentate gyrus (DG) granule cell reactivity and synaptic plasticity in naïve and in MDA-kindled anaesthetised rats. We found that both the fatty acid amide hydrolase (FAAH) inhibitor URB597 and the synthetic cannabinoid agonist WIN55,212-2 displayed AM…

Male0301 basic medicinemedicine.medical_treatmentLong-Term Potentiationlcsh:MedicineBrain -- Diseases -- DiagnosisSynaptic TransmissionEpilepsy -- Alternative treatmentchemistry.chemical_compoundEpilepsy0302 clinical medicineFatty acid amide hydrolaselcsh:ScienceTemporal lobe epilepsyInhibitionNeuronal PlasticityMultidisciplinaryLong-term potentiationmedicine.anatomical_structureAnesthesiaBenzamidesHippocampus (Brain)medicine.medical_specialtyArticleAmidohydrolases03 medical and health sciencesSeizuresInternal medicinemedicineAnimalsAuthor CorrectionEpilepsyCannabinoidsDentate gyruslcsh:RURB597medicine.diseaseGranule cellHippocampus (Brain) -- PhysiologyRats030104 developmental biologyEndocrinologychemistryDentate GyrusSynaptic plasticitylcsh:QNeuroplasticityCarbamatesCannabinoid030217 neurology & neurosurgery
researchProduct

Lamotrigine differently modulates 7-Nitroindazole and L-Arginine influence on Rat Maximal Dentate Gyrus Activation

2007

The effects induced on the maximal dentate gyrus activation (MDA) by administering the anticonvulsant lamotrigine (LTG), the selective inhibitor of neuronal nitric oxide synthase 7-nitroindazole (7-NI) and the precursor of nitric oxide (NO) synthesis L-arginine, alone or in combination, were studied in urethane anaesthetized rats. Either 7-NI or LTG alone administration reduced the number of convulsing animals following angular bundle (AB) stimulation; their combined treatment induced a further increase of the anticonvulsant effect as also demonstrated by the decrease of MDA and afterdischarge (AD) durations in the animals still responding to AB stimulation. On the contrary, the injection o…

Male7-NitroindazoleIndazolesArgininemedicine.medical_treatmentStimulationPharmacologyLamotrigineArginineLamotrigineNitric OxideSettore BIO/09 - FisiologiaNitric oxidechemistry.chemical_compoundSeizuresmedicineAnimalsEnzyme InhibitorsRats WistarBiological PsychiatryTriazinesDentate gyrusElectric StimulationRatsPsychiatry and Mental healthAnticonvulsantNeurologychemistryDentate GyrusAnticonvulsantsNeurology (clinical)Neuronal Nitric Oxide Synthasemedicine.drugLAMOTRIGINE NITRIC OXIDE EPILEPSY CONTROL
researchProduct

Connexin-30 mRNA Is Up-Regulated in Astrocytes and Expressed in Apoptotic Neuronal Cells of Rat Brain Following Kainate-Induced Seizures

2002

Glial connexins (Cxs) make an extensively interconnected functional syncytium created by a network of gap junctions between astrocytes and oligodendrocytes. Among Cxs expressed in the brain, Cx30 is expressed in grey matter astrocytes, as shown at the protein level by immunoistochemistry. In the present study we aimed to perform a detailed study of the regional distribution of Cx30 mRNA in the adult and postnatal developing rat brain, analyzing its expression by in situ hybridization, and determining its cell type localization by double labeling. Recently, it has been suggested that neuronal activity may control the level of intercellular communication between astrocytes through gap junctio…

MaleAgingCell typeGene ExpressionConnexinApoptosisKainate receptorCell CommunicationIn situ hybridizationGrey matterBiologyConnexinsCellular and Molecular NeuroscienceStatus EpilepticusSeizuresExcitatory Amino Acid AgonistsmedicineAnimalsPremovement neuronal activityRNA MessengerRats WistarMolecular BiologyNeuronsSyncytiumKainic AcidGap junctionBrainCell BiologyImmunohistochemistryRatsUp-RegulationCell biologymedicine.anatomical_structureAnimals NewbornAstrocytesNeuroscienceMolecular and Cellular Neuroscience
researchProduct

Cellular expression of connexins in the rat brain: neuronal localization, effects of kainate-induced seizures and expression in apoptotic neuronal ce…

2003

The identification of connexins (Cxs) expressed in neuronal cells represents a crucial step for understanding the direct communication between neurons and between neuron and glia. In the present work, using a double-labelling method combining in situ hybridization for Cx mRNAs with immunohistochemical detection for neuronal markers, we provide evidence that, among cerebral connexins (Cx26, Cx32, Cx36, Cx37, Cx40, Cx43, Cx45 and Cx47), only Cx45 and Cx36 mRNAs are localized in neuronal cells in both developing and adult rat brain. In order to establish whether connexin expression is influenced in vivo by abnormal neuronal activity, we examined the short-term effects of kainate-induced seizur…

MaleAgingTime FactorsgliaHippocampusConnexinbrain developmentKainate receptorApoptosisIn situ hybridizationBiologyConnexinsgap junctionbrain development; gap junction; gliaSeizuresTubulinmedicineExcitatory Amino Acid AgonistsIn Situ Nick-End LabelingPremovement neuronal activityAnimalsRNA MessengerOrganic ChemicalsRats WistarIn Situ HybridizationFluorescent DyesNeuronsMessenger RNAKainic AcidReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceGap junctionBrainGene Expression Regulation DevelopmentalFluoresceinsImmunohistochemistryCell biologyRatsmedicine.anatomical_structurenervous systemAnimals NewbornPhosphopyruvate HydrataseAutoradiographysense organsNeuronNeuroscienceDensitometryThe European journal of neuroscience
researchProduct