Brandt, Andreas

[["dc.bibliographiccitation.firstpage","11577"],["dc.bibliographiccitation.issue","50"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","11585"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Brandt, Andreas"],["dc.contributor.author","Khimich, Darina"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2017-09-07T11:53:40Z"],["dc.date.available","2017-09-07T11:53:40Z"],["dc.date.issued","2005"],["dc.description.abstract","Hearing relies on faithful sound coding at hair cell ribbon synapses, which use Ca2+-triggered glutamate release to signal with submillisecond precision. Here, we investigated stimulus-secretion coupling at mammalian inner hair cell (IHC) synapses to explore the mechanisms underlying this high temporal fidelity. Using nonstationary fluctuation analysis on Ca2+ tail currents, we estimate that IHCs contain similar to 1700 Ca2+ channels, mainly of Ca(V)1.3 type. We show by immunohistochemistry that the Ca(V)1.3 Ca2+ channels are localized preferentially at the ribbon-type active zones of IHCs. We argue that each active zone holds similar to 80 Ca2+ channels, of which probably < 10 open simultaneously during physiological stimulation. We then manipulated the Ca2+ current by primarily changing single-channel current or open-channel number. Effects on exocytosis of the readily releasable vesicle pool (RRP) were monitored by membrane capacitance recordings. Consistent with the high intrinsic Ca2+ cooperativity of exocytosis, RRP exocytosis changed nonlinearly with the Ca2+ current when varying the single-channel current. In contrast, the apparent Ca2+ cooperativity of RRP exocytosis was close to unity when primarily manipulating the number of open channels. Our findings suggest a Ca2+ channel-release site coupling in which few nearby Ca(V)1.3 channels impose high nanodomain [Ca2+] on release sites in IHCs during physiological stimulation. We postulate that the IHC ribbon synapse uses this Ca2+ nanodomain control of exocytosis to signal with high temporal precision already at low sound intensities."],["dc.identifier.doi","10.1523/JNEUROSCI.3411-05.2005"],["dc.identifier.gro","3143772"],["dc.identifier.isi","000233942200011"],["dc.identifier.pmid","16354915"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1322"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Few Ca(V)1.3 channels regulate the exocytosis of a synaptic vesicle at the hair cell ribbon synapse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","The Journal of Physiological Sciences"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Frank, Thomas"],["dc.contributor.author","Pangsric, Tina"],["dc.contributor.author","Neef, Jakob"],["dc.contributor.author","Brandt, Andreas"],["dc.contributor.author","Meyer, Alexander C."],["dc.contributor.author","Egner, Alexander"],["dc.contributor.author","Striessnig, Joerg"],["dc.contributor.author","Gregg, Ronald R."],["dc.contributor.author","Petit, Christine"],["dc.contributor.author","Schwaller, Beat"],["dc.contributor.author","Khimich, Darina"],["dc.date.accessioned","2018-11-07T08:34:55Z"],["dc.date.available","2018-11-07T08:34:55Z"],["dc.date.issued","2009"],["dc.format.extent","30"],["dc.identifier.isi","000271023100099"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17937"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Tokyo"],["dc.relation.issn","1880-6546"],["dc.title","Molecular Physiology Of The Hair Cell Ribbon Synapse"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","347"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","359"],["dc.bibliographiccitation.volume","326"],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Brandt, Andreas"],["dc.contributor.author","Lysakowski, Anna"],["dc.date.accessioned","2017-09-07T11:52:28Z"],["dc.date.available","2017-09-07T11:52:28Z"],["dc.date.issued","2006"],["dc.description.abstract","Hearing and balance rely on the faithful synaptic coding of mechanical input by the auditory and vestibular hair cells of the inner ear. Mechanical deflection of their stereocilia causes the opening of mechanosensitive channels, resulting in hair cell depolarization, which controls the release of glutamate at ribbon-type synapses. Hair cells have a compact shape with strong polarity. Mechanoelectrical transduction and active membrane turnover associated with stereociliar renewal dominate the apical compartment. Transmitter release occurs at several active zones along the basolateral membrane. The astonishing capability of the hair cell ribbon synapse for temporally precise and reliable sensory coding has been the subject of intense investigation over the past few years. This research has been facilitated by the excellent experimental accessibility of the hair cell. For the same reason, the hair cell serves as an important model for studying presynaptic Ca(2+) signaling and stimulus-secretion coupling. In addition to common principles, hair cell synapses differ in their anatomical and functional properties among species, among the auditory and vestibular organs, and among hair cell positions within the organ. Here, we briefly review synaptic morphology and connectivity and then focus on stimulus-secretion coupling at hair cell synapses."],["dc.identifier.doi","10.1007/s00441-006-0276-3"],["dc.identifier.gro","3143595"],["dc.identifier.isi","000240714000013"],["dc.identifier.pmid","16944206"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1127"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","0302-766X"],["dc.title","Hair cell ribbon synapses"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","10832"],["dc.bibliographiccitation.issue","34"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","10840"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Brandt, Andreas"],["dc.contributor.author","Striessnig, Joerg"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2021-06-01T10:48:24Z"],["dc.date.available","2021-06-01T10:48:24Z"],["dc.date.issued","2003"],["dc.description.abstract","Cochlear inner hair cells (IHCs) release neurotransmitter onto afferent auditory nerve fibers in response to sound stimulation. During early development, afferent synaptic transmission is triggered by spontaneous Ca2+ spikes of IHCs, which are under efferent cholinergic control. Around the onset of hearing, large-conductance Ca2+-activated K+ channels are acquired, and Ca2+ spikes as well as the cholinergic innervation are lost. Here, we performed patch-clamp measurements in IHCs of mice lacking the Ca(V)1.3 channel (Ca(V)1.3(-/-)) to investigate the role of this prevailing voltage-gated Ca2+ channel in IHC development and synaptic function. The small Ca2+ current remaining in IHCs from 3-week- old Ca(V)1.3(-/-) mice was mainly mediated by L-type Ca2+ channels, because it was sensitive to dihydropyridines but resistant to inhibitors of non-L-type Ca2+ channels such as omega-conotoxins GVIA and MVIIC and SNX-482. Depolarization induced only marginal exocytosis in Ca(V)1.3(-/-) IHC, which was solely mediated by L-type Ca2+ channels, whereas robust exocytic responses were elicited by photolysis of caged Ca2+. Secretion triggered by short depolarizations was reduced proportionally to the Ca2+ current, suggesting that the coupling of the remaining channels to exocytosis was unchanged. Ca(V)1.3(-/-) IHCs lacked the Ca2+ action potentials and displayed a complex developmental failure. Most strikingly, we observed a continued presence of efferent cholinergic synaptic transmission and a lack of functional large-conductance Ca2+-activated K+ channels up to 4 weeks after birth. We conclude that Ca(V)1.3 channels are essential for normal hair cell development and synaptic transmission."],["dc.identifier.doi","10.1523/JNEUROSCI.23-34-10832.2003"],["dc.identifier.gro","3144034"],["dc.identifier.isi","000186902500011"],["dc.identifier.pmid","14645476"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85923"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","Ca V 1.3 Channels Are Essential for Development and Presynaptic Activity of Cochlear Inner Hair Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","27"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","HNO"],["dc.bibliographiccitation.lastpage","36"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Strenzke, N."],["dc.contributor.author","Pauli-Magnus, D."],["dc.contributor.author","Meyer, A."],["dc.contributor.author","Brandt, A."],["dc.contributor.author","Maier, H."],["dc.contributor.author","Moser, T."],["dc.date.accessioned","2017-09-07T11:48:49Z"],["dc.date.available","2017-09-07T11:48:49Z"],["dc.date.issued","2008"],["dc.identifier.doi","10.1007/s00106-007-1640-7"],["dc.identifier.gro","3143378"],["dc.identifier.isi","000252715900006"],["dc.identifier.pmid","18210004"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/885"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0017-6192"],["dc.title","Update on physiology and pathophysiology of the inner ear. Pathomechanisms of sensorineural hearing loss"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]