Search results for "CB"

showing 10 items of 647 documents

The endocannabinoid system controls key epileptogenic circuits in the hippocampus.

2006

SummaryBalanced control of neuronal activity is central in maintaining function and viability of neuronal circuits. The endocannabinoid system tightly controls neuronal excitability. Here, we show that endocannabinoids directly target hippocampal glutamatergic neurons to provide protection against acute epileptiform seizures in mice. Functional CB1 cannabinoid receptors are present on glutamatergic terminals of the hippocampal formation, colocalizing with vesicular glutamate transporter 1 (VGluT1). Conditional deletion of the CB1 gene either in cortical glutamatergic neurons or in forebrain GABAergic neurons, as well as virally induced deletion of the CB1 gene in the hippocampus, demonstrat…

MaleVesicular glutamate transporter 1HUMDISEASEHippocampusGene ExpressionHippocampal formationHippocampusMembrane Potentialschemistry.chemical_compoundMice0302 clinical medicineReceptor Cannabinoid CB1Premovement neuronal activitygamma-Aminobutyric Acid0303 health sciencesKainic AcidbiologyBehavior AnimalReverse Transcriptase Polymerase Chain Reactionmusculoskeletal neural and ocular physiologyGeneral NeurosciencePyramidal CellsCalcium Channel BlockersEndocannabinoid systemlipids (amino acids peptides and proteins)psychological phenomena and processesmedicine.drugKainic acidNeuroscience(all)MorpholinesGlutamic AcidMice TransgenicNaphthalenesMOLNEUROgamma-Aminobutyric acid03 medical and health sciencesGlutamatergicCannabinoid Receptor ModulatorsmedicineAnimals030304 developmental biologyAnalysis of VarianceEpilepsyBenzoxazinesMice Inbred C57BLnervous systemchemistryCalcium-Calmodulin-Dependent Protein KinasesVesicular Glutamate Transport Protein 1biology.proteinNerve NetSYSNEUROCalcium-Calmodulin-Dependent Protein Kinase Type 2Neuroscience030217 neurology & neurosurgeryEndocannabinoidsNeuron
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Biallelic mutations in neurofascin cause neurodevelopmental impairment and peripheral demyelination

2019

See Karakaya and Wirth (doi:10.1093/brain/awz273) for a scientific commentary on this article. Neurofascin (NFASC) isoforms are immunoglobulin cell adhesion molecules involved in node of Ranvier assembly. Efthymiou et al. identify biallelic NFASC variants in ten unrelated patients with a neurodevelopmental disorder characterized by variable degrees of central and peripheral involvement. Abnormal expression of Nfasc155 is accompanied by severe loss of myelinated fibres.

Male[SDV]Life Sciences [q-bio][SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyNerve Fibers MyelinatedGene FrequencyNeurodevelopmental Disorder[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]Nerve Growth FactorProtein IsoformsChildComputingMilieux_MISCELLANEOUSMyelin Sheathneurofascin; neurodevelopment; peripheral demyelinationAlleleneurodevelopmentDemyelinating DiseaseGenomicsneurodevelopment neurofascin peripheral demyelinationSettore MED/39 - Neuropsichiatria InfantilePedigree[SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunologyChild PreschoolPeripheral Nerve[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Femaleneurodevelopment; neurofascin; peripheral demyelinationNeurogliaHumanAdultAdolescentNervous System MalformationsGuillain-Barre SyndromeAxonNervous System MalformationneurofascinRanvier's NodesHumansNerve Growth FactorsPeripheral NervesAllelesAutoantibodiesperipheral demyelinationInfantProtein IsoformOriginal ArticlesAxonsnervous systemNeurodevelopmental DisordersCell Adhesion MoleculeMutationCell Adhesion MoleculesDemyelinating Diseases
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Adolescent Exposure to the Synthetic Cannabinoid WIN 55212-2 Modifies Cocaine Withdrawal Symptoms in Adult Mice

2017

Chronic cannabinoid consumption is an increasingly common behavior among teenagers and has been shown to cause long-lasting neurobehavioral alterations. Besides, it has been demonstrated that cocaine addiction in adulthood is highly correlated with cannabis abuse during adolescence. Cocaine consumption and subsequent abstinence from it can cause psychiatric symptoms, such as psychosis, cognitive impairment, anxiety, and depression. The aim of the present research was to study the consequences of adolescent exposure to cannabis on the psychiatric-like effects promoted by cocaine withdrawal in adult mice. We pre-treated juvenile mice with the cannabinoid CB1 receptor agonist WIN 55212-2 (WIN)…

MalecannabisCannabinoid receptormedicine.medical_treatment0302 clinical medicineCocaineDopamine Uptake InhibitorsReceptor Cannabinoid CB1Spectroscopymedia_commoncocaine withdrawalBehavior Animalbiologyadolescence; cannabis; WIN 55212-2; cocaine withdrawal; miceGeneral MedicineSubstance Withdrawal SyndromeComputer Science ApplicationsHindlimb SuspensionElevated plus mazePsychosismedicine.medical_specialtymiceMorpholinesmedia_common.quotation_subjectNaphthalenesArticleCatalysisInorganic ChemistryCocaine-Related Disorders03 medical and health sciencesMemoryInternal medicinemedicineAnimalsWIN 55212-2Physical and Theoretical ChemistryPsychiatryMolecular BiologyCannabinoid Receptor Agonistsbusiness.industryAddictionOrganic ChemistryAbstinencemedicine.diseasebiology.organism_classificationBenzoxazines030227 psychiatryEndocrinologyAnxiogenicExploratory BehavioradolescenceCannabisCannabinoidbusiness030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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Elevated AA/EPA Ratio Represents an Inflammatory Biomarker in Tumor Tissue of Metastatic Colorectal Cancer Patients

2019

Chronic inflammation increases the risk of developing certain types of cancer, such as colorectal cancer (CRC). The oxidative metabolism of polyunsaturated fatty acids (PUFAs) has a strong effect on colonic tumorigenesis and the levels of arachidonic acid (AA) and eicosapentaenoic acid (EPA) can contribute to the development of an inflammatory microenvironment. Aim of this study was to evaluate the possible differences in the AA/EPA ratio tissue levels between CRC patients with and without synchronous metastases. Moreover, the expression of the most important inflammatory enzymes and mediators, linked with the AA/EPA ratio, have been also assessed. Sixty-eight patients with CRC were enrolle…

Maleeicosapentaenoic acidColorectal cancermedicine.disease_causeMetastasislcsh:ChemistryReceptor Cannabinoid CB2chemistry.chemical_compoundMedicineArachidonate 15-LipoxygenaseNeoplasm Metastasislcsh:QH301-705.5Spectroscopychemistry.chemical_classificationGeneral MedicineEicosapentaenoic acidComputer Science ApplicationsGene Expression Regulation NeoplasticArachidonic acidArachidonic acidFemalelipids (amino acids peptides and proteins)medicine.symptomColorectal NeoplasmsPolyunsaturated fatty acidInflammationcolorectal cancerCatalysisArticleInorganic ChemistryBiomarkers TumorHumansmetastasisRNA MessengerPhysical and Theoretical ChemistryMolecular BiologyAgedInflammationbusiness.industryOrganic Chemistryinflammatory biomarkerCancermedicine.diseasePPAR gammalcsh:Biology (General)lcsh:QD1-999chemistryCancer researchbusinessCarcinogenesisInternational Journal of Molecular Sciences
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Dietary antioxidant supplementation did not affect declining sperm function with age in the mouse but did increase head abnormalities and reduced spe…

1998

The present study aims to ascertain whether dietary administration of a mixture of vitamins C and E may prevent the negative effects of paternal age on male fertility variables in the mouse. Experimental males were fed a standard diet supplemented with either a low or high dose of vitamins C and E. Oocytes enclosed in cumulus masses were inseminated using a 2 x 2 factorial design established according to whether males were young (3-4 months of age) or aged (22-24 months of age) and whether they were fed a control or antioxidant diet. Aged males showed a significant decrease in number of spermatozoa/mg epididymis when compared to young males. Dietary supplementation with low doses of vitamin…

Maleendocrine systemmedicine.medical_specialtyAgingAntioxidantmedicine.medical_treatmentAscorbic AcidFertilization in VitroBiologyAntioxidantsMiceInternal medicine[SDV.BDD] Life Sciences [q-bio]/Development BiologymedicineConceptusAnimalsVitamin ESpermatogenesis[SDV.BDLR] Life Sciences [q-bio]/Reproductive Biologyurogenital systemVitamin EEpididymisAscorbic acidSertoli cellSpermSpermatozoaDietMice Inbred C57BL[SDV.AEN] Life Sciences [q-bio]/Food and Nutritionmedicine.anatomical_structureEndocrinologyMice Inbred CBASperm HeadFemaleSpermatogenesis
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Prenatal exposure to PCB-153, p,p'-DDE and birth outcomes in 9000 mother-child pairs: exposure-response relationship and effect modifiers.

2014

Low-level exposure to polychlorinated biphenyl-153 (PCB-153) and dichlorodiphenyldichloroethylene (p-p′-DDE) can impair fetal growth; however, the exposure–response relationship and effect modifiers of such association are not well established. This study is an extension of an earlier European meta-analysis. Our aim was to explore exposure–response relationship between PCB-153 and p-p′-DDE and birth outcomes; to evaluate whether any no exposure–effect level and susceptible subgroups exist; and to assess the role of maternal gestational weight gain (GWG). We used a pooled dataset of 9377 mother–child pairs enrolled in 14 study populations from 11 European birth cohorts. General additive mode…

Malemedicine.medical_specialtyBirth weightDichlorodiphenyl Dichloroethylene[SDV]Life Sciences [q-bio]Biomarkers of exposurechemistry.chemical_compoundPregnancyInternal medicinemedicineBirth WeightHumansBiologyPrenatal exposureExposure responselcsh:Environmental sciencesGeneral Environmental Sciencelcsh:GE1-350Polychlorinated biphenyls (PCBs)PregnancyPersistent organic pollutantsDichlorodiphenyldichloroethylene (DDE)Infant NewbornPregnancy Outcomemedicine.diseaseMother child pairsPolychlorinated Biphenyls3. Good healthChemistryEndocrinologyDichlorodiphenyldichloroethylenechemistryMaternal ExposureGestationEnvironmental PollutantsFemalemedicine.symptomWeight gainDemography
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Adipocyte cannabinoid CB1 receptor deficiency alleviates high fat diet-induced memory deficit, depressive-like behavior, neuroinflammation and impair…

2019

Abstract Background Obesity is a low-grade inflammation condition that facilitates the development of numerous comorbidities and the dysregulation of brain homeostasis. Additionally, obesity also causes distinct behavioral alterations both in humans and rodents. Here, we investigated the effect of inducible genetic deletion of the cannabinoid type 1 receptor (CB1) in adipocytes (Ati-CB1-KO mice) on obesity-induced memory deficits, depressive-like behavior, neuroinflammation and adult neurogenesis. Methods Behavioral, mRNA expression and immunohistochemical studies were performed in Ati-CB1-KO mice and corresponding wild-type controls under standard and high-fat diet. Results Adipocyte-speci…

Malemedicine.medical_specialtyCannabinoid receptorNeurogenesisEndocrinology Diabetes and Metabolismmedicine.medical_treatmentInflammationDiet High-FatMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyNeural Stem CellsNeuritisReceptor Cannabinoid CB1AdipocyteInternal medicineAdipocytesmedicineAnimalsBiological PsychiatryNeuroinflammationMice KnockoutMemory DisordersBehavior AnimalDepressionEndocrine and Autonomic Systemsbusiness.industryNeurogenesisBrain030227 psychiatryAdult Stem CellsPsychiatry and Mental healthEndocrinologynervous systemchemistryGliosisOrgan SpecificityCannabinoidmedicine.symptombusinessGene Deletion030217 neurology & neurosurgeryHomeostasisPsychoneuroendocrinology
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Antidepressant-like behavioral effects of impaired cannabinoid receptor type 1 signaling coincide with exaggerated corticosterone secretion in mice.

2007

Hypothalamic-pituitary-adrenocortical (HPA) axis hyperactivity is associated with major depressive disorders, and treatment with classical antidepressants ameliorates not only psychopathological symptoms, but also the dysregulation of the HPA axis. Here, we further elucidated the role of impaired cannabinoid type 1 receptor (CB1) signaling for neuroendocrine and behavioral stress coping in the mouse forced swim test (FST). We demonstrate that the genetic inactivation of CB1 is accompanied by increased plasma corticosterone levels both under basal conditions and at different time points following exposure to the FST. The latter effect could be mimicked in C57BL/6N mice by acute, subchronic, …

Malemedicine.medical_specialtyCannabinoid receptorTime FactorsEndocrinology Diabetes and Metabolismmedicine.medical_treatmentAntidepressive Agents TricyclicStatistics NonparametricArticlechemistry.chemical_compoundMiceEndocrinologyRimonabantPiperidinesReceptor Cannabinoid CB1CorticosteroneDesipramineInternal medicineCannabinoid receptor type 1Adaptation PsychologicalmedicineAnimalsBiological PsychiatrySwimmingMice KnockoutAnalysis of VarianceEndocrine and Autonomic SystemsDepressionDesipramineMice Inbred C57BLPsychiatry and Mental healthDisease Models AnimalEndocrinologychemistrynervous systemPyrazoleslipids (amino acids peptides and proteins)FemaleCannabinoidRimonabantPsychologyCorticosteronehuman activitiesGlucocorticoidStress Psychologicalmedicine.drugBehavioural despair testSignal TransductionPsychoneuroendocrinology
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Impaired cannabinoid receptor type 1 signaling interferes with stress-coping behavior in mice.

2007

Dysregulation of the endocannabinoid system is known to interfere with emotional processing of stressful events. Here, we studied the role of cannabinoid receptor type 1 (CB1) signaling in stress-coping behaviors using the forced swim test (FST) with repeated exposures. We compared effects of genetic inactivation with pharmacological blockade of CB1 receptors both in male and female mice. In addition, we investigated potential interactions of the endocannabinoid system with monoaminergic and neurotrophin systems of the brain. Naive CB1 receptor-deficient mice (CB1-/-) showed increased passive stress-coping behaviors as compared to wild-type littermates (CB1+/+) in the FST, independent of se…

Malemedicine.medical_specialtyCannabinoid receptormedicine.medical_treatmentBiologyPharmacologyHippocampusMicePiperidinesReceptor Cannabinoid CB1Internal medicineCannabinoid receptor type 1MonoaminergicAdaptation PsychologicalGeneticsmedicineAnimalsBiogenic MonoaminesRNA MessengerReceptorMonoamine OxidaseSwimmingPharmacologyBrain-derived neurotrophic factormusculoskeletal neural and ocular physiologyBrain-Derived Neurotrophic FactorDesipraminefood and beveragesEndocannabinoid systemMice Inbred C57BLMonoamine neurotransmitterEndocrinologynervous systemVesicular Glutamate Transport Protein 1Molecular MedicinePyrazoleslipids (amino acids peptides and proteins)FemaleCannabinoidRimonabantpsychological phenomena and processesStress PsychologicalSignal TransductionThe pharmacogenomics journal
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Chronic l-DOPA treatment increases striatal cannabinoid CB1 receptor mRNA expression in 6-hydroxydopamine-lesioned rats

2000

Abstract The effect of a unilateral 6-hydroxydopamine (6-OHDA) lesion of the left medial forebrain bundle and 3 weeks treatment with l -DOPA of normal and 6-OHDA lesioned rats on CB1r mRNA expression was investigated by in situ hybridization. A 6-OHDA lesion of nigrostriatal pathway alone, confirmed by the loss of nigral tyrosine hydroxylase mRNA, did not alter CB1r mRNA levels in the dopamine depleted striatum. Similarly, chronic l -DOPA treatment of normal rats had no effect on striatal CB1r mRNA expression. In contrast, chronic l -DOPA treatment of 6-OHDA-lesioned rats significantly increased CB1r mRNA expression in the denervated striatum. These results suggest that the CB1r activity ma…

Malemedicine.medical_specialtyLevodopaanimal structuresTyrosine 3-MonooxygenaseReceptors DrugDopamine Agents-DOPANigrostriatal pathwayStriatumBiologySubthalamic nucleusStriatumLevodopaLesionAdrenergic AgentsDopamineInternal medicinemedicineAnimalsRNA MessengerRats WistarOxidopamineReceptors CannabinoidMedial forebrain bundleHydroxydopamineTyrosine hydroxylaseGeneral NeuroscienceMedial Forebrain BundleParkinson DiseaseCorpus StriatumRatsmedicine.anatomical_structureEndocrinologynervous systemSettore BIO/14 - Farmacologiamedicine.symptomCannabinoid CB1 receptor mRNA6-Hydroxydopaminemedicine.drugNeuroscience Letters
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