Search results for "Knockout mouse"

showing 10 items of 81 documents

Altered brain concentrations of citalopram and escitalopram in P-glycoprotein deficient mice after acute and chronic treatment

2013

Background: According to both in vitro and in vivo data P-glycoprotein (P-gp) may restrict the uptake of several antidepressants into the brain, thus contributing to the poor success rate of current antidepressant therapies. The therapeutic activity of citalopram resides in the Senantiomer, whereas the R-enantiomer is practically devoid of serotonin reuptake potency. To date, no in vivo data are available that address whether the enantiomers of citalopram and its metabolites are substrates of P-gp. Methods: P-gp knockout (abcb1ab (-/-)) and wild-type (abcb1ab (+/+)) mice underwent acute (single-dose) and chronic (two daily doses for 10 days) treatment with citalopram (10 mg/kg) or escitalop…

MaleMedicin och hälsovetenskapescitalopramenantiomersCitaloprammice knockoutP-glycoproteinCitalopramPharmacologyMedical and Health Sciencesbehavioral disciplines and activitiesMiceIn vivomental disordersmedicineAnimalsEscitalopramPotencyPharmacology (medical)ATP Binding Cassette Transporter Subfamily B Member 1Biological PsychiatryP-glycoproteinMice KnockoutPharmacologybiologybusiness.industryBrainPsychiatry and Mental healthNeurologyKnockout mousebiology.proteinAntidepressive Agents Second-GenerationAntidepressantNeurology (clinical)Enantiomerbusinessmedicine.drugEuropean Neuropsychopharmacology
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Changes in the expression of neurotransmitter receptors in Parkin and DJ-1 knockout mice – A quantitative multireceptor study

2015

Parkinson's disease (PD) is a well-characterized neurological disorder with regard to its neuropathological and symptomatic appearance. At the genetic level, mutations of particular genes, e.g. Parkin and DJ-1, were found in human hereditary PD with early onset. Neurotransmitter receptors constitute decisive elements in neural signal transduction. Furthermore, since they are often altered in neurological and psychiatric diseases, receptors have been successful targets for pharmacological agents. However, the consequences of PD-associated gene mutations on the expression of transmitter receptors are largely unknown. Therefore, we studied the expression of 16 different receptor binding sites …

MaleMice KnockoutOncogene ProteinsUbiquitin-Protein LigasesGeneral NeuroscienceProtein Deglycase DJ-1Glutamate receptorBrainKainate receptorPeroxiredoxinsAMPA receptorNeurotransmissionBiologyParkinReceptors NeurotransmitterMice Inbred C57BLParkinsonian DisordersNeurotransmitter receptorKnockout mouseAnimalsAutoradiographyReceptorNeuroscienceNeuroscience
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Toll-like receptor 4 defective mice carrying point or null mutations do not show increased susceptibility toCandida albicansin a model of hematogenou…

2006

We have studied the role of TLR4 in murine defenses against Candida albicans in two TLR4-defective mouse strains: C3H/HeJ mice which have defective TLR4 signaling, and TLR4-/- knockout mice. Both TLR4-defective mice strains experimentally infected with virulent C. albicans cells showed no significant difference in survival as compared with their respective controls. Recruitment of neutrophils to the peritoneal cavity of i.p. infected mice was not affected in TLR4-/-animals, but significantly enhanced in C3H/HeJ mice, compared with their control mice. In vitro production of TNF-alpha by macrophages from both types of TLR4-defective mice, in response to yeasts and hyphae of C. albicans, was n…

MaleNeutrophilsBiologyMicrobiologyInterferon-gammaMicePeritoneal cavityCandida albicansSplenocytemedicineAnimalsPoint MutationGenetic Predisposition to DiseaseCandida albicansMice KnockoutMice Inbred C3HToll-like receptorTumor Necrosis Factor-alphaCandidiasisGeneral MedicineTh1 CellsFlow Cytometrybiology.organism_classificationInterleukin-12Corpus albicansMice Inbred C57BLToll-Like Receptor 4Infectious Diseasesmedicine.anatomical_structureKnockout mouseMacrophages PeritonealTLR4Femalelipids (amino acids peptides and proteins)Tumor necrosis factor alphaMedical Mycology
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Connexin36 (Cx36) expression and protein detection in the mouse carotid body and myenteric plexus

2013

AbstractAlthough connexin36 (Cx36) has been studied in several tissues, it is notable that no data are available on Cx36 expression in the carotid body and the intestine. The present study was undertaken to evaluate using immunohistochemistry, PCR and Western blotting procedures, whether Cx36 was expressed in the mouse carotid body and in the intestine at ileum and colon level. In the carotid body, Cx36 was detected as diffuse punctate immunostaining and as protein by Western blotting and mRNA by RT-PCR. Cx36 punctate immunostaining was also evident in the intestine with localization restricted to the myenteric plexus of both the ileum and the colon, and this detection was also confirmed by…

MalePathologymedicine.medical_specialtyHistologyMousegenetic structuresMyenteric plexusBlotting WesternIleumConnexinBiologySettore BIO/09 - FisiologiaConnexinsMice03 medical and health sciences0302 clinical medicinemedicineAnimalsGap junctionsMyenteric plexus030304 developmental biologyMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionGap junctions Carotid body Myenteric plexus Connexin Cx36 MouseCell BiologyGeneral MedicineImmunohistochemistryMolecular biologyMice Inbred C57BLBlotCarotid bodymedicine.anatomical_structureReal-time polymerase chain reactionCx36Knockout mouseImmunohistochemistryCarotid bodysense organs030217 neurology & neurosurgeryImmunostaining
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Synaptic vesicle alterations in rod photoreceptors of synaptophysin-deficient mice.

2001

Abstract The abundance of the integral membrane protein synaptophysin in synaptic vesicles and its multiple possible functional contributions to transmitter exocytosis and synaptic vesicle formation stand in sharp contrast to the observed lack of defects in synaptophysin knockout mice. Assuming that deficiencies are compensated by the often coexpressed synaptophysin isoform synaptoporin, we now show that retinal rod photoreceptors, which do not synthesize synaptoporin either in wild-type or in knockout mice, are affected by the loss of synaptophysin. Multiple pale-appearing photoreceptors, as seen by electron microscopy, possess reduced cytoplasmic electron density, swollen mitochondria, an…

MalePresynaptic TerminalsSynaptophysinAction PotentialsFluorescent Antibody TechniqueDark AdaptationBiologyRibbon synapseSynaptic vesicleSynaptic TransmissionExocytosisExocytosisMiceRetinal Rod Photoreceptor CellsElectroretinographySynaptic vesicle recyclingAnimalsMice KnockoutSex CharacteristicsGeneral NeuroscienceVesicleMembrane ProteinsClathrin-Coated VesiclesSynaptoporinCell biologyMice Inbred C57BLMicroscopy ElectronProtein TransportKnockout mouseSynaptophysinbiology.proteinFemaleSynaptic VesiclesNeurosciencePhotic StimulationNeuroscience
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Detection of behavioral alterations and learning deficits in mice lacking synaptophysin.

2009

The integral membrane protein synaptophysin is one of the most abundant polypeptide components of synaptic vesicles. It is not essential for neurotransmission despite its abundance but is believed to modulate the efficiency of the synaptic vesicle cycle. Detailed behavioral analyses were therefore performed on synaptophysin knockout mice to test whether synaptophysin affects higher brain functions. We find that these animals are more exploratory than their wild type counterparts examining novel objects more closely and intensely in an enriched open field arena. We also detect impairments in learning and memory, most notably reduced object novelty recognition and reduced spatial learning. Th…

Mice KnockoutbiologyBehavior AnimalGeneral NeuroscienceWild typeSynaptophysinVisual AcuityLong-term potentiationRecognition PsychologyNeurotransmissionSynaptic vesicle cycleSynaptic vesicleOpen fieldMiceMemoryKnockout mouseSynaptophysinbiology.proteinElectroretinographyExploratory BehaviorAnimalsLearningPsychologyNeuroscienceNeuroscience
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Lack of GDAP1 induces neuronal calcium and mitochondrial defects in a knockout mouse model of Charcot-Marie-tooth neuropathy

2015

27 páginas, 9 figuras.

Mitochondrial proteinCancer Researchlcsh:QH426-470Nerve Tissue ProteinsBiologyMitochondrionCharcot-Marie-Tooth diseaseGDAP1 geneMiceGeneticsAutophagyAnimalsCalcium SignalingMolecular BiologyGenetics (clinical)Ecology Evolution Behavior and SystematicsCytoskeletonCalcium signalingGeneticsVoltage-dependent calcium channelEndoplasmic reticulumAutophagyBiología y Biomedicina / BiologíaAxonsCell biologyMitochondriaMitochondrialMice Inbred C57BLAlpha tubulinlcsh:Geneticsmitochondrial fusionKnockout mouseMitochondrial fissionCalcium ChannelsAnimal cellGene DeletionResearch Article
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Transcriptome comparison of murine wild-type and synaptophysin-deficient retina reveals complete identity

2005

Loss of synaptophysin, one of the major synaptic vesicle membrane proteins, is surprisingly well tolerated in knockout mice. To test whether compensatory gene transcription accounts for the apparent lack of functional deficiencies, comparative transcriptome analyses were carried out. The retina was selected as the most suitable tissue since morphological alterations were observed in mutant photoreceptors, most notably a reduction of synaptic vesicles and concomitant increase in clathrin-coated vesicles. Labeled cRNA was prepared in triplicate from retinae of age- and sex-matched wild-type and mutant litter mates and hybridized to high-density microarray chips. Only three differentially expr…

MutantSynaptophysinSynaptic vesicleRetinaTranscriptomeMiceMicroscopy Electron TransmissionGene expressionAnimalsPhotoreceptor CellsRNA MessengerEye ProteinsMolecular BiologyMice KnockoutbiologyReverse Transcriptase Polymerase Chain ReactionSynaptic vesicle membraneGeneral NeuroscienceWild typeGlucan 13-beta-GlucosidaseMicroarray AnalysisMolecular biologyClathrinMice Inbred C57BLGene Expression RegulationKnockout mouseSynaptophysinbiology.proteinSynaptic VesiclesNeurology (clinical)Developmental BiologyBrain Research
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Disruption of Slc4a10 augments neuronal excitability and modulates synaptic short-term plasticity

2015

Slc4a10 is a Na(+)-coupled Cl(-)-HCO3 (-) exchanger, which is expressed in principal and inhibitory neurons as well as in choroid plexus epithelial cells of the brain. Slc4a10 knockout (KO) mice have collapsed brain ventricles and display an increased seizure threshold, while heterozygous deletions in man have been associated with idiopathic epilepsy and other neurological symptoms. To further characterize the role of Slc4a10 for network excitability, we compared input-output relations as well as short and long term changes of evoked field potentials in Slc4a10 KO and wildtype (WT) mice. While responses of CA1 pyramidal neurons to stimulation of Schaffer collaterals were increased in Slc4a1…

Neocortexsynaptic plasticitySeizure thresholdGABAergic inhibitionNeural facilitationHippocampusLong-term potentiationBiologyInhibitory postsynaptic potentiallcsh:RC321-571field potentialCellular and Molecular Neurosciencemedicine.anatomical_structureKnockout mouseSynaptic plasticitymedicineLTPNeuroscienceSLC4A10lcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal ResearchNeuroscienceFrontiers in Cellular Neuroscience
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the role of mitochondrial aldehyde dehydrognase (ALDH-2) for bioactivation of organic nitrates: “Proof of concept” through investigations in ALDH-2 k…

2006

Pharmacologychemistry.chemical_classificationchemistrybiologyBiochemistryPhysiologyStereochemistryKnockout mousebiology.proteinMolecular MedicineAldehyde dehydrogenaseAldehydeOrganic nitratesVascular Pharmacology
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