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showing 10 items of 667 documents

Effects of Hippocampal State-Contingent Trial Presentation on Hippocampus-Dependent Nonspatial Classical Conditioning and Extinction

2014

Hippocampal local field potentials are characterized by two mutually exclusive states: one characterized by regular θ oscillations (∼4–8 Hz) and the other by irregular sharp-wave ripples. Presenting stimuli during dominant θ oscillations leads to expedited learning, suggesting that θ indexes a state in which encoding is most effective. However, ripple-contingent training also expedites learning, suggesting that any discrete brain state, much like the external context, can affect learning. We trained adult rabbits in trace eyeblink conditioning, a hippocampus-dependent nonspatial task, followed by extinction. Trials were delivered either in the presence or absence of θ or regardless of hippo…

General NeuroscienceConditioning ClassicalClassical conditioningHippocampusContext (language use)ArticlesLocal field potentialExtinction (psychology)Hippocampal formationHippocampusConditioning EyelidExtinction PsychologicalDevelopmental psychologyEyeblink conditioningAnimalsConditioningFemaleRabbitsPsychologyNeuroscienceThe Journal of Neuroscience
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Effects of histamine on dentate granule cells in vitro

1990

Abstract Hippocampal slices from rat brain were exposed to histamine and related substances in a perfusion chamber. Granule cells of the dentate gyrus were studied with conventional extra- and intracellular recording and a single electrode voltage clamp. Histamine caused, through activation of H 2 -receptors, a small depolarization, an increase in the number of synaptic and action potentials, a block of the long lasting (but not the early) component of spike afterhyperpolarizations and a reduction of the accommodation of action potential firing. These effects were mimicked by forskolin (suggests activation of adenylate cyclase). In voltage clamp, histamine blocked a long lasting calcium-dep…

General NeuroscienceDentate gyrusColforsinHistaminergicAction PotentialsRats Inbred StrainsIn Vitro TechniquesPerforant pathInhibitory postsynaptic potentialHippocampusMembrane PotentialsRatschemistry.chemical_compoundmedicine.anatomical_structurechemistryHistamine H2 receptormedicineExcitatory postsynaptic potentialBiophysicsAnimalsHistamine H3 receptorNeuroscienceHistamineAdenylyl CyclasesHistamineNeuroscience
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Identification of the cannabinoid receptor type 1 in serotonergic cells of raphe nuclei in mice.

2007

The endocannabinoid system (ECS) possesses neuromodulatory functions by influencing the release of various neurotransmitters, including GABA, noradrenaline, dopamine, glutamate and acetylcholine. Even though there are studies indicating similar interactions between the ECS and the serotonergic system, there are no results showing clear evidence for type 1 cannabinoid receptor (CB1) location on serotonergic neurons. In this study, we show by in situ hybridization that a low but significant fraction of serotonergic neurons in the raphe nuclei of mice contains CB1 mRNA as illustrated by the coexpression with the serotonergic marker gene tryptophane hydroxylase 2, the rate limiting enzyme for t…

Genetic MarkersSerotoninSerotonin uptakeBiologyTryptophan HydroxylaseSerotonergicHippocampuschemistry.chemical_compoundMiceNerve FibersReceptor Cannabinoid CB1Cannabinoid receptor type 1AnimalsRNA MessengerNeurotransmitterIn Situ HybridizationSerotonin Plasma Membrane Transport ProteinsMicroscopy ConfocalTPH2General NeuroscienceAmygdalaEndocannabinoid systemImmunohistochemistryIsoenzymesMice Inbred C57BLnervous systemchemistryDentate GyrusSynapsesRaphe NucleiFemaleSerotoninRaphe nucleiNeuroscienceNeuroscience
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A Novel 1,4-Dihydropyridine Derivative Improves Spatial Learning and Memory and Modifies Brain Protein Expression in Wild Type and Transgenic APPSweD…

2015

Ca2+ blockers, particularly those capable of crossing the blood-brain barrier (BBB), have been suggested as a possible treatment or disease modifying agents for neurodegenerative disorders, e.g., Alzheimer's disease. The present study investigated the effects of a novel 4-(N-dodecyl) pyridinium group-containing 1,4-dihydropyridine derivative (AP-12) on cognition and synaptic protein expression in the brain. Treatment of AP-12 was investigated in wild type C57BL/6J mice and transgenic Alzheimer's disease model mice (Tg APPSweDI) using behavioral tests and immunohistochemistry, as well as mass spectrometry to assess the blood-brain barrier (BBB) penetration. The data demonstrated the ability …

Genetically modified mouseMalePathologymedicine.medical_specialtyDihydropyridinesTime Factorsmedicine.drug_classTransgeneSpatial Learninglcsh:MedicineMice TransgenicBlood–brain barrierAnxiolyticGyrus CinguliHippocampus03 medical and health sciences0302 clinical medicineHomer Scaffolding ProteinsMemorymedicineAnimalsHumanslcsh:Science030304 developmental biology0303 health sciencesMultidisciplinaryAmyloid beta-PeptidesGlutamate Decarboxylaselcsh:RDihydropyridineWild typeBrainmedicine.disease3. Good healthMice Inbred C57BLmedicine.anatomical_structureAnti-Anxiety AgentsBlood-Brain BarrierSynaptic plasticitylcsh:QAlzheimer's diseaseCarrier ProteinsNeuroscience030217 neurology & neurosurgerymedicine.drugResearch ArticlePloS one
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Aβ and tau toxicities in Alzheimer’s are linked via oxidative stress-induced p38 activation: Protective role of vitamin E

2014

AbstractOxidative stress is a hallmark of Alzheimer’s disease (AD). We propose that rather than causing damage because of the action of free radicals, oxidative stress deranges signaling pathways leading to tau hyperphosphorylation, a hallmark of the disease. Indeed, incubation of neurons in culture with 5 µM beta-amyloid peptide (Aβ) causes an activation of p38 MAPK (p38) that leads to tau hyperphosphorylation. Inhibition of p38 prevents Aβ-induced tau phosphorylation. Aβ-induced effects are prevented when neurons are co-incubated with trolox (the water-soluble analog of vitamin E).We have confirmed these results in vivo, in APP/PS1 double transgenic mice of AD. We have found that APP/PS1 …

Genetically modified mouseMalemedicine.medical_specialtyCell signalingAntioxidantP-p38p38 mitogen-activated protein kinasesmedicine.medical_treatmentClinical BiochemistryMice Transgenictau ProteinsBiologyBeta-amyloidmedicine.disease_causeProtective AgentsBiochemistryHippocampusp38 Mitogen-Activated Protein KinasesArticlechemistry.chemical_compoundMiceAlzheimer DiseaseInternal medicinemental disordersmedicineVitamin EAnimalsPhosphorylationlcsh:QH301-705.5Cells CulturedNeuronslcsh:R5-920Amyloid beta-PeptidesVitamin EOrganic Chemistrymedicine.diseaseRatsDisease Models AnimalOxidative StressEndocrinologylcsh:Biology (General)chemistryTroloxAlzheimer's diseaseAntioxidantlcsh:Medicine (General)Oxidative stressRedox Biology
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A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model

2004

Alzheimer disease (AD) is characterized by excessive deposition of amyloid beta-peptides (A beta peptides) in the brain. In the nonamyloidogenic pathway, the amyloid precursor protein (APP) is cleaved by the alpha-secretase within the A beta peptide sequence. Proteinases of the ADAM family (adisintegrin and metalloproteinase) are the main candidates as physiologically relevant alpha-secretases, but early lethality of knockout animals prevented a detailed analysis in neuronal cells. To overcome this restriction, we have generated transgenic mice that overexpress either ADAM10 or a catalytically inactive ADAM10 mutant. In this report we show that a moderate neuronal overexpression of ADAM10 i…

Genetically modified mousePathologymedicine.medical_specialtyAmyloidAmyloidADAM10BACE1-ASGene ExpressionMice TransgenicHippocampusArticleAmyloid beta-Protein PrecursorMiceAlzheimer DiseaseEndopeptidasesAmyloid precursor proteinmedicineAnimalsAspartic Acid EndopeptidasesHumansbiologybusiness.industryP3 peptideAmyloidosisGeneral Medicinemedicine.diseaseCell biologyEnzyme ActivationDisease Models AnimalCommentarybiology.proteinErratumAlzheimer's diseaseAmyloid Precursor Protein SecretasesbusinessAmyloid precursor protein secretaseJournal of Clinical Investigation
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Mildronate improves cognition and reduces amyloid-β pathology in transgenic Alzheimer's disease mice

2013

Mildronate, a carnitine congener drug, previously has been shown to provide neuroprotection in an azidothymidine-induced mouse model of neurotoxicity and in a Parkinson's disease rat model. The aim of this study was to investigate the effects of mildronate treatment on cognition and pathology in Alzheimer's disease (AD) model mice (APP(SweDI)). Mildronate was administered i.p. daily at 50 or 100 mg/kg for 28 days. At the end of treatment, the animals were behaviorally and cognitively tested, and brains were assessed for AD-related pathology, inflammation, synaptic markers, and acetylcholinesterase (AChE). The data show that mildronate treatment significantly improved animal performance in w…

Genetically modified mousePathologymedicine.medical_specialtybiologyNeurotoxicityHippocampusWater mazemedicine.diseaseAcetylcholinesteraseNeuroprotectionCellular and Molecular Neurosciencechemistry.chemical_compoundchemistrySynaptic plasticitymedicineSynaptophysinbiology.proteinPsychologyJournal of Neuroscience Research
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P3‐039: Axonal neuritic pathology induces early presynaptic alterations in ps1/APP Alzheimer's mice hippocampus

2011

Loss of neurons in the hippocampus correlates with memory impairment in AD. Significant early reduction in the numerical density of hippocampal SOM interneurons was found in single (APPswe) and double (APPswe/ PS1dE9 and APPswe/TauP301S-G272V) transgenic models based on APP over expression and amyloid production. However, this inhibitory population was unaffected in age-matched single PS1 and tau transgenic mice as well as nontransgenic controls. Whereas SOM neuron loss in APPswe/PS1dE9 was associated to the onset of extracellular amyloid pathology in double APP/ tau mice this loss preceded plaque formation. Conclusions: As in human AD, somatostatin cell loss is a common early pathological …

Genetically modified mouseeducation.field_of_studyAmyloidEpidemiologyHealth PolicyTransgenePopulationHippocampusBiologyHippocampal formationInhibitory postsynaptic potentialPsychiatry and Mental healthCellular and Molecular NeuroscienceSomatostatinnervous systemDevelopmental Neurosciencemental disordersNeurology (clinical)Geriatrics and GerontologyeducationNeuroscienceAlzheimer's & Dementia
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Effects of neuron-specific ADAM10 modulation in an in vivo model of acute excitotoxic stress.

2008

A disintegrin and metalloprotease (ADAM) 10 is the main candidate enzyme for the alpha-secretase processing of the amyloid precursor protein (APP). Neuron-specific ADAM10 overexpression proved beneficial in the APP[V717I] mutant Alzheimer mouse model [Postina R, Schroeder A, Dewachter I, Bohl J, Schmitt U, Kojro E, Prinzen C, Endres K, Hiemke C, Blessing M, Flamez P, Dequenne A, Godaux E, van Leuven F, Fahrenholz F (2004) A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model. J Clin Invest 113:1456-1464]. Since Alzheimer patients have a high prevalence for epileptic seizures, we investigated the effects of ADAM10 modula…

Genetically modified mousemedicine.medical_specialtyIndolesADAM10TransgeneExcitotoxicityMice Transgenicmedicine.disease_causeNeuroprotectionHippocampusADAM10 ProteinAmyloid beta-Protein PrecursorMiceLeucineSeizuresStress PhysiologicalInternal medicineGlial Fibrillary Acidic ProteinmedicineAmyloid precursor proteinAnimalsNeuroinflammationNeuronsAnalysis of VarianceKainic AcidbiologyCell DeathDose-Response Relationship DrugChemistryGeneral NeuroscienceNeurodegenerationMembrane ProteinsValinemedicine.diseaseADAM ProteinsDisease Models AnimalEndocrinologyGene Expression RegulationMutationbiology.proteinAmyloid Precursor Protein SecretasesPlant LectinsNeuroscienceNeuroscience
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29 Elevated acetylcholine release in the hippocampus of transgenic mice expressing the human acetylcholinesterase

1998

Genetically modified mousemedicine.medical_specialtychemistry.chemical_compoundEndocrinologychemistryPhysiology (medical)General NeuroscienceInternal medicinemedicineHippocampusAcetylcholinesteraseAcetylcholinemedicine.drugJournal of Physiology-Paris
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