Differential Control of Vesicle Priming and Short-Term Plasticity by Munc13 Isoforms

Presynaptic short-term plasticity is an important adaptive mechanism regulating synaptic transmitter release at varying action potential frequencies. However, the underlying molecular mechanisms are unknown. We examined genetically defined and functionally unique axonal subpopulations of synapses in...

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Bibliographic Details
Published in:Neuron (Cambridge, Mass.) Mass.), 2002-01, Vol.33 (3), p.411-424
Main Authors: Rosenmund, Christian, Sigler, Albrecht, Augustin, Iris, Reim, Kerstin, Brose, Nils, Rhee, Jeong-Seop
Format: Article
Language:English
Subjects:
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid - pharmacology
Animals
Bridged Bicyclo Compounds, Heterocyclic - pharmacology
Calcium - metabolism
Cells, Cultured
Dizocilpine Maleate - pharmacology
Electric Stimulation
Enzyme Inhibitors - chemistry
Enzyme Inhibitors - pharmacology
Excitatory Amino Acid Antagonists - pharmacology
Excitatory Postsynaptic Potentials - physiology
Experiments
Glutamic Acid - metabolism
Hippocampus - cytology
Hippocampus - metabolism
Insects
Intracellular Signaling Peptides and Proteins
Kinases
Mice
Mice, Knockout
Munc13 protein
N-Methylaspartate - pharmacology
Nerve Tissue Proteins - genetics
Nerve Tissue Proteins - metabolism
Neuronal Plasticity - physiology
Neurons
Neurons - cytology
Neurons - drug effects
Neurons - metabolism
Protein Isoforms - genetics
Protein Isoforms - metabolism
Synaptic Transmission - physiology
Synaptic Vesicles - metabolism
Thiazoles - pharmacology
Thiazolidines
Transmitters
Type C Phospholipases - antagonists & inhibitors
Type C Phospholipases - metabolism
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Summary:Presynaptic short-term plasticity is an important adaptive mechanism regulating synaptic transmitter release at varying action potential frequencies. However, the underlying molecular mechanisms are unknown. We examined genetically defined and functionally unique axonal subpopulations of synapses in excitatory hippocampal neurons that utilize either Munc13-1 or Munc13-2 as synaptic vesicle priming factor. In contrast to Munc13-1-dependent synapses, Munc13-2-driven synapses show pronounced and transient augmentation of synaptic amplitudes following high-frequency stimulation. This augmentation is caused by a Ca 2+-dependent increase in release probability and releasable vesicle pool size, and requires phospholipase C activity. Thus, differential expression of Munc13 isoforms at individual synapses represents a general mechanism that controls short-term plasticity and contributes to the heterogeneity of synaptic information coding.
ISSN:0896-6273
1097-4199
DOI:10.1016/S0896-6273(02)00568-8