Search results for "hippocampu"

showing 10 items of 628 documents

Non-granule PSA-NCAM immunoreactive neurons in the rat hippocampus

2002

The polysialylated form of the neural cell adhesion molecule (PSA-NCAM) continues to be expressed in the adult hippocampus, mainly in a subset of neurons located in the innermost portion of the granule cell layer. PSA-NCAM immunoreactive neurons have also been described outside this layer in humans, where they are severely reduced in schizophrenic brains. Given this important clinical implication, we were interested in finding whether similar neurons existed in the adult rat hippocampus and to characterize their distribution, morphology and phenotype. PSA-NCAM immunocytochemistry reveals labeled neurons in the subiculum, fimbria, alveus, hilus, and stratum oriens, lucidum and radiatum of CA…

MaleInterneuronNeural Cell Adhesion Molecule L1Hippocampal formationHippocampusCalbindinImage Processing Computer-AssistedmedicineAnimalsNeuropeptide YFluorescent Antibody Technique IndirectNeural Cell Adhesion MoleculesMolecular Biologygamma-Aminobutyric AcidNeuronsbiologyGeneral NeuroscienceSubiculumGranule cellImmunohistochemistryRatsPhenotypemedicine.anatomical_structurenervous systemSialic Acidsbiology.proteinNeural cell adhesion moleculeNeurology (clinical)CalretininSomatostatinNeuroscienceParvalbuminDevelopmental BiologyBrain Research
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Hippocampal GABAergic Synapses Possess the Molecular Machinery for Retrograde Nitric Oxide Signaling

2007

Nitric oxide (NO) plays an important role in synaptic plasticity as a retrograde messenger at glutamatergic synapses. Here we describe that, in hippocampal pyramidal cells, neuronal nitric oxide synthase (nNOS) is also associated with the postsynaptic active zones of GABAergic symmetrical synapses terminating on their somata, dendrites, and axon initial segments in both mice and rats. The NO receptor nitric oxide-sensitive guanylyl cyclase (NOsGC) is present in the brain in two functional subunit compositions: α1β1and α2β1. The β1subunit is expressed in both pyramidal cells and interneurons in the hippocampus. Using immunohistochemistry andin situhybridization methods, we describe that the …

MaleInterneuronReceptors Cytoplasmic and NuclearNitric Oxide Synthase Type IBiologyNitric OxideHippocampusSynapseMiceSoluble Guanylyl CyclasemedicineAnimalsHumansRNA MessengerRats Wistargamma-Aminobutyric AcidMice Knockoutmusculoskeletal neural and ocular physiologyGeneral NeuroscienceArticlesAxon initial segmentRatsMice Inbred C57BLmedicine.anatomical_structurenervous systemGuanylate CyclaseSynaptic plasticitySynapsesbiology.proteinRetrograde signalingGABAergicSoluble guanylyl cyclaseNeuroscienceParvalbuminSignal Transduction
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The antibiotic erythromycin induces tolerance against transient global cerebral ischemia in rats (pharmacologic preconditioning).

2006

Background Cerebral ischemic tolerance can be induced by a variety of noxious stimuli, but no clinically applicable regimen for preconditioning has been described. Therefore, the authors tested the ability of a pharmacologic preconditioning strategy using the well-known macrolide antibiotic erythromycin to induce tolerance against transient global cerebral ischemia in vivo. They also investigated whether tolerance induction by erythromycin involves transcriptional and translational changes of cerebral B-cell leukemia/lymphoma-2 (bcl-2) expression. Methods Male Wistar rats were treated with erythromycin (25 mg/kg intramuscularly) or vehicle and subjected to 15 min of transient global cerebr…

MaleIschemiaHippocampusErythromycinPharmacologyNeuroprotectionHippocampusIn vivomedicineAnimalsRNA MessengerRats WistarIschemic PreconditioningAntibacterial agentNeuronsbusiness.industrymedicine.diseaseAnti-Bacterial AgentsErythromycinRatsTolerance inductionAnesthesiology and Pain MedicineProto-Oncogene Proteins c-bcl-2Ischemic Attack TransientImmunologyReperfusionIschemic preconditioningbusinessmedicine.drugAnesthesiology
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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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Bruce/apollon promotes hippocampal neuron survival and is downregulated by kainic acid

2005

Prolonged or excess stimulation of excitatory amino acid receptors leads to seizures and the induction of excitotoxic nerve cell injury. Kainic acid acting on glutamate receptors produces degeneration of vulnerable neurons in parts of the hippocampus and amygdala, but the exact mechanisms are not fully understood. We have here investigated whether the anti-apoptotic protein Bruce is involved in kainic acid-induced neurodegeneration. In the rat hippocampus and cortex, Bruce was exclusively expressed by neurons. The levels of Bruce were rapidly downregulated by kainic acid in hippocampal neurons as shown both in vivo and in cell culture. Caspase-3 was activated in neurons exhibiting low level…

MaleKainic acidCell SurvivalBiophysicsExcitotoxicityBruce/apollon Hippocampus Kainic acid Excitotoxicity Neuronal death Caspase-3 Cytochrome cDown-RegulationHippocampusStimulationBiologyHippocampal formationmedicine.disease_causeHippocampusBiochemistrychemistry.chemical_compoundDownregulation and upregulationmedicineAnimalsRats WistarMolecular BiologyCells CulturedNeuronsKainic AcidDose-Response Relationship DrugNeurodegenerationGlutamate receptorCell Biologymedicine.diseaseRatsCell biologynervous systemchemistryBiochemistryUbiquitin-Conjugating Enzymeshuman activitiescirculatory and respiratory physiology
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Zinc chelation during non-lesioning overexcitation results in neuronal death in the mouse hippocampus

2003

In the hippocampus, chelatable zinc is accumulated in vesicles of glutamatergic presynaptic terminals, abounding specially in the mossy fibers, from where it is released with activity and can exert a powerful inhibitory action upon N-methyl-D-aspartate receptors. Zinc is therefore in a strategic situation to control overexcitation at the zinc-rich excitatory synapses, and consequently zinc removal during high activity might result in excitotoxic neuronal damage. We analyzed the effect of zinc chelation with sodium dietyldithiocarbamate under overexcitation conditions induced by non-lesioning doses of kainic acid in the mouse hippocampus, to get insight into the role of zinc under overexcita…

MaleKainic acidSodiumchemistry.chemical_elementAMPA receptorPharmacologyInhibitory postsynaptic potentialHippocampusMicechemistry.chemical_compoundSeizuresmedicineAnimalsPremovement neuronal activityCell damageChelating AgentsNeuronsKainic AcidCell DeathGeneral NeuroscienceGlutamate receptormedicine.diseaseZincnervous systemBiochemistrychemistryNMDA receptorDitiocarbNeuroscience
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Neural overexcitation and implication of NMDA and AMPA receptors in a mouse model of temporal lobe epilepsy implying zinc chelation.

2006

Summary: Purpose: Zinc chelation with diethyldithiocarbamate (DEDTC) during nondamaging kainic acid administration enhances excitotoxicity to the level of cell damage. The objective of this work was to study the developing of the lesion in this model of temporal lobe epilepsy and the implications of the different types of glutamate receptors. Methods: The antagonist of the N-methyl-d-aspartate (NMDA) receptor MK-801, and the antagonist of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor GYKI52466, were used concomitantly with intraperitoneal administration of kainic acid (15 mg/kg) followed by DEDTC (150 mg/kg) in mouse. The animals were killed at different times from 4 …

MaleKainic acidmedicine.medical_specialtyExcitotoxicityHippocampusKainate receptorHSP72 Heat-Shock ProteinsAMPA receptorBiologymedicine.disease_causeHippocampusReceptors N-Methyl-D-AspartateSynaptic Transmissionchemistry.chemical_compoundBenzodiazepinesMiceReceptors Kainic AcidInternal medicinemedicineAnimalsReceptors AMPACell damageChelating AgentsKainic AcidCell DeathGlutamate receptormedicine.diseaseDisease Models AnimalZincEndocrinologyNeuroprotective Agentsnervous systemNeurologychemistryEpilepsy Temporal LobeNMDA receptorNeurology (clinical)Dizocilpine MaleateDitiocarbProto-Oncogene Proteins c-fosEpilepsia
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Role of the amygdala in antidepressant effects on hippocampal cell proliferation and survival and on depression-like behavior in the rat

2021

The stimulation of adult hippocampal neurogenesis by antidepressants has been associated with multiple molecular pathways, but the potential influence exerted by other brain areas has received much less attention. The basolateral complex of the amygdala (BLA), a region involved in anxiety and a site of action of antidepressants, has been implicated in both basal and stress-induced changes in neural plasticity in the dentate gyrus. We investigated here whether the BLA modulates the effects of the SSRI antidepressant fluoxetine on hippocampal cell proliferation and survival in relation to a behavioral index of depression-like behavior (forced swim test). We used a lesion approach targeting th…

MaleLong-Term Potentiationlcsh:MedicineHippocampal formationElement-Binding ProteinAmygdala/*drug effects/physiopathologyHippocampusMemory FormationRats Sprague-Dawleyddc:616.890302 clinical medicineMedial Prefrontal CortexElevated Plus-MazeSerotonin Uptake Inhibitors/*pharmacologylcsh:ScienceBasolateral Amygdala0303 health sciencesMultidisciplinaryNeuroscience/Behavioral NeuroscienceDepressionNeurogenesisBLAAmygdalaImmunohistochemistryChronic FluoxetineAdult-RatNeuroscience/Psychologymedicine.anatomical_structureFluoxetine/*pharmacologyDepression/*pathologyAntidepressantAntidepressive Agents Second-GenerationSelective Serotonin Reuptake InhibitorsResearch ArticleEstrèsElevated plus mazemedicine.medical_specialtyAnimal-ModelAntidepressive Agents Second-Generation/*pharmacologyCell SurvivalAmygdala03 medical and health sciencesFluoxetineNeuroplasticityHippocampus/cytology/*drug effectsmedicineAnimalsPsychiatryMaze Learning030304 developmental biologyCell Proliferationbusiness.industryDentate gyrusMental Health/Mood Disorderslcsh:RBasolateral complex of the amygdaleRatsCell Proliferation/*drug effectsDentate Gyruslcsh:QCell Survival/*drug effectsbusinessNeuroscience030217 neurology & neurosurgeryBasolateral amygdala
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Inactivation of glycogen synthase kinase-3β protects against kainic acid-induced neurotoxicity in vivo

2004

Many neurodegenerative diseases involve oxidative stress and excitotoxic cell death. In an attempt to further elucidate the signal transduction pathways involved in the cell death/cell survival associated with excitotoxicity, we have used an in vivo model of excitotoxicity employing kainic acid (KA)-induced neurotoxicity. Here, we show that extracellular signal-related kinase (ERK) 2, but not ERK 1, is phosphorylated and thereby activated in the hippocampus and cerebellum of kainic acid-treated mice. Phosphorylation and hence inactivation of glycogen synthase kinase 3beta (GSK-3beta), a general survival factor, is often a downstream consequence of mitogen-activated protein kinase pathway ac…

MaleMAPK/ERK pathwayKainic acidProgrammed cell deathTime FactorsCell SurvivalBlotting WesternExcitotoxicityTetrazolium Saltsmacromolecular substancesBiologymedicine.disease_causeHippocampusGlycogen Synthase Kinase 3Micechemistry.chemical_compoundOrgan Culture TechniquesGSK-3CerebellumNitrilesButadienesSerinemedicineAnimalsEnzyme InhibitorsPhosphorylationProtein kinase AMolecular BiologyMitogen-Activated Protein Kinase 1Glycogen Synthase Kinase 3 betaKainic AcidBehavior AnimalCell DeathKinaseGeneral NeuroscienceImmunohistochemistryCell biologyEnzyme ActivationThiazolesBiochemistrychemistryTyrosineNeurotoxicity SyndromesNeurology (clinical)Signal transductionLithium ChlorideDevelopmental BiologyBrain Research
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Understanding Cannabinoid Psychoactivity with Mouse Genetic Models

2007

Marijuana and its main psychotropic ingredient Δ9-tetrahydrocannabinol (THC) exert a plethora of psychoactive effects through the activation of the neuronal cannabinoid receptor type 1 (CB1), which is expressed by different neuronal subpopulations in the central nervous system. The exact neuroanatomical substrates underlying each effect of THC are, however, not known. We tested locomotor, hypothermic, analgesic, and cataleptic effects of THC in conditional knockout mouse lines, which lack the expression of CB1 in different neuronal subpopulations, including principal brain neurons, GABAergic neurons (those that release γ aminobutyric acid), cortical glutamatergic neurons, and neurons expres…

MaleMESH: Body TemperatureCannabinoid receptormedicine.medical_treatmentGene ExpressionMESH: Receptor Cannabinoid CB1NeocortexMESH: gamma-Aminobutyric AcidMESH: CatalepsyPharmacologyHippocampusMESH: Mice KnockoutMESH: Corpus StriatumBody TemperatureMESH: Autonomic Nervous SystemMESH: NeocortexMice0302 clinical medicineReceptor Cannabinoid CB1MESH: Behavior AnimalCannabinoid receptor type 1MESH: AnimalsMESH: Gene SilencingDronabinolMESH: NociceptorsBiology (General)gamma-Aminobutyric AcidMice Knockout0303 health sciencesBehavior Animalmusculoskeletal neural and ocular physiologyGeneral NeuroscienceMESH: Pain ThresholdNociceptorsMESH: Glutamic AcidMESH: InterneuronsMESH: Motor Activity3. Good healthGABAergicMESH: TetrahydrocannabinolGeneral Agricultural and Biological SciencesResearch Articlemedicine.drugPain ThresholdMESH: Gene ExpressionMESH: Psychotropic DrugsQH301-705.5Glutamic AcidMotor ActivityBiologyAutonomic Nervous SystemGeneral Biochemistry Genetics and Molecular Biologygamma-Aminobutyric acid03 medical and health sciencesGlutamatergicDopamine receptor D1InterneuronsCannabinoid Receptor Modulatorsmental disorders[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineAnimalsGenetic Predisposition to Disease[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyGene SilencingTetrahydrocannabinolMESH: MiceAnesthesiology and Pain Management030304 developmental biologyPharmacologyCatalepsyPsychotropic DrugsModels GeneticGeneral Immunology and MicrobiologyCannabinoidsIllicit Drugsorganic chemicalsMESH: MaleCorpus StriatumPrimerDisease Models Animalnervous systemCannabinoidNervous System Diseases030217 neurology & neurosurgeryNeurosciencePLoS Biology
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