Search results for "Neuroligin"

showing 4 items of 4 documents

Autism Related Neuroligin-4 Knockout Impairs Intracortical Processing but not Sensory Inputs in Mouse Barrel Cortex

2016

Neuroligin-4 (Nlgn4) is a cell adhesion protein that regulates synapse organization and function. Mutations in human NLGN4 are among the causes of autism spectrum disorders. In mouse, Nlgn4 knockout (KO) perturbs GABAergic synaptic transmission and oscillatory activity in hippocampus, and causes social interaction deficits. The complex profile of cellular and circuit changes that are caused by Nlgn4-KO is still only partly understood. Using Nlgn4-KO mice, we found that Nlgn4-KO increases the power in the alpha frequency band of spontaneous network activity in the barrel cortex under urethane anesthesia in vivo. Nlgn4-KO did not affect single-whisker-induced local field potentials, but suppr…

0301 basic medicineCell Adhesion Molecules NeuronalCognitive NeuroscienceHippocampusNeocortexNeuroliginSensory systemIn Vitro TechniquesNeurotransmissionMice03 medical and health sciencesCellular and Molecular NeuroscienceGlutamatergic0302 clinical medicineAnimalsEvoked PotentialsSynapse organizationMice KnockoutNeuronsAfferent PathwaysNeurotransmitter AgentsChemistryBarrel cortexElectric StimulationVoltage-Sensitive Dye Imaging030104 developmental biologyAnimals NewbornVibrissaeExcitatory postsynaptic potentialNerve NetNeuroscience030217 neurology & neurosurgeryCerebral Cortex
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Impaired hippocampal neuroligin-2 function by chronic stress or synthetic peptide treatment is linked to social deficits and increased aggression.

2014

Neuroligins (NLGNs) are cell adhesion molecules that are important for proper synaptic formation and functioning, and are critical regulators of the balance between neural excitation/inhibition (E/I). Mutations in NLGNs have been linked to psychiatric disorders in humans involving social dysfunction and are related to similar abnormalities in animal models. Chronic stress increases the likelihood for affective disorders and has been shown to induce changes in neural structure and function in different brain regions, with the hippocampus being highly vulnerable to stress. Previous studies have shown evidence of chronic stress-induced changes in the neural E/I balance in the hippocampus. Ther…

MaleRestraint PhysicalhippocampusmoodCell Adhesion Molecules NeuronalNeurexinstress disordersHippocampusPoison controlNeuroliginNerve Tissue ProteinsReceptors Cell Surfacebehavioral scienceHippocampal formationneuropharmacologyHippocampussocial behaviorRats Sprague-DawleystressmedicineNeuritesAnimalsChronic stressRats WistarSocial BehaviorCells CulturedPharmacologyNeuronsAggressionaggressionneuropeptideschronic restraint stressOrgan SizeanxietyRatsAggressionsociabilityPsychiatry and Mental healthChronic DiseaseOriginal Articleneuroliginmedicine.symptomPsychologyCorticosteronePeptidesNeuroscienceStress PsychologicalSocial behaviorNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
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The NG2 Protein Is Not Required for Glutamatergic Neuron-NG2 Cell Synaptic Signaling.

2014

NG2 glial cells (as from now NG2 cells) are unique in receiving synaptic input from neurons. However, the components regulating formation and maintenance of these neuron–glia synapses remain elusive. The transmembrane protein NG2 has been considered a potential mediator of synapse formation and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) clustering, because it contains 2 extracellular Laminin G/Neurexin/Sex Hormone-Binding Globulin domains, which in neurons are crucial for formation of transsynaptic neuroligin– neurexin complexes. NG2 is connected via Glutamate Receptor-Interacting Protein with GluA2/3-containing AMPARs, thereby possibly mediating receptor clus…

0301 basic medicineCognitive NeuroscienceNeurexinSynaptogenesisGlutamic AcidNeuroliginMice TransgenicBiologyNeurotransmissionHippocampusSynaptic Transmission03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinePostsynaptic potentialAnimalsReceptors AMPAAntigensNeuronsMembrane Proteins030104 developmental biologynervous systemSynaptic plasticitySynapsesProteoglycansSynaptic signalingNeurosciencePostsynaptic densityNeuroglia030217 neurology & neurosurgeryCerebral cortex (New York, N.Y. : 1991)
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A paradigmatic autistic phenotype associated with loss of PCDH11Y and NLGN4Y genes

2021

Abstract Background Most studies relative to Y chromosome abnormalities are focused on the sexual developmental disorders. Recently, a few studies suggest that some genes located on Y chromosome may be related to different neurodevelopment disorders. Case presentation We report a child with sexual developmental disorder associated with a peculiar phenotype characterized by severe language impairment and autistic behaviour associated with a mosaicism [45,X(11)/46,XY(89)] and a partial deletion of the short and long arm of Y chromosome (del Yp11.31q11.23) that also involves the loss of both PCDH11Y and NLGN4Y genes. To our knowledge no study has ever reported the occurrence of the lack of bot…

Male0301 basic medicinelcsh:Internal medicineMixed gonadal dysgenesilcsh:QH426-470Autism Spectrum DisorderCell Adhesion Molecules NeuronalNeuroliginProtocadherinCase ReportNeuroliginDevelopmental global delayBiologyY chromosome03 medical and health sciences0302 clinical medicineProtocadherinSettore M-PSI/08 - Psicologia ClinicaGeneticsmedicineHumanslcsh:RC31-1245ChildGenetics (clinical)GeneticsMosaicismMixed gonadal dysgenesismedicine.diseasePhenotypeSettore MED/39 - Neuropsichiatria InfantileHuman geneticsDevelopmental disorderlcsh:GeneticsPhenotype030104 developmental biologymedicine.anatomical_structureCerebral cortexAutism spectrum disorder030217 neurology & neurosurgeryBMC Medical Genomics
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