Search results for "LONG-TERM POTENTIATION"

showing 10 items of 101 documents

Presynaptic nitric oxide/cGMP facilitates glutamate release via hyperpolarization-activated cyclic nucleotide-gated channels in the hippocampus

2011

In hippocampal neurons, synaptic transmission is affected by a variety of modulators, including nitric oxide (NO), which was proposed as a retrograde messenger as long as two decades ago. NO signals via two NO-sensitive guanylyl cyclases (NO-GCs) (NO-GC1 and NO-GC2) and the subsequent increase in cGMP. Lack of long-term potentiation in mice deficient in either one of the two NO-GCs demonstrates the involvement of both NO-GCs in synaptic transmission. However, the physiological consequences of NO/cGMP and the cellular mechanisms involved are unknown. Here, we analyzed glutamatergic synaptic transmission, most likely reflecting glutamate release, in the hippocampal CA1 region of NO-GC knockou…

General NeuroscienceGlutamate receptorLong-term potentiationHyperpolarization (biology)BiologyNeurotransmissionNitric oxideCell biologychemistry.chemical_compoundGlutamatergicBiochemistrychemistryRetrograde signalingSoluble guanylyl cyclaseEuropean Journal of Neuroscience
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Lack of APP and APLP2 in GABAergic Forebrain Neurons Impairs Synaptic Plasticity and Cognition.

2020

AbstractAmyloid-β precursor protein (APP) is central to the pathogenesis of Alzheimer’s disease, yet its physiological functions remain incompletely understood. Previous studies had indicated important synaptic functions of APP and the closely related homologue APLP2 in excitatory forebrain neurons for spine density, synaptic plasticity, and behavior. Here, we show that APP is also widely expressed in several interneuron subtypes, both in hippocampus and cortex. To address the functional role of APP in inhibitory neurons, we generated mice with a conditional APP/APLP2 double knockout (cDKO) in GABAergic forebrain neurons using DlxCre mice. These DlxCre cDKO mice exhibit cognitive deficits i…

InterneuronCognitive NeuroscienceLong-Term PotentiationSpatial LearningHippocampusAction PotentialsInhibitory postsynaptic potentialHippocampusNesting Behavior03 medical and health sciencesCellular and Molecular NeuroscienceAmyloid beta-Protein PrecursorMice0302 clinical medicineCognitionProsencephalonAmyloid precursor proteinmedicineAnimalsGABAergic NeuronsCA1 Region Hippocampal030304 developmental biologySpatial MemoryMice Knockout0303 health sciencesNeuronal PlasticitybiologyPyramidal CellsExcitatory Postsynaptic PotentialsLong-term potentiationmedicine.anatomical_structurenervous systemInhibitory Postsynaptic PotentialsSynaptic plasticityForebrainExcitatory postsynaptic potentialbiology.proteinNeuroscience030217 neurology & neurosurgeryCerebral cortex (New York, N.Y. : 1991)
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The expression mechanism of the residual LTP in the CA1 region of BDNF k.o. mice is insensitive to NO synthase inhibition

2011

Abstract BDNF and nitric oxide signaling both contribute to long-term potentiation (LTP) at glutamatergic synapses, but to date, few studies analyzed the interaction of both signaling cascades in the same synaptic pathway. Here we addressed the question whether the residual LTP in the CA1 region of hippocampal slices from heterozygous BDNF knockout mice (BDNF +/− ) is dependent on nitric oxide (NO) signaling. Extracellular recording of synaptic field potentials elicited by presynaptic Schaffer collateral stimulation was performed in the CA1 region of hippocampal slices of 4- to 6-week-old mice, and LTP was induced by a theta burst stimulation protocol. Application of the nitric oxide inhibi…

Long-Term PotentiationBiophysicsTropomyosin receptor kinase BIn Vitro TechniquesBiologyNitric oxideMicechemistry.chemical_compoundmedicineAnimalsEnzyme InhibitorsCA1 Region HippocampalMolecular BiologyMice KnockoutBrain-derived neurotrophic factorBrain-Derived Neurotrophic Factormusculoskeletal neural and ocular physiologyGeneral NeuroscienceExcitatory Postsynaptic PotentialsLong-term potentiationElectric StimulationCell biologyMice Inbred C57BLNG-Nitroarginine Methyl EsterSynaptic fatiguemedicine.anatomical_structureAnimals Newbornnervous systemchemistrySchaffer collateralSynaptic plasticityRetrograde signalingNeurology (clinical)Nitric Oxide SynthaseNeuroscienceDevelopmental BiologyBrain Research
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Cannabinoid CB1 Receptor Calibrates Excitatory Synaptic Balance in the Mouse Hippocampus

2015

The endocannabinoid system negatively regulates the release of various neurotransmitters in an activity-dependent manner, thereby influencing the excitability of neuronal circuits. In the hippocampus, cannabinoid type 1 (CB1) receptor is present on both GABAergic and glutamatergic axon terminals. CB1 receptor-deficient mice were previously shown to have increased hippocampal long-term potentiation (LTP). In this study, we have investigated the consequences of cell-type-specific deletion of the CB1 receptor on the induction of hippocampal LTP and on CA1 pyramidal cell morphology. Deletion of CB1 receptor in GABAergic neurons in GABA-CB1-KO mice leads to a significantly decreased hippocampal …

Long-Term PotentiationHippocampusHippocampal formationBiologyHippocampusSynaptic TransmissionMiceGlutamatergicReceptor Cannabinoid CB1medicineAnimalsAxonMice KnockoutNeuronal Plasticitymusculoskeletal neural and ocular physiologyGeneral NeuroscienceExcitatory Postsynaptic Potentialsfood and beveragesLong-term potentiationArticlesEndocannabinoid systemMice Inbred C57BLmedicine.anatomical_structurenervous systemSynapsesSynaptic plasticityGABAergiclipids (amino acids peptides and proteins)NeuroscienceThe Journal of Neuroscience
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Potentiation of the antitumor effects of both selective cyclooxygenase-1 and cyclooxygenase-2 inhibitors in human hepatic cancer cells by inhibition …

2007

The molecular mechanisms behind the anti-neoplastic effects of non-steroidal anti-inflammatory drugs (NSAIDs) are not completely understood and cannot be explained by the inhibition of the cyclooxygenase (COX) enzymes COX-1 and COX-2 alone. We previously reported that both the selective COX-1 inhibitor SC-560 and the selective COX-2 inhibitor CAY10404 exhibit anti-tumor effects in human hepatoma cells. NSAID inhibitors have many COX-independent actions and, among others, the mitogen-activated protein kinase (MAPK) pathways are targets for NSAIDs. Here, we examined the role of MEK/ERK1/2 signaling in the anti-neoplastic effects of both selective COX-1 and COX-2 inhibitors in two human hepato…

MAPK/ERK pathwayCancer ResearchCarcinoma HepatocellularTime FactorsBlotting WesternApoptosisPharmacologyCOX-1 COX-2 NSAIDs MEK1/2 ERK1/2NitrilesButadienesTumor Cells CulturedHumansCyclooxygenase InhibitorsSulfonesEnzyme InhibitorsPhosphorylationProtein kinase ACell ProliferationPharmacologychemistry.chemical_classificationMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinase 3biologyDose-Response Relationship DrugLiver NeoplasmsCytochromes cLong-term potentiationDrug SynergismIsoxazolesFlow CytometryEnzymeOncologychemistryCyclooxygenase 2CaspasesCancer cellbiology.proteinCyclooxygenase 1Molecular MedicineMEK-ERK PathwayPyrazolesDrug Therapy CombinationCyclooxygenaseHepatoma cellCancer biologytherapy
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Neural stem cell lineage-specific cannabinoid type-1 receptor regulates neurogenesis and plasticity in the adult mouse hippocampus

2018

Abstract Neural stem cells (NSCs) in the adult mouse hippocampus occur in a specific neurogenic niche, where a multitude of extracellular signaling molecules converges to regulate NSC proliferation as well as fate and functional integration. However, the underlying mechanisms how NSCs react to extrinsic signals and convert them to intracellular responses still remains elusive. NSCs contain a functional endocannabinoid system, including the cannabinoid type-1 receptor (CB1). To decipher whether CB1 regulates adult neurogenesis directly or indirectly in vivo, we performed NSC-specific conditional inactivation of CB1 by using triple-transgenic mice. Here, we show that lack of CB1 in NSCs is su…

Male0301 basic medicineCell signalingCannabinoid receptorNeurogenesisCognitive NeuroscienceLong-Term PotentiationMice Transgenicmouse hippocampus ; neural stem cells ; neurogenesis-dependent behavior ; CB1 ; adult neurogenesisHippocampal formationBiologyHippocampus03 medical and health sciencesCellular and Molecular Neurosciencemouse hippocampus0302 clinical medicineNeural Stem CellsReceptor Cannabinoid CB1Animalsreproductive and urinary physiologySpatial MemoryBehavior AnimalNeurogenesisLong-term potentiationOriginal ArticlesCB1Endocannabinoid systemneurogenesis-dependent behaviorNeural stem cellCell biologyadult neurogenesisMice Inbred C57BL030104 developmental biologynervous systemlipids (amino acids peptides and proteins)biological phenomena cell phenomena and immunityStem cell030217 neurology & neurosurgeryCerebral Cortex
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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
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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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High dose of 8-OH-DPAT decreases maximal dentate gyrus activation and facilitates granular cell plasticity in vivo.

2013

Although several studies have emphasized a crucial role for the serotonergic system in the control of hippocampal excitability, the role of serotonin (5-HT) and its receptors in normal and pathologic conditions, such as temporal lobe epilepsy (TLE), is still unclear. The present study was therefore designed firstly to investigate the acute effect of 8-OH-DPAT, a mixed 5-HT1A/7 receptor agonist, at a high dose (1 mg/kg, i.p.) known to have antiepileptic properties, in a model of acute partial epilepsy in rats. For this purpose, a maximal dentate activation (MDA) protocol was used to measure electrographic seizure onset and duration. In addition, the effect of 8-OH-DPAT on in vivo dentate gyr…

MaleAgonistSerotoninmedicine.medical_specialtymedicine.drug_classSerotonergic1AHippocampal formationDentate gyruSerotonergicSettore BIO/09 - FisiologiaRats Sprague-Dawleychemistry.chemical_compoundEpilepsyMemoryInternal medicineAnimalsMedicineDentate gyrusTemporal lobe epilepsySerotonin receptor5-HT receptor8-Hydroxy-2-(di-n-propylamino)tetralinNeuronal PlasticityDepressionbusiness.industry8-OH-DPATGeneral NeuroscienceDentate gyrusLong-term potentiationmedicine.diseaseRatsSerotonin Receptor AgonistsEndocrinologyDepression Mentalnervous systemchemistryReceptors SerotoninDentate Gyrusbusinessdrugs.Neuroscience
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Different electrophysiological actions of 24- and 72-hour aggregated amyloid-beta oligomers on hippocampal field population spike in both anesthetize…

2010

Diffusible oligomeric assemblies of the amyloid beta-protein (Abeta) could be the primary factor in the pathogenic pathway leading to Alzheimer's disease (AD). Converging lines of evidence support the notion that AD begins with subtle alterations in synaptic efficacy, prior to the occurrence of extensive neuronal degeneration. Recently, however, a shared or overlapping pathogenesis for AD and epileptic seizures occurred as aberrant neuronal hyperexcitability, as well as nonconvulsive seizure activity were found in several different APP transgenic mouse lines. This generated a renewed attention to the well-known comorbidity of AD and epilepsy and interest in how Abeta oligomers influence neu…

MaleAmyloidAmyloid betaHippocampusHippocampal formationMicroscopy Atomic ForceSettore BIO/09 - FisiologiaHippocampusRats Sprague-DawleyAtomic force microscopyAlzheimer's disease; Amyloid; Excitability; Oligomer; Atomic force microscopymental disordersAnimalsMolecular BiologyNeuronsAnalysis of VarianceExcitabilityAmyloid beta-PeptidesbiologyPerforant PathwayChemistryGeneral NeuroscienceDentate gyrusLong-term potentiationPopulation spikeAlzheimer's diseaseElectric StimulationPeptide FragmentsRatsElectrophysiologyElectrophysiologyOligomerbiology.proteinNeurology (clinical)NeuroscienceDevelopmental BiologyBrain research
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