Search results for "Cephalon"

showing 10 items of 99 documents

Modifications in Evoked Activity in the Visual Cortex Induced by the Caudate Nucleus

1971

The visual system, like the other sensorial systems, is subjected to intrinsic, complex control, originating both in the retina (CHANG et al., 1959; ARDUINI and HIRAO, 1960; STERIADE, 1967) and in the visual cortex (BUSER et a/., 1963; JASSIK-GERSCHENFELD and ASCHER, 1963; MEULDERS, 1965), which regulates its input at various levels of the specific pathways. However, the visual system is also influenced by subcortical structures which, though not exerting on it a strictly selective control, determine notable modifications in the level of excitability of the cortical sensorial neurons. It is in fact we11 known that activation of the mesencephalic reticular formation, by increasing the level …

LightPhysiologyCaudate nucleusStimulationInhibitory postsynaptic potentialReticular formationBiochemistryMidbrainMesencephalonNeural PathwaysmedicineAnimalsEvoked PotentialsVisual CortexChemistryReticular FormationGeniculate BodiesOptic NerveParamedian pontine reticular formationElectric StimulationRadiation EffectsVisual cortexmedicine.anatomical_structureCerebral cortexCatsCaudate NucleusNeuroscienceArchives Internationales de Physiologie et de Biochimie
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Functional Plasticity after Unilateral Vestibular Midbrain Infarction in Human Positron Emission Tomography.

2016

The aim of the study was to uncover mechanisms of central compensation of vestibular function at brainstem, cerebellar, and cortical levels in patients with acute unilateral midbrain infarctions presenting with an acute vestibular tone imbalance. Eight out of 17 patients with unilateral midbrain infarctions were selected on the basis of signs of a vestibular tone imbalance, e.g., graviceptive (tilts of perceived verticality) and oculomotor dysfunction (skew deviation, ocular torsion) in F18-fluordeoxyglucose (FDG)-PET at two time points: A) in the acute stage, and B) after recovery 6 months later. Lesion-behavior mapping analyses with MRI verified the exact structural lesion sites. Group su…

Male0301 basic medicineBrain Stem Infarctionslcsh:MedicinePathology and Laboratory MedicineMidbrainDiagnostic Radiology0302 clinical medicineThalamusMesencephalonCortex (anatomy)Medicine and Health SciencesMedicinelcsh:ScienceTomographyPostural BalanceVestibular systemNeuronal PlasticityMultidisciplinaryRadiology and ImagingBrainAnatomyFrontal eye fieldsMagnetic Resonance Imagingmedicine.anatomical_structureVestibular DiseasesInfarctionThalamic NucleiFemaleBrainstemAnatomyBrainstemResearch ArticleImaging TechniquesThalamusNeuroimagingResearch and Analysis Methods03 medical and health sciencesSigns and SymptomsDiagnostic MedicineOcular SystemHumansSkew deviationAgedbusiness.industrylcsh:RBiology and Life SciencesVestibular cortex030104 developmental biologyVisual cortexCase-Control StudiesPositron-Emission TomographyLesionsEyeslcsh:QbusinessHeadNeurosciencePositron Emission Tomography030217 neurology & neurosurgeryNeurosciencePLoS ONE
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Protective effects of mirtazapine in mice lacking the Mbnl2 gene in forebrain glutamatergic neurons: Relevance for myotonic dystrophy 1

2019

Myotonic dystrophy type 1 (DM1) is a multisystemic disorder characterized by muscle weakness and wasting and by important central nervous system-related symptoms including impairments in executive functions, spatial abilities and increased anxiety and depression. The Mbnl2 gene has been implicated in several phenotypes consistent with DM1 neuropathology. In this study, we developed a tissue-specific knockout mouse model lacking the Mbnl2 gene in forebrain glutamatergic neurons to examine its specific contribution to the neurobiological perturbations related to DM1. We found that these mice exhibit long-term cognitive deficits and a depressive-like state associated with neuronal loss, increa…

Male0301 basic medicineMirtazapineGlutamic AcidHippocampusMice TransgenicMirtazapineMyotonic dystrophyAnimals Genetically ModifiedMice03 medical and health sciencesCellular and Molecular NeuroscienceGlutamatergicProsencephalon0302 clinical medicinemedicineAnimalsMyotonic DystrophyDentate gyrusInflammationMice KnockoutNeuronsPharmacologyDepressionbusiness.industryCognitive deficitsDentate gyrusNeurogenesisRNA-Binding Proteinsmedicine.disease3. Good healthMice Inbred C57BLNeuroprotective Agents030104 developmental biologynervous systemKnockout mouseForebrainNeuronal lossDrosophilaFemaleDM1businessNeuroscience030217 neurology & neurosurgerymedicine.drugNeuropharmacology
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Retrotransposon activation by distressed mitochondria in neurons

2020

Retrotransposon activation occurs in a variety of neurological disorders including multiple sclerosis and Alzheimer's Disease. While the origins of disease-related retrotransposon activation have remained mostly unidentified, this phenomenon may well contribute to disease progression by inducing inflammation, disrupting transcription and, potentially, genomic insertion. Here, we report that the inhibition of mitochondrial respiratory chain complex I by pharmacological agents widely used to model Parkinson's disease leads to a significant increase in expression of the ORF1 protein of the long interspersed nucleotide element 1 (LINE1) retrotransposon in human dopaminergic LUHMES cells. These …

Male0301 basic medicineParkinson's diseaseRetroelementsBiophysicsInflammationRetrotransposonMitochondrionBiologyBiochemistryCell Line03 medical and health sciences0302 clinical medicineMesencephalonTranscription (biology)medicineAnimalsHumansMitochondrial respiratory chain complex IMolecular BiologyNeuronsElectron Transport Complex INeurodegenerationfood and beveragesCell BiologyDNA Methylationmedicine.diseaseMitochondriaCell biologyMice Inbred C57BLLong Interspersed Nucleotide Elements030104 developmental biology030220 oncology & carcinogenesisDNA methylationmedicine.symptomBiochemical and Biophysical Research Communications
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Downregulation of PMCA2 increases the vulnerability of midbrain neurons to mitochondrial complex I inhibition

2013

Parkinson's disease is an age-associated disorder characterized by selective degeneration of dopaminergic neurons. The molecular mechanisms underlying the selective vulnerability of this subset of neurons are, however, not fully understood. Employing SH-SY5Y neuroblastoma cells and primary mesencephalic neurons, we here demonstrate a significant increase in cytosolic calcium after inhibition of mitochondrial complex I by means of MPP(+), which is a well-established environmental toxin-based in vitro model of Parkinson's disease. This increase in calcium is correlated with a downregulation of the neuron-specific plasma membrane Ca(2+)-ATPase isoform 2 (PMCA2). Interestingly, two other import…

Male1-Methyl-4-phenylpyridiniummedicine.medical_specialtySERCADown-Regulationchemistry.chemical_elementCalciumToxicologyCREBRats Sprague-DawleyPlasma Membrane Calcium-Transporting ATPaseschemistry.chemical_compoundDownregulation and upregulationMesencephalonCell Line TumorInternal medicinemedicineAnimalsHumansCyclic AMP Response Element-Binding ProteinNeuronsCalcium metabolismElectron Transport Complex IbiologyGeneral NeuroscienceMPTPNeurodegenerationmedicine.diseaseRatsEndocrinologychemistrybiology.proteinCalciumsense organsIntracellularNeuroToxicology
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Loss of all three APP family members during development impairs synaptic function and plasticity, disrupts learning, and causes an autism-like phenot…

2021

The key role of APP for Alzheimer pathogenesis is well established. However, perinatal lethality of germline knockout mice lacking the entire APP family has so far precluded the analysis of its physiological functions for the developing and adult brain. Here, we generated conditional APP/APLP1/APLP2 triple KO (cTKO) mice lacking the APP family in excitatory forebrain neurons from embryonic day 11.5 onwards. NexCre cTKO mice showed altered brain morphology with agenesis of the corpus callosum and disrupted hippocampal lamination. Further, NexCre cTKOs revealed reduced basal synaptic transmission and drastically reduced long-term potentiation that was associated with reduced dendritic length …

Male10017 Institute of AnatomyLong-Term PotentiationHippocampal formationSynaptic TransmissionAmyloid beta-Protein Precursor0302 clinical medicine2400 General Immunology and MicrobiologyAmyloid precursor proteinMolecular Biology of DiseaseAutism spectrum disorderMice KnockoutNeurons0303 health sciencesbiologyBehavior AnimalGeneral NeuroscienceBrain2800 General NeuroscienceLong-term potentiationArticlesPhenotype10076 Center for Integrative Human PhysiologyKnockout mouseFemalelearning and memory610 Medicine & healthGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesProsencephalon1300 General Biochemistry Genetics and Molecular Biologymental disorders1312 Molecular BiologyAnimalsLearningAPLP1Autistic DisorderSocial BehaviorMolecular BiologyAPLP2CA1 Region Hippocampal030304 developmental biologysynaptic plasticityGeneral Immunology and MicrobiologyAmyloid precursor proteinSynaptic plasticityForebrainSynapsesbiology.proteinAlzheimer570 Life sciences; biologyNeuroscience030217 neurology & neurosurgeryNeuroscienceThe EMBO journal
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CB1 Cannabinoid Receptors and On-Demand Defense Against Excitotoxicity

2003

Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protecti…

MaleCannabinoid receptorReceptors Drugmedicine.medical_treatment2-ArachidonoylglycerolExcitotoxicityHippocampal formationmedicine.disease_causeHippocampusMicechemistry.chemical_compoundPiperidinesCannabinoid receptor type 1Excitatory Amino Acid AgonistsReceptors Cannabinoidgamma-Aminobutyric AcidMice KnockoutNeuronsKainic AcidMultidisciplinaryBrainEndocannabinoid systemNeuroprotective AgentsMitogen-Activated Protein KinasesRimonabantSignal Transductionmedicine.medical_specialtyKainic acidPolyunsaturated AlkamidesGlutamic AcidMice TransgenicArachidonic AcidsIn Vitro TechniquesBiologyGlyceridesProsencephalonInternal medicinemedicineAnimalsFuransGenes Immediate-EarlyEpilepsyCannabinoidsBrain-Derived Neurotrophic FactorExcitatory Postsynaptic PotentialsMice Inbred C57BLEndocrinologyGene Expression Regulationnervous systemchemistryMutationPyrazolesCannabinoidNeuroscienceEndocannabinoidsScience
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Inverse behaviour of "synaptic" ribbon and spherule numbers in the pineal gland of male guinea-pigs exposed to continuous illumination.

1986

There is increasing evidence that pineal “synaptic” ribbons are a heterogeneous population of organelles. In addition to “synaptic” ribbons (SR) sensu stricto, which consist of an electron-dense rod surrounded by electronlucent vesicles, “synaptic” spherules (SS) exist, the electrondense core of which is round and much wider than that of the SR. In the guinea-pig SR and SS numbers exhibit an inverse day/night rhythmicity. To gain more insight into the functional significance of SR and SS, guinea-pigs were exposed to continuous illumination for approximately 4 months (LL) and the respective structures in the pineal gland were quantitated under the electron microscope and compared with contro…

MaleEmbryologyLightGuinea PigsSynaptic MembranesBiologyPineal GlandPinealocytelaw.inventionGuinea pigDiencephalonPineal glandlawParenchymaOrganellemedicineAnimalsSynaptic ribbonDose-Response Relationship RadiationCell BiologyAnatomyOrganoidsmedicine.anatomical_structureSynapsesBiophysicsAnatomyElectron microscopeDevelopmental BiologyAnatomy and embryology
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Nucleus incertus contribution to hippocampal theta rhythm generation.

2006

The hippocampal theta rhythm is generated by the pacemaker activity of the medial septum-diagonal band of Broca (MS/DBB) neurons. These nuclei are influenced by brainstem structures that modulate the theta rhythm. The aim of the present work is to determine whether the nucleus incertus (NI), which has important anatomical connections with the MS/DBB, contributes to the hippocampal theta rhythm generation in rats. Hippocampal field activity was recorded in urethane-anaesthetized rats. Electrical stimulation of the NI not only evoked theta rhythm in the hippocampus, but also decreased the amplitude of delta waves. Unit recordings in the NI revealed either a non-rhythm discharge pattern in mos…

MaleHippocampusStimulationHippocampal formationDiagonal Band of BrocaHippocampuschemistry.chemical_compoundRhythmMesencephalonNeural PathwaysmedicineAnimalsRats WistarTheta RhythmBrain MappingGeneral NeuroscienceNucleus IncertusDiagonal band of BrocaElectric StimulationRatsmedicine.anatomical_structurenervous systemMuscimolchemistryFemaleSeptum of BrainNeuroscienceNucleusMicroelectrodesThe European journal of neuroscience
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Neuroprotection of S(+) ketamine isomer in global forebrain ischemia

2001

The non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist ketamine can block the action of excitotoxic amino acids in the central nervous system. S(+) ketamine has a 2-3 times higher anesthetic potency compared with the ketamine-racemate and also shows a higher neuroprotective efficacy in vitro. To determine the neuroprotective activity of S(+) ketamine compared with its R(-) stereoisomer in vivo, we examined the functional and neurohistological outcome in rats treated 15 min after global forebrain ischemia with S(+) ketamine in different dosages compared with R(-) ketamine. Influence of the treatment on regional cerebral blood flow (rCBF) and cortical oxygen saturation (HbO2) was…

MaleIschemiaHippocampusPharmacologyNeuroprotectionBrain IschemiaOxygen ConsumptionProsencephalonmedicineAnimalsKetamineRats WistarMolecular BiologyCell DeathDose-Response Relationship Drugbusiness.industryGeneral NeuroscienceGlutamate receptorAntagonistStereoisomerismmedicine.diseaseRatsNeuroprotective AgentsAnesthesiaAnestheticNMDA receptorKetamineNeurology (clinical)businessExcitatory Amino Acid AntagonistsDevelopmental Biologymedicine.drugBrain Research
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