0000000000501478

AUTHOR

Susanne Tom Dieck

showing 2 related works from this author

Effects of Presynaptic Mutations on a Postsynaptic Cacna1s Calcium Channel Colocalized with mGluR6 at Mouse Photoreceptor Ribbon Synapses

2008

Purpose Photoreceptor ribbon synapses translate light-dependent changes of membrane potential into graded transmitter release via L-type voltage-dependent calcium channel (VDCC) activity. Functional abnormalities (e.g., a reduced electroretinogram b-wave), arising from mutations of presynaptic proteins, such as Bassoon and the VDCCalpha1 subunit Cacna1f, have been shown to altered transmitter release. L-type VDCCalpha1 subtype expression in wild-type and mutant mice was examined, to investigate the underlying pathologic mechanism. Methods Two antisera against Cacna1f, and a Cacna1f mouse mutant (Cacna1fDeltaEx14-17) were generated. Immunocytochemistry for L-type VDCCalpha1 subunits and addi…

MaleCalcium Channels L-TypeBlotting WesternPresynaptic TerminalsRibbon synapseBiologyReceptors Metabotropic GlutamateSynaptic TransmissionEpitopesMicePostsynaptic potentialAnimalsCalcium SignalingActive zoneFluorescent Antibody Technique IndirectMicroscopy ImmunoelectronSequence DeletionMembrane potentialSheepVoltage-dependent calcium channelReverse Transcriptase Polymerase Chain ReactionCalcium channelMetabotropic glutamate receptor 6ColocalizationAnatomyBlotting NorthernMice Mutant StrainsPeptide FragmentsCell biologyMice Inbred C57BLFemaleCalcium ChannelsRabbitssense organsPhotoreceptor Cells VertebrateInvestigative Opthalmology & Visual Science
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Proper synaptic vesicle formation and neuronal network activity critically rely on syndapin I

2011

Synaptic transmission relies on effective and accurate compensatory endocytosis. F-BAR proteins may serve as membrane curvature sensors and/or inducers and thereby support membrane remodelling processes; yet, their in vivo functions urgently await disclosure. We demonstrate that the F-BAR protein syndapin I is crucial for proper brain function. Syndapin I knockout (KO) mice suffer from seizures, a phenotype consistent with excessive hippocampal network activity. Loss of syndapin I causes defects in presynaptic membrane trafficking processes, which are especially evident under high-capacity retrieval conditions, accumulation of endocytic intermediates, loss of synaptic vesicle (SV) size cont…

General Immunology and MicrobiologyGeneral NeuroscienceEndocytic cycleBiologyNeurotransmissionEndocytosisActin cytoskeletonSynaptic vesicleGeneral Biochemistry Genetics and Molecular BiologyBulk endocytosisCell biologyMolecular BiologyDynaminMembrane invaginationThe EMBO Journal
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