Rickmann, Michael J.

[["dc.bibliographiccitation.firstpage","2575"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA"],["dc.bibliographiccitation.lastpage","2580"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","Kunwar, Ajaya J."],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Backofen, Bianca"],["dc.contributor.author","Browski, Sascha M."],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Schoening, Susanne"],["dc.contributor.author","Fleischmann, Thomas"],["dc.contributor.author","Krieglstein, Kerstin"],["dc.contributor.author","von Mollard, Gabriele Fischer"],["dc.date.accessioned","2018-11-07T08:59:16Z"],["dc.date.available","2018-11-07T08:59:16Z"],["dc.date.issued","2011"],["dc.description.abstract","Fusion between membranes is mediated by specific SNARE complexes. Here we report that fibroblasts survive the absence of the trans-Golgi network/early endosomal SNARE vti1a and the late endosomal SNARE vti1b with intact organelle morphology and minor trafficking defects. Because vti1a and vti1b are the only members of their SNARE subclass and the yeast homolog Vti1p is essential for cell survival, these data suggest that more distantly related SNAREs acquired the ability to function in endosomal traffic during evolution. However, absence of vti1a and vti1b resulted in perinatal lethality. Major axon tracts were missing, reduced in size, or misrouted in Vti1a(-/-) Vti1b(-/-) embryos. Progressive neurodegeneration was observed in most Vti1a(-/-) Vti1b(-/-) peripheral ganglia. Neurons were reduced by more than 95% in Vti1a(-/-) Vti1b(-/-) dorsal root and geniculate ganglia at embryonic day 18.5. These data suggest that special demands for endosomal membrane traffic could not be met in Vti1a(-/-) Vti1b(-/-) neurons. Vti1a(-/-) and Vti1b(-/-) single deficient mice were viable without these neuronal defects, indicating that they can substitute for each other in these processes."],["dc.identifier.doi","10.1073/pnas.1013891108"],["dc.identifier.isi","000287084500073"],["dc.identifier.pmid","21262811"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23851"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","123"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","136"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Betz, Andrea"],["dc.contributor.author","Ashery, Uri"],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Augustin, Iris"],["dc.contributor.author","Neher, Erwin"],["dc.contributor.author","Südhof, Thomas C."],["dc.contributor.author","Rettig, Jens"],["dc.contributor.author","Brose, Nils"],["dc.date.accessioned","2017-09-07T11:48:09Z"],["dc.date.available","2017-09-07T11:48:09Z"],["dc.date.issued","1998"],["dc.description.abstract","Munc13-1, a mammalian homolog of C. elegans unc-13p, is thought to be involved in the regulation of synaptic transmission. We now demonstrate that Munc13-1 is a presynaptic high-affinity phorbol ester and diacylglycerol receptor with ligand affinities similar to those of protein kinase C. Munc13-1 associates with the plasma membrane in response to phorbol ester binding and acts as a phorbol ester-dependent enhancer of transmitter release when overexpressed presynaptically in the Xenopus neuromuscular junction. These observations establish Munc13-1 as a novel presynaptic target of the diacylglycerol second messenger pathway that acts in parallel with protein kinase C to regulate neurotransmitter secretion."],["dc.identifier.doi","10.1016/S0896-6273(00)80520-6"],["dc.identifier.gro","3144539"],["dc.identifier.isi","000075061900012"],["dc.identifier.pmid","9697857"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2174"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.eissn","1097-4199"],["dc.relation.issn","0896-6273"],["dc.title","Munc13-1 is a presynaptic phorbol ester receptor that enhances neurotransmitter release"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","97"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Developmental Neuroscience"],["dc.bibliographiccitation.lastpage","102"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Rahhal, Belal"],["dc.contributor.author","Heermann, Stephan"],["dc.contributor.author","Ferdinand, Anika"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Krieglstein, Kerstin"],["dc.date.accessioned","2018-11-07T08:33:04Z"],["dc.date.available","2018-11-07T08:33:04Z"],["dc.date.issued","2009"],["dc.description.abstract","Neurotrophic factors are well-recognized extracellular signaling molecules that regulate neuron development including neurite growth, survival and maturation of neuronal phenotypes in the central and peripheral nervous system. Previous studies have suggested that TGF-beta plays a key role in the regulation of neuron survival and death and potentiates the neurotrophic activity of several neurotrophic factors, most strikingly of GDNF. To test the physiological relevance of this finding, TGF-beta 2/GDNF double mutant (d-ko) mice were generated. Double mutant mice die at birth like single mutants due to kidney agenesis(GDNF / )and congential cyanosis (TGF-beta 2-/-), respectively. To test for the in vivo relevance of TCF-beta 2/GDNF cooperativity to regulate neuron survival, mesencephalic dopaminergic neurons, lumbar motoneurons, as well as neurons of the lumbar dorsal root ganglion and the superior cervical ganglion were investigated. No loss of mesencephalic dopaminergic neurons was observed in double mutant mice at E18.5. A partial reduction in neuron numbers was observed in lumbar motoneurons, sensory and sympathetic neurons in GDNF single mutants, which was further reduced in TGF-beta 2/GDNF double mutant mice at E18.5. However, TGF-beta 2 single mutant mice showed no loss of neurons. These data point towards a cooperative role of TGF-beta 2 and GDNF with regard to promotion of survival within the peripheral motor and sensory systems investigated. (C) 2008 ISDN. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ijdevneu.2008.08.003"],["dc.identifier.isi","000263387300013"],["dc.identifier.pmid","18824086"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17490"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","1873-474X"],["dc.relation.issn","0736-5748"],["dc.title","In vivo requirement of TGF-beta/GDNF cooperativity in mouse development: focus on the neurotrophic hypothesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","229"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neurogenetics"],["dc.bibliographiccitation.lastpage","238"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Mannan, Ashraf U."],["dc.contributor.author","Roussa, Eleni"],["dc.contributor.author","Kraus, Cornelia"],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Maenner, Joerg"],["dc.contributor.author","Nayernia, K."],["dc.contributor.author","Krieglstein, Kerstin"],["dc.contributor.author","Reis, A."],["dc.contributor.author","Engel, Wolfgang"],["dc.date.accessioned","2018-11-07T10:43:34Z"],["dc.date.available","2018-11-07T10:43:34Z"],["dc.date.issued","2004"],["dc.description.abstract","We report a novel spontaneous mutation named nax in mice, which exhibit delayed hair appearance and ataxia in a homozygote state. Histological analyses of nax brain revealed an overall impairment of the cerebellar cortex. The classical cortical cytoarchitecture was disrupted, the inner granule cell layer was not obvious, the Purkinje cells were not aligned as a Purkinje cell layer, and Bergmann glias did not span the molecular layer. Furthermore, histological analyses of skin showed that the hair follicles were also abnormal. We mapped the nax locus between marker D2Mit158 and D2Mit100 within a region of 800 kb in the middle of chromosome 2 and identified a missense mutation (Gly244Glu) in Acp2, a lysosomal monoesterase. The Glu244 mutation does not affect the stability of the Acp2 transcript, however it renders the enzyme inactive. Ultrastructural analysis of nax cerebellum showed lysosomal storage bodies in nucleated cells, suggesting progressive degeneration as the underlying mechanism. Identification of Acp2 as the gene mutated in nax mice provides a valuable model system for studying the role of Acp2 in cerebellum and skin homeostasis."],["dc.identifier.doi","10.1007/s10048-004-0197-9"],["dc.identifier.isi","000226285100005"],["dc.identifier.pmid","15503243"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47086"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1364-6745"],["dc.title","Mutation in the gene encoding lysosomal acid phosphatase (Acp2) causes cerebellum and skin malformation in mouse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","584"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular and Cellular Neuroscience"],["dc.bibliographiccitation.lastpage","601"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Bohm, D."],["dc.contributor.author","Schwegler, H."],["dc.contributor.author","Kotthaus, L."],["dc.contributor.author","Nayernia, K."],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Kohler, M."],["dc.contributor.author","Rosenbusch, J."],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Flugge, G."],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T09:46:43Z"],["dc.date.available","2018-11-07T09:46:43Z"],["dc.date.issued","2002"],["dc.description.abstract","Aberrant reorganization of hippocampal mossy fibers occurs in human temporal lobe epilepsy and rodent epilepsy models. We generated a mouse model showing massive late-onset aberrant mossy fiber sprouting in the adult hippocampus. The mutation in this mouse model derives from an intronic insertion of transgene DNA in the mouse PLC-beta1 gene (PLC-beta1(TC)(-/-) mutation) leading to a splice mutation of the PLC-beta1 gene and a complete loss of downstream PLC-beta1 expression. PLC-beta1(TC)(-/-) mutants develop a loss of NMDA-receptors in the stratum oriens of region CA1, apoptotic neuronal death, and reduced hippocampal PKC activity. The phenotype of these mice further consists of a late-onset epileptiform hyperexcitability, behavioral modifications in a radial maze and in an open field, female nurturing defect, and male infertility. In the present study, we provide evidence that the arising of the behavioral phenotype in PLC-beta1(TC)(-/-) mice correlates in time with the development of the aberrant mossy fiber projections and that the disruption of the PLC-beta1-mediated signal transduction pathway may lead to a functional cholinergic denervation, which could cause hippocampal remodeling and, in consequence, epileptiform hyperexcitability."],["dc.identifier.doi","10.1006/mcne.2002.1199"],["dc.identifier.isi","000180026300006"],["dc.identifier.pmid","12504592"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34945"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1044-7431"],["dc.title","Disruption of PLC-beta 1-mediated signal transduction in mutant mice causes age-dependent hippocampal mossy fiber sprouting and neurodegeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","253"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","262"],["dc.bibliographiccitation.volume","323"],["dc.contributor.author","Oehlke, O."],["dc.contributor.author","Sprysch, P."],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Roussa, Eleni"],["dc.date.accessioned","2018-11-07T10:21:05Z"],["dc.date.available","2018-11-07T10:21:05Z"],["dc.date.issued","2006"],["dc.description.abstract","Acute metabolic acidosis and alkalosis cause a series of homeostatic adaptive responses in the kidney and other epithelia. We hypothesized that acid/base disturbances might affect the expression of Na+/H+ stop exchanger (NHE) isoforms in salivary glands and determined the expression and cellular distribution of NHE3 and NHE4 in rat submandibular glands of controls and after imposed acute or chronic metabolic acidosis or alkalosis in vivo. Reverse transcription/polymerase chain reaction, in situ hybridization, and immunohistochemistry were applied by using specific primers, antisense probes, and antibodies, respectively. The results showed NHE3 and NHE4 transcript expression and protein abundance in rat submandibular gland. NHE3 was apically localized in duct cells, whereas NHE4 was found basolaterally distributed in acinar and duct cells. Acute acidosis and alkalosis and chronic acidosis had no effect on NHE3 and NHE4 expression and localization. In contrast, chronic metabolic alkalosis significantly decreased the number of apically stained NHE3 duct cells but had no effect on NHE3 mRNA expression. The results demonstrate, for the first time, the presence of NHE4 protein in salivary glands. The data also indicate the distinct regulation and adaptive changes of different isoforms of the same transporter in rat submandibular gland as a response to acid/base disturbances."],["dc.identifier.doi","10.1007/s00441-005-0055-6"],["dc.identifier.isi","000234689500007"],["dc.identifier.pmid","16158325"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42024"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0302-766X"],["dc.title","Na+/H+ exchanger isoforms are differentially regulated in rat submandibular gland during acid/base disturbances in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","303"],["dc.bibliographiccitation.journal","Neuroscience"],["dc.bibliographiccitation.lastpage","316"],["dc.bibliographiccitation.volume","463"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Kunwar, Ajaya J."],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Tuoc, Tran"],["dc.contributor.author","Rizzoli, Silvio O."],["dc.contributor.author","Tarabykin, Victor"],["dc.contributor.author","von Mollard, Gabriele Fischer"],["dc.contributor.author","Krieglstein, Kerstin"],["dc.contributor.author","Staiger, Jochen F."],["dc.date.accessioned","2021-06-01T09:41:26Z"],["dc.date.available","2021-06-01T09:41:26Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.neuroscience.2021.03.021"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84922"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","0306-4522"],["dc.title","Ablation of Vti1a/1b Triggers Neural Progenitor Pool Depletion and Cortical Layer 5 Malformation in Late-embryonic Mouse Cortex"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","25"],["dc.bibliographiccitation.journal","Neural Development"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Heupel, Katharina"],["dc.contributor.author","Sargsyan, Vardanush"],["dc.contributor.author","Plomp, Jaap J."],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Varoqueaux, Frederique"],["dc.contributor.author","Zhang, W."],["dc.contributor.author","Krieglstein, Kerstin"],["dc.date.accessioned","2018-11-07T11:10:04Z"],["dc.date.available","2018-11-07T11:10:04Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: The formation of functional synapses is a crucial event in neuronal network formation, and with regard to regulation of breathing it is essential for life. Members of the transforming growth factor-beta (TGF-beta) superfamily act as intercellular signaling molecules during synaptogenesis of the neuromuscular junction of Drosophila and are involved in synaptic function of sensory neurons of Aplysia. Results: Here we show that while TGF-beta 2 is not crucial for the morphology and function of the neuromuscular junction of the diaphragm muscle of mice, it is essential for proper synaptic function in the pre-Botzinger complex, a central rhythm organizer located in the brainstem. Genetic deletion of TGF-beta 2 in mice strongly impaired both GABA/glycinergic and glutamatergic synaptic transmission in the pre-Botzinger complex area, while numbers and morphology of central synapses of knock-out animals were indistinguishable from their wild-type littermates at embryonic day 18.5. Conclusion: The results demonstrate that TGF-beta 2 influences synaptic function, rather than synaptogenesis, specifically at central synapses. The functional alterations in the respiratory center of the brain are probably the underlying cause of the perinatal death of the TGF-beta 2 knock-out mice."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft through GRK [632]; SFB [406, 780]"],["dc.identifier.doi","10.1186/1749-8104-3-25"],["dc.identifier.isi","000260872000001"],["dc.identifier.pmid","18854036"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4952"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53134"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1749-8104"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Loss of transforming growth factor-beta 2 leads to impairment of central synapse function"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3043"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","3052"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Juranek, Judyta"],["dc.contributor.author","Mukherjee, Konark"],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Calka, Jaroslaw"],["dc.contributor.author","Suedhof, Thomas C."],["dc.contributor.author","Jahn, Reinhard"],["dc.date.accessioned","2018-11-07T08:53:11Z"],["dc.date.available","2018-11-07T08:53:11Z"],["dc.date.issued","2006"],["dc.description.abstract","Nerve terminals of the central nervous system (CNS) contain specialized release sites for synaptic vesicles, referred to as active zones. They are characterized by electron-dense structures that are tightly associated with the presynaptic plasma membrane and organize vesicle docking and priming sites. Recently, major protein constituents of active zones have been identified, including the proteins Piccolo, Bassoon, RIM, Munc13, ERCs/ELKs/CASTs and liprins. While it is becoming apparent that each of these proteins is essential for synaptic function in the CNS, it is not known to what extent these proteins are involved in synaptic function of the peripheral nervous system. Somatic neuromuscular junctions contain morphologically and functionally defined active zones with similarities to CNS synapses. In contrast, sympathetic neuromuscular varicosities lack active zone-like morphological specializations. Using immunocytochemistry at the light and electron microscopic level we have now performed a systematic investigation of all five major classes of active zone proteins in peripheral neuromuscular junctions. Our results show that somatic neuromuscular endplates contain a full complement of all active zone proteins. In contrast, varicosities of the vas deferens contain a subset of active zone proteins including Bassoon and ELKS2, with the other four components being absent. We conclude that Bassoon and ELKS2 perform independent and specialized functions in synaptic transmission of autonomic synapses."],["dc.identifier.doi","10.1111/j.1460-9568.2006.05183.x"],["dc.identifier.isi","000243361700008"],["dc.identifier.pmid","17156365"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22346"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0953-816X"],["dc.title","Differential expression of active zone proteins in neuromuscular junctions suggests functional diversification"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","10"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","17"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Augustin, Iris"],["dc.contributor.author","Korte, Stefan"],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Südhof, Thomas C."],["dc.contributor.author","Herms, Jochen W."],["dc.contributor.author","Brose, Nils"],["dc.date.accessioned","2022-03-01T11:44:15Z"],["dc.date.available","2022-03-01T11:44:15Z"],["dc.date.issued","2001"],["dc.description.abstract","Munc13 proteins form a family of three, primarily brain-specific phorbol ester receptors (Munc13-1/2/3) in mammals. Munc13-1 is a component of presynaptic active zones in which it acts as an essential synaptic vesicle priming protein. In contrast to Munc13-1, which is present in most neurons throughout the rat and mouse CNS, Munc13-3 is almost exclusively expressed in the cerebellum. Munc13-3 mRNA is present in granule and Purkinje cells but absent from glia cells. Munc13-3 protein is localized to the synaptic neuropil of the cerebellar molecular layer but is not found in Purkinje cell dendrites, suggesting that Munc13-3, like Munc13-1, is a presynaptic protein at parallel fiber-Purkinje cell synapses. To examine the role of Munc13-3 in cerebellar physiology, we generated Munc13-3-deficient mutant mice. Munc13-3 deletion mutants exhibit increased paired-pulse facilitation at parallel fiber-Purkinje cell synapses. In addition, mutant mice display normal spontaneous motor activity but have an impaired ability to learn complex motor tasks. Our data demonstrate that Munc13-3 regulates synaptic transmission at parallel fiber-Purkinje cell synapses. We propose that Munc13-3 acts at a similar step of the synaptic vesicle cycle as does Munc13-1, albeit with less efficiency. In view of the present data and the well established vesicle priming function of Munc13-1, it is likely that Munc13-3-loss leads to a reduction in release probability at parallel fiber-Purkinje cell synapses by interfering with vesicle priming. This, in turn, would lead to increases in paired-pulse facilitation and could contribute to the observed deficit in motor learning."],["dc.identifier.doi","10.1523/JNEUROSCI.21-01-00010.2001"],["dc.identifier.gro","3144325"],["dc.identifier.isi","000166278500005"],["dc.identifier.pmid","11150314"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102970"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["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","The Cerebellum-Specific Munc13 Isoform Munc13-3 Regulates Cerebellar Synaptic Transmission and Motor Learning in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]