Neher, Erwin

[["dc.bibliographiccitation.firstpage","196"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Pflügers Archiv European Journal of Physiology"],["dc.bibliographiccitation.lastpage","203"],["dc.bibliographiccitation.volume","431"],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Chow, Robert H."],["dc.contributor.author","Neher, Erwin"],["dc.date.accessioned","2017-09-07T11:51:10Z"],["dc.date.available","2017-09-07T11:51:10Z"],["dc.date.issued","1995"],["dc.description.abstract","We have studied osmotically induced catecholamine secretion from bovine adrenal chromaffin cells by combining patch-damp measurements, electrochemical detection of secretion, and Fura-2. measurements of intracellular free calcium concentration ([Ca2+](i)). We find that osmotically induced catecholamine release is exocytotic and calcium dependent. Furthermore, we demonstrate that cell swelling is coupled to such secretion via a volume-activated current, carrying predominantly chloride, which causes a plateau depolarization of the cell membrane potential and thus promotes voltage-activated calcium influx. Therefore, cell volume changes may modulate the secretory activity."],["dc.identifier.doi","10.1007/BF00410191"],["dc.identifier.gro","3144670"],["dc.identifier.isi","A1995TN61000007"],["dc.identifier.pmid","9026779"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2319"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","0031-6768"],["dc.title","Swelling-induced catecholamine secretion recorded from single chromaffin cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2314"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","2323"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Neher, Erwin"],["dc.date.accessioned","2017-09-07T11:51:02Z"],["dc.date.available","2017-09-07T11:51:02Z"],["dc.date.issued","1997"],["dc.description.abstract","We report here that brief depolarizations such as action potentials trigger exocytosis in thin mouse adrenal slices. The secretory rates obtained in membrane capacitance recordings from chromaffin cells in slices are faster than those observed in isolated cells. Fast exocytosis in slices is attributable to the rapid release of a small pool of vesicles. The pool recovers from depletion with a time constant of 10 sec. Recruitment of the rapidly released vesicles is strongly hindered by the fast Ca2+ chelator BAPTA and much less by the slower chelator EGTA. We suggest that these vesicles are located in close proximity to Ca2+ channels. Spatial coupling of Ca2+ entry and exocytosis may be sensitive to cell isolation and culture."],["dc.identifier.gro","3144608"],["dc.identifier.isi","A1997WQ58500007"],["dc.identifier.pmid","9065492"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2251"],["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","Rapid exocytosis in single chromaffin cells recorded from mouse adrenal slices"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","11680"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","11685"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Voets, T."],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Lund, P. E."],["dc.contributor.author","Chow, Robert H."],["dc.contributor.author","Geppert, M."],["dc.contributor.author","Suedhof, Thomas C."],["dc.contributor.author","Neher, Erwin"],["dc.date.accessioned","2017-09-07T11:46:01Z"],["dc.date.available","2017-09-07T11:46:01Z"],["dc.date.issued","2001"],["dc.description.abstract","Synaptotagmin I is a synaptic vesicle-associated protein essential for synchronous neurotransmission. We investigated its impact on the intracellular Ca2+-dependence of large dense-core vesicle (LDCV) exocytosis by combining Ca2+-uncaging and membrane capacitance measurements in adrenal slices from mouse synapto-tagmin I null mutants. Synaptotagmin I-deficient chromaffin cells displayed prolonged exocytic delays and slow, yet Ca2+-dependent fusion rates, resulting in strongly reduced LDCV release in response to short depolarizations. Vesicle recruitment, the shape of individual amperometric events, and endocytosis appeared unaffected. These findings demonstrate that synaptotagmin I is required for rapid, highly Ca2+-sensitive LDCV exocytosis and indicate that it regulates the equilibrium between a slowly releasable and a readily releasable state of the fusion machinery. Alternatively, synaptotagmin I could function as calcium sensor for the readily releasable pool, leading to the destabilization of the pool in its absence."],["dc.identifier.doi","10.1073/pnas.201398798"],["dc.identifier.gro","3144254"],["dc.identifier.isi","000171237100124"],["dc.identifier.pmid","11562488"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1858"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Intracellular calcium dependence of large dense-core vesicle exocytosis in the absence of synaptotagmin I"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","681"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","690"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Beutner, D."],["dc.contributor.author","Voets, T."],["dc.contributor.author","Neher, Erwin"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2017-09-07T11:46:40Z"],["dc.date.available","2017-09-07T11:46:40Z"],["dc.date.issued","2001"],["dc.description.abstract","Release of neurotransmitter at the inner hair cell (IHC) afferent synapse is a fundamental step in translating sound into auditory nerve excitation. To study the Ca2+ dependence of the underlying vesicle fusion and subsequent endocytosis, we combined Ca2+ uncaging with membrane capacitance measurements in mouse IHCs. Rapid elevations in [Ca2+](i) above 8 muM caused a biphasic capacitance increase corresponding to the fusion of similar to 40,000 vesicles. The kinetics of exocytosis displayed a fifth-order Ca2+ dependence reaching maximal rates of >3 x 10(7) vesicle/s. Exocytosis was always followed by slow, compensatory endocytosis (tau approximate to 15 s). Higher [Ca2+](i) increased the contribution of a faster mode of endocytosis with a Ca2+-independent time constant of similar to 300 ms. These properties provide for rapid and sustained transmitter release from this large presynaptic terminal."],["dc.identifier.doi","10.1016/S0896-6273(01)00243-4"],["dc.identifier.gro","3144301"],["dc.identifier.isi","000167868900017"],["dc.identifier.pmid","11301027"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1910"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","0896-6273"],["dc.title","Calcium dependence of exocytosis and endocytosis at the Cochlear inner hair cell afferent synapse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8377"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","8383"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Dinkelacker, V"],["dc.contributor.author","Voets, T."],["dc.contributor.author","Neher, Erwin"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2017-09-07T11:46:45Z"],["dc.date.available","2017-09-07T11:46:45Z"],["dc.date.issued","2000"],["dc.description.abstract","Maturation of exocytic vesicles to the release-ready state is regulated by several factors, including intracellular calcium concentration ([Ca2+](int)) and the state of protein phosphorylation. Here we investigated the effects of temperature on the recovery from depletion of the readily releasable pool (RRP) of vesicles in adrenal chromaffin cells. Exocytosis and [Ca2+](int) were monitored by combined membrane capacitance and fura-2 measurements. At higher temperatures, a faster pool refilling and a larger RRP size were observed. The time constants of the recovery from depletion ranged from 3.6 to 1.1 sec (22 and 37 degreesC, respectively) yielding a Q(10) of 2.3. The changes of the Ca2+ signal between the different temperatures could not account for the differences in recovery kinetics. At 32 and 37 degreesC, we observed a transient overfilling of the RRP after pool depletion, which stands in clear contrast to the sustained secretory depression seen at lower temperatures. The overshoot in RRP size was very prominent in cells with lower basal [Ca2+](int), hence with a large difference between prestimulus and poststimulus [Ca2+](int). In cells with higher basal [Ca2+](int), the pool was larger under steady-state conditions but showed less overfilling on stimulation. We conclude that vesicle maturation is markedly accelerated at physiological temperature, thus allowing for a rapid adaptation of the pool size to the relatively short-lived Ca2+ transient."],["dc.identifier.gro","3144343"],["dc.identifier.isi","000165131500022"],["dc.identifier.pmid","11069944"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1957"],["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","The readily releasable pool of vesicles in chromaffin cells is replenished in a temperature-dependent manner and transiently overfills at 37 degrees C"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8377"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","8383"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Dinkelacker, Vera"],["dc.contributor.author","Voets, Thomas"],["dc.contributor.author","Neher, Erwin"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2022-03-01T11:44:14Z"],["dc.date.available","2022-03-01T11:44:14Z"],["dc.date.issued","2000"],["dc.identifier.doi","10.1523/JNEUROSCI.20-22-08377.2000"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102969"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","The Readily Releasable Pool of Vesicles in Chromaffin Cells Is Replenished in a Temperature-Dependent Manner and Transiently Overfills at 37°C"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8323"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","8330"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Albillos, Almudena"],["dc.contributor.author","Neher, Erwin"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2021-06-01T10:48:23Z"],["dc.date.available","2021-06-01T10:48:23Z"],["dc.date.issued","2000"],["dc.description.abstract","Patch-clamp measurements of Ca2+ currents and membrane capacitance were performed on slices of mouse adrenal glands, using the perforated-patch configuration of the patch-clamp technique. These recording conditions are much closer to the in vivo situation than those used so far in most electrophysiological studies in adrenal chromaffin cells (isolated cells maintained in culture and whole-cell configuration). We observed profound discrepancies in the quantities of Ca2+ channel subtypes (P-, Q-, N-, and L- type Ca2+ channels) described for isolated mouse chromaffin cells maintained in culture. Differences with respect to previous studies may be attributable not only to culture conditions, but also to the patch-clamp configuration used. Our experiments revealed the presence of a Ca2+ channel subtype never before described in chromaffin cells, a toxin and dihydropyridine-resistant Ca2+ channel with fast inactivation kinetics, similar to the R-type Ca2+ channel described in neurons. This channel contributes 22% to the total Ca2+ current and controls 55% of the rapid secretory response evoked by short depolarizing pulses. Our results indicate that R-type Ca2+ channels are in close proximity with the exocytotic machinery to rapidly regulate the secretory process."],["dc.identifier.doi","10.1523/JNEUROSCI.20-22-08323.2000"],["dc.identifier.gro","3144342"],["dc.identifier.isi","000165131500017"],["dc.identifier.pmid","11069939"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85918"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Soc Neuroscience"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","R-Type Ca 2+ Channels Are Coupled to the Rapid Component of Secretion in Mouse Adrenal Slice Chromaffin Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6735"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","6740"],["dc.bibliographiccitation.volume","94"],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Neher, Erwin"],["dc.date.accessioned","2017-09-07T11:50:58Z"],["dc.date.available","2017-09-07T11:50:58Z"],["dc.date.issued","1997"],["dc.description.abstract","Whole-cell membrane capacitance measurements are frequently used to monitor neuronal and nonneuronal secretory activity, However, unless individual fusion events can be resolved, the type of the fusing vesicles cannot be identified in these experiments. Here we apply statistical analysis of trial-to-trial variations between depolarization-induced capacitance increases of mouse adrenal chromaffin cells and obtain estimates for the capacitance contribution of individual exocytic vesicles between 0.6 and 2 fF, For com parison, measurements of membrane capacitance were combined with amperometric recordings of catecholamine release during intracellular perfusion of chromaffin cells with high [Ca2+], Crosscorrelation of both signals yielded a mean capacitance contribution of individual catecholaminergic vesicles of 1.3 fF. We suggest that depolarization-induced capacitance increases in mouse adrenal chromaffin cells mainly represent fusion of chromaffin granules."],["dc.identifier.doi","10.1073/pnas.94.13.6735"],["dc.identifier.gro","3144599"],["dc.identifier.isi","A1997XH03400028"],["dc.identifier.pmid","9192634"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2241"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Estimation of mean exocytic vesicle capacitance in mouse adrenal chromaffin cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1243"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","1253"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Smith, Colin A."],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Xu, T"],["dc.contributor.author","Neher, Erwin"],["dc.date.accessioned","2017-09-07T11:48:09Z"],["dc.date.available","2017-09-07T11:48:09Z"],["dc.date.issued","1998"],["dc.description.abstract","Recovery from depletion of the readily releasable pool of vesicles (RRP) in adrenal chromaffin cells was studied at differing basal [Ca2+](i) or following protein kinase C (PKC) activation by phorbol esters. Following depletion, the pool size was estimated at varied times from cell capacitance jumps in response to paired depolarizations. The experimentally observed RRP recovery time course and steady-state size could be predicted from the measured [Ca2+](i) signal assuming a Michaelis-Menten-type regulation of the vesicle supply by Ca2+. An elevated recruitment activity was observed at increased [Ca2+](i) even when protein kinase C was blocked, but maximum effects could be obtained only after stimulation of PKC by phorbol esters or by prolonged elevations in [Ca2+](i). We suggest that, in chromaffin cells, elevated cytosolic Ca2+ modulates exocytotic plasticity via PKC-dependent and -independent pathways."],["dc.identifier.doi","10.1016/S0896-6273(00)80504-8"],["dc.identifier.gro","3144547"],["dc.identifier.isi","000074627300019"],["dc.identifier.pmid","9655511"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2183"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","0896-6273"],["dc.title","Cytosolic Ca2+ acts by two separate pathways to modulate the supply of release-competent vesicles in chromaffin cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","581"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","591"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Voets, T."],["dc.contributor.author","Toonen, R. F."],["dc.contributor.author","Brian, E. C."],["dc.contributor.author","Wit, Heidi de"],["dc.contributor.author","Moser, Tobias"],["dc.contributor.author","Rettig, Jens"],["dc.contributor.author","Suedhof, Thomas C."],["dc.contributor.author","Neher, Erwin"],["dc.contributor.author","Verhage, Matthijs"],["dc.date.accessioned","2017-09-07T11:46:04Z"],["dc.date.available","2017-09-07T11:46:04Z"],["dc.date.issued","2001"],["dc.description.abstract","Secretory vesicles dock at the plasma membrane before Ca2+ triggers their exocytosis. Exocytosis requires the assembly of SNARE complexes formed by the vesicle protein Synaptobrevin and the membrane proteins Syntaxin-1 and SNAP-25. We analyzed the role of Munc18-1, a cytosolic binding partner of Syntaxin-1, in large dense-core vesicle (LDCV) secretion. Calcium-dependent LDCV exocytosis was reduced 10-fold in mouse chromaffin cells lacking Munc18-1, but the kinetic properties of the remaining release, including single fusion events, were not different from controls. Concomitantly, mutant cells displayed a 10-fold reduction in morphologically docked LDCVs. Moreover, acute overexpression of Munc18-1 in bovine chromaffin cells increased the amount of releasable vesicles and accelerated vesicle supply. We conclude that Munc18-1 functions upstream of SNARE complex formation and promotes LDCV docking."],["dc.identifier.doi","10.1016/S0896-6273(01)00391-9"],["dc.identifier.gro","3144258"],["dc.identifier.isi","000170759200012"],["dc.identifier.pmid","11545717"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1862"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","0896-6273"],["dc.title","Munc18-1 promotes large dense-core vesicle docking"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]