Search results for " Neurologic Mutants"

showing 4 items of 4 documents

Hedgehog signaling and primary cilia are required for the formation of adult neural stem cells.

2008

Neural stem cells that continue to produce neurons are retained in the adult hippocampal dentate gyrus. The mechanisms by which embryonic neural progenitors expand and transform into postnatal neural stem cells, an essential process for the continual production of neurons throughout life, remain unknown. We found that radial astrocytes, the postnatal progenitors in the dentate gyrus, failed to develop after embryonic ablation of ciliary genes or Smoothened (Smo), an essential component for Sonic hedgehog (Shh) signaling. Postnatal dentate neurogenesis failed in these mutant mice, and the dentate gyrus became severely hypotrophic. In contrast, expression of a constitutively active Smo (SmoM2…

AgingKinesinsHippocampal formationHippocampusReceptors G-Protein-CoupledMiceMice Neurologic MutantsAnimalsHedgehog ProteinsCiliaSonic hedgehogCells CulturedCell ProliferationMice KnockoutbiologyGeneral NeuroscienceDentate gyrusStem CellsNeurogenesisCell DifferentiationSmoothened ReceptorNeural stem cellHedgehog signaling pathwaySmoothened Receptornervous systemAstrocytesDentate Gyrusbiology.proteinSmoothenedNeuroscienceSignal TransductionNature neuroscience
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Retinal oxidation, apoptosis and age- and sex-differences in the mnd mutant mouse, a model of neuronal ceroid lipofuscinosis

2004

Retinal degeneration is an early and progressive event in many forms of neuronal ceroid lipofuscinoses (NCLs), a heterogeneous group of neurodegenerative disorders with unknown pathogenesis. We here used the mutant motor neuron degeneration (mnd) mouse, a late-infantile NCL variant, to investigate the retinal oxidative state and apoptotic cell death as a function of age and sex. Total superoxide dismutase (SOD) activities and thiobarbituric acid-reactive substance (TBARS) levels revealed progressive increases in retinal oxyradicals and lipid peroxides of mnd mice of both sexes. Female mnd retinas showed a higher oxidation rate and consistently exhibited the 4-hydroxy-2-nonenal (4-HNE)-adduc…

MaleRetinal degenerationPathologymedicine.medical_specialtyApoptosisBiologymedicine.disease_causeThiobarbituric Acid Reactive SubstancesRetinaMiceMice Neurologic Mutantschemistry.chemical_compoundSex FactorsNeuronal Ceroid-LipofuscinosesIn Situ Nick-End LabelingmedicineAnimalsOuter nuclear layerMolecular BiologyAldehydesRetinaTUNEL assayLipid peroxideCaspase 3Superoxide DismutaseGeneral NeuroscienceRetinal DegenerationRetinalmedicine.diseaseImmunohistochemistryEnzyme ActivationMice Inbred C57BLDisease Models AnimalOxidative Stressmedicine.anatomical_structureBiochemistrychemistryCaspasesFemaleNeuronal ceroid lipofuscinosisNeurology (clinical)Oxidation-ReductionOxidative stressDevelopmental BiologyBrain Research
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Antiabsence effects of carbenoxolone in two genetic animal models of absence epilepsy (WAG/Rij rats and lh/lh mice).

2005

Carbenoxolone (CBX), the succinyl ester of glycyrrhetinic acid, is an inhibitor of gap junctional intercellular communication. We have tested its possible effects upon two genetic animal models of epilepsy (WAG/Rij rats and lethargic (lh/lh) mice). Systemic administration of CBX was unable to significantly affect the occurrence of absence seizures in WAG/Rij rats. In particular, intravenous (5-40 mg/kg) or intraperitoneal (i.p.; 10-80 mg/kg) administration of CBX was unable to significantly modify the number and duration of spike-wave discharges (SWDs) in WAG/Rij rats, whereas the bilateral microinjection (0.05, 0.1, 0.5 and 1 microg/0.5 microl) of CBX into nucleus reticularis thalami (NRT)…

Malemedicine.medical_specialtyTime FactorsCarbenoxoloneConnexinConnexinsCellular and Molecular Neurosciencechemistry.chemical_compoundEpilepsyMiceMice Neurologic MutantsInternal medicinemedicineAnimalsGlycyrrhizinMicroinjectionGap junctionsPharmacologyDose-Response Relationship DrugGap junctionElectroencephalographyRats Inbred StrainsEpilepsy Carbenoxolone WAG/Rij rat Lethargic mouse Gap junction Connexin Absence seizuresmedicine.diseaseRatsDisease Models AnimalEndocrinologymedicine.anatomical_structurechemistryEpilepsy AbsenceGene Expression RegulationThalamic NucleiSystemic administrationCarbenoxoloneepilepsyAutoradiographyNucleusmedicine.drugGap junctions; Carbenoxolone ; epilepsyNeuropharmacology
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Perturbed interactions of mutant proteolipid protein/DM20 with cholesterol and lipid rafts in oligodendroglia: implications for dysmyelination in spa…

2006

Missense mutations in the humanPLP1gene lead to dysmyelinating diseases with a broad range of clinical severity, ranging from severe Pelizaeus–Merzbacher disease (PMD) to milder spastic paraplegia type 2 (SPG-2). The molecular pathology has been generally attributed to endoplasmic reticulum (ER) retention of misfolded proteolipid protein (PLP) (and its splice isoform DM20) and induction of the unfolded protein response. As opposed to previous studies of heterologous expression systems, we have analyzed PLP/DM20 trafficking in oligodendroglial cells, thereby revealing differences between PMD and SPG-2-associated PLP/DM20 isoforms. PLPA242Vand DM20A242V(jimpy-msdin mice), associated with seve…

Proteolipid protein 1Time FactorsLeupeptinsBlotting WesternGene Expressionchemical and pharmacologic phenomenaNerve Tissue ProteinsBiologyProtein degradationCysteine Proteinase InhibitorsTransfectionMiceMice Neurologic MutantsCricetulusMembrane MicrodomainsMutant proteinimmune system diseasesCricetinaeAnimalsImmunoprecipitationMyelin Proteolipid ProteinLipid raftCells CulturedGeneral NeuroscienceEndoplasmic reticulumCholesterol bindingER retentionArticlesImmunohistochemistryCell biologynervous system diseasesOligodendrogliaProtein TransportCholesterolBiochemistryUnfolded protein responselipids (amino acids peptides and proteins)Mutant ProteinsSubcellular FractionsThe Journal of neuroscience : the official journal of the Society for Neuroscience
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