Search results for "Schaffer collateral"

showing 4 items of 4 documents

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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Gene Expression Profiling of Facilitated L-LTP in VP16-CREB Mice Reveals that BDNF Is Critical for the Maintenance of LTP and Its Synaptic Capture

2011

Expression of VP16-CREB, a constitutively active form of CREB, in hippocampal neurons of the CA1 region lowers the threshold for eliciting the late, persistent phase of long-term potentiation (L-LTP) in the Schaffer collateral pathway. This VP16-CREB-mediated L-LTP differs from the conventional late phase of LTP in not being dependent on new transcription. This finding suggests that in the transgenic mice the mRNA transcript(s) encoding the protein(s) necessary for this form of L-LTP might already be present in CA1 neurons in the basal condition. We used high-density oligonucleotide arrays to identify the mRNAs differentially expressed in the hippocampus of transgenic and wild-type mice. We…

MalePatch-Clamp TechniquesTime FactorsTransgeneNeuroscience(all)Long-Term PotentiationNerve Tissue ProteinsDynorphinHippocampal formationCREBHippocampusSynaptic TransmissionMiceNeurotrophic factorsMHC class ImedicineAnimalsRNA MessengerIn Situ HybridizationMice KnockoutNeuronsNeuronal PlasticitybiologyReverse Transcriptase Polymerase Chain ReactionBrain-Derived Neurotrophic FactorGene Expression Profilingmusculoskeletal neural and ocular physiologyGeneral NeuroscienceExcitatory Postsynaptic PotentialsHerpes Simplex Virus Protein Vmw65Long-term potentiationExonsCREB-Binding ProteinMolecular biologyCell biologymedicine.anatomical_structurenervous systemSchaffer collateralSynapsesbiology.proteinFemaleNeuron
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Neurocalcin-immunoreactive cells in the rat hippocampus are GABAergic interneurons

1998

Neurocalcin (NC) is a recently described calcium-binding protein isolated and characterized from bovine brain. NC belongs to the neural calcium-sensor proteins defined by the photoreceptor cell-specific protein recoverin that have been proposed to be involved in the regulation of calcium-dependent phosphorylation in signal transduction pathways. We analyzed the distribution and morphology of the NC-immunoreactive (IR) neurons in the rat dorsal hippocampus and the coexistence of NC with GABA and different neurochemical markers which label perisomatic inhibitory cells [parvalbumin (PV) and cholecystokinin (CCK)], mid-proximal dendritic inhibitory cells [calbindin D28k (CB)], distal dendritic …

NeurocalcinbiologyChemistryCognitive NeuroscienceDentate gyrusHippocampusHippocampal formationGranule cellmedicine.anatomical_structurenervous systemSchaffer collateralbiology.proteinmedicineCalretininNeuroscienceParvalbuminHippocampus
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A common thread for pain and memory synapses? Brain-derived neurotrophic factor and trkB receptors.

2003

Recent evidence indicates that trophic factors can exert fast effects on neurones and so alter synaptic plasticity. Here, we focus on brain-derived neurotrophic factor (BDNF), which exerts a modulatory action at hippocampal synapses that are involved in learning and memory, and at the first pain synapse between primary sensory neurones and dorsal horn neurones. Hippocampal and sensory neurones share some properties for the release of endogenous BDNF. In the Schaffer collateral pathway of the hippocampus, binding of BDNF to high-affinity trkB receptors is essential for the induction of long-term potentiation, a specific type of synaptic plasticity. However, the consequences of BDNF binding t…

PharmacologyBrain-derived neurotrophic factorBrain-Derived Neurotrophic FactorPainLong-term potentiationTropomyosin receptor kinase BToxicologyHippocampusSynapsemedicine.anatomical_structurenervous systemSchaffer collateralNeurotrophic factorsMemorySynaptic plasticityMetaplasticitySynapsesmedicineHumansReceptor trkBNeurons AfferentPsychologyNeuroscienceTrends in pharmacological sciences
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