Search results for " In utero"

showing 6 items of 6 documents

Neuronal LRP4 regulates synapse formation in the developing CNS

2017

The low-density lipoprotein receptor-related protein 4 (LRP4) is essential in muscle fibers for the establishment of the neuromuscular junction. Here, we show that LRP4 is also expressed by embryonic cortical and hippocampal neurons, and that downregulation of LRP4 in these neurons causes a reduction in density of synapses and number of primary dendrites. Accordingly, overexpression of LRP4 in cultured neurons had the opposite effect inducing more but shorter primary dendrites with an increased number of spines. Transsynaptic tracing mediated by rabies virus revealed a reduced number of neurons presynaptic to the cortical neurons in which LRP4 was knocked down. Moreover, neuron-specific kno…

0301 basic medicineDendritic spineRabiesSynaptogenesisHippocampusBiologyHippocampal formationHippocampusNeuromuscular junctionGene Knockout TechniquesMice03 medical and health sciences0302 clinical medicinemedicineAnimalsLrp4 ; Central Nervous System Development ; Synapse Formation ; Dendritogenesis ; Transsynaptic Tracing ; Agrin ; In Utero Electroporation ; Psd95 ; Bassoon ; MouseMolecular BiologyCells CulturedLDL-Receptor Related ProteinsCerebral CortexGene knockdownAgrinDendritesCortex (botany)Cell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureReceptors LDLnervous systemRabies virusSynapsesImmunology030217 neurology & neurosurgeryDevelopmental Biology
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NEGR1 and FGFR2 cooperatively regulate cortical development and core behaviours related to autism disorders in mice.

2018

See Contreras and Hippenmeyer (doi:10.1093/brain/awy218) for a scientific commentary on this article. Autism spectrum disorders (ASDs) are complex conditions with diverse aetiologies. Szczurkowska et al. demonstrate that two ASD-related molecules – FGFR2 and Negr1 – physically interact to act on the same downstream pathway, and regulate cortical development and ASD-relevant behaviours in mice. Identifying common mechanisms in ASDs may reveal targets for pharmacological intervention.

0301 basic medicineMAPK/ERK pathwaygenetic structuresAutism Spectrum DisorderFGFR2 signalingFibroblast growth factorReceptor tyrosine kinaseMiceautism; development; cell adhesion; in utero electroporation; FGFR2 signaling0302 clinical medicineCell MovementCerebral CortexMice KnockoutbiologyBehavior AnimalKinaseCell adhesion moleculeCell biologyProtein TransportSignal Transductionmusculoskeletal diseasesMAP Kinase Signaling SystemCell Adhesion Molecules NeuronalDendritic SpinesNeurogenesisautismDown-Regulationbehavioral disciplines and activities03 medical and health sciencesmental disordersmedicineAnimalsHumansAutistic DisorderReceptor Fibroblast Growth Factor Type 2developmentProtein kinase BFibroblast growth factor receptor 2Cell Membranecell adhesionOriginal Articlesin utero electroporationmedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologyHEK293 Cellsbiology.proteinAutismNeurology (clinical)030217 neurology & neurosurgeryBrain : a journal of neurology
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Prenatal diazepam exposure functionally alters the GABA(A) receptor that modulates [3H]noradrenaline release from rat hippocampal synaptosomes.

2002

In rats, exposure to diazepam (DZ) during the last week of gestation is associated with behavioral alterations (in some cases sexually dimorphic) that appear when the animals reach adulthood. This study was conducted to evaluate the effects of prenatal DZ exposure on the function of the gamma-aminobutyric (GABA)(A) receptor complex. The method used - perfusion of rat hippocampal nerve terminals labeled with [3H]noradrenaline (NA) - allowed us to evaluate the effects of DZ on a specific native GABA(A) receptor subtype which is located on hippocampal noradrenergic nerve endings and mediates the release of NA. Muscimol stimulated synaptosomal release of [3H]NA in a concentration-dependent mann…

Fetal ProteinsMaleBaclofenNerve Tissue ProteinsPregnanoloneBicucullinein uteroHippocampusGABA AntagonistsNorepinephrineAllosteric RegulationPregnancyAnimalsPicrotoxinRats WistarGABA AgonistsDiazepam In utero [3H]Noradrenaline release Synaptosomes GABAA receptor Allosteric modulationallosteric modulationDiazepamMental DisordersGABAA receptorReceptors GABA-ARatsProtein SubunitsPrenatal Exposure Delayed EffectsSettore BIO/14 - FarmacologiaFemaleSynaptosomesDevelopmental neuroscience
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Prospettive di terapia fetale.

2009

Terapia fetale terapia in uteroSettore MED/40 - Ginecologia E Ostetricia
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Valutazione dell'attività dell'asse ipotalamo-ipofisi-surrene, in seguito all'esposizione in utero a stress acuto e cronico nella progenie di ratto a…

2011

asse ipotalamo-ipofisi-surreneSettore BIO/14 - Farmacologiaprogenie di ratto adulta.esposizione in utero a stress acuto e cronico
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Indagini genetiche e trattamenti prenatali in utero della Sindrome Adreno Genitale (SAG) in una Coorte Siciliana.

2008

La deficienza dell'enzima 21 idrossilasi (21OHD) è la causa più comune di sindrome adrenogenitale (SAG). Il gene implicato è il CYP21 (6p21.3). La SAG è un problema clinico-sociale in quanto nel 95% dei casi genera l'iperandrogenismo dei neonati di sesso femminile. Il trattamento più effettuato in corso di virilizzazzione dei genitali femminili esterni è di tipo chirurgico (genitoplastica). Il trattamento prenatale in utero è una alternativa medica con il fine di compensare il difetto enzimatico e prevenire l'eccesso di androgeni in corso di morfogenesi fetale. Un nuovo protocollo diagnostico-terapeutico prenatale è stato sviluppato sulla base di una terapia precoce (alla 5° WG) con Desamet…

sindrome adrenogenitale Il gene CYP21 trattamento prenatale in utero.Settore MED/38 - Pediatria Generale E Specialistica
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