Source:http://linkedlifedata.com/resource/pubmed/id/11150314
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2001-1-19
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| pubmed:abstractText |
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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotransmitter Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Isoforms,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Unc13c protein, mouse
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
1529-2401
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
1
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| pubmed:volume |
21
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
10-7
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:11150314-Animals,
pubmed-meshheading:11150314-Cerebellum,
pubmed-meshheading:11150314-Electric Stimulation,
pubmed-meshheading:11150314-Female,
pubmed-meshheading:11150314-Gene Deletion,
pubmed-meshheading:11150314-Gene Targeting,
pubmed-meshheading:11150314-Glutamic Acid,
pubmed-meshheading:11150314-Learning,
pubmed-meshheading:11150314-Male,
pubmed-meshheading:11150314-Mice,
pubmed-meshheading:11150314-Mice, Inbred C57BL,
pubmed-meshheading:11150314-Mice, Knockout,
pubmed-meshheading:11150314-Mice, Mutant Strains,
pubmed-meshheading:11150314-Nerve Tissue Proteins,
pubmed-meshheading:11150314-Neurotransmitter Agents,
pubmed-meshheading:11150314-Organ Specificity,
pubmed-meshheading:11150314-Patch-Clamp Techniques,
pubmed-meshheading:11150314-Phenotype,
pubmed-meshheading:11150314-Protein Isoforms,
pubmed-meshheading:11150314-Psychomotor Performance,
pubmed-meshheading:11150314-Purkinje Cells,
pubmed-meshheading:11150314-RNA, Messenger,
pubmed-meshheading:11150314-Synapses,
pubmed-meshheading:11150314-Synaptic Transmission
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| pubmed:year |
2001
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| pubmed:articleTitle |
The cerebellum-specific Munc13 isoform Munc13-3 regulates cerebellar synaptic transmission and motor learning in mice.
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| pubmed:affiliation |
AG Molekulare Neurobiologie, Max-Planck-Institut für experimentelle Medizin, D-37075 Göttingen, Germany.
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| pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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