scholarly journals Dynamic Control of Synaptic Vesicle Replenishment and Short-Term Plasticity by Ca2+-Calmodulin-Munc13-1 Signaling

Neuron ◽  
2013 ◽  
Vol 79 (1) ◽  
pp. 82-96 ◽  
Author(s):  
Noa Lipstein ◽  
Takeshi Sakaba ◽  
Benjamin H. Cooper ◽  
Kun-Han Lin ◽  
Nicola Strenzke ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Dynamic Control ◽  
Short Term ◽  
Short Term Plasticity

scholarly journals Separation of presynaptic Cav2 and Cav1 channel function in synaptic vesicle exo- and endocytosis by the membrane anchored Ca2+ pump PMCA

2021 ◽  
Vol 118 (28) ◽  
pp. e2106621118
Author(s):  
Niklas Krick ◽  
Stefanie Ryglewski ◽  
Aylin Pichler ◽  
Arthur Bikbaev ◽  
Torsten Götz ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Neurotransmitter Release ◽  
Calcium Currents ◽  
Short Term ◽  
Triggered Release ◽  
Presynaptic Terminals ◽  
Dynamic Regulation ◽  
Short Term Plasticity ◽  
Separate Control ◽  
Active Zones

Synaptic vesicle (SV) release, recycling, and plastic changes of release probability co-occur side by side within nerve terminals and rely on local Ca2+ signals with different temporal and spatial profiles. The mechanisms that guarantee separate regulation of these vital presynaptic functions during action potential (AP)–triggered presynaptic Ca2+ entry remain unclear. Combining Drosophila genetics with electrophysiology and imaging reveals the localization of two different voltage-gated calcium channels at the presynaptic terminals of glutamatergic neuromuscular synapses (the Drosophila Cav2 homolog, Dmca1A or cacophony, and the Cav1 homolog, Dmca1D) but with spatial and functional separation. Cav2 within active zones is required for AP-triggered neurotransmitter release. By contrast, Cav1 localizes predominantly around active zones and contributes substantially to AP-evoked Ca2+ influx but has a small impact on release. Instead, L-type calcium currents through Cav1 fine-tune short-term plasticity and facilitate SV recycling. Separate control of SV exo- and endocytosis by AP-triggered presynaptic Ca2+ influx through different channels demands efficient measures to protect the neurotransmitter release machinery against Cav1-mediated Ca2+ influx. We show that the plasma membrane Ca2+ ATPase (PMCA) resides in between active zones and isolates Cav2-triggered release from Cav1-mediated dynamic regulation of recycling and short-term plasticity, two processes which Cav2 may also contribute to. As L-type Cav1 channels also localize next to PQ-type Cav2 channels within axon terminals of some central mammalian synapses, we propose that Cav2, Cav1, and PMCA act as a conserved functional triad that enables separate control of SV release and recycling rates in presynaptic terminals.

scholarly journals Synapsin Controls Both Reserve and Releasable Synaptic Vesicle Pools during Neuronal Activity and Short-Term Plasticity inAplysia

2001 ◽  
Vol 21 (12) ◽  
pp. 4195-4206 ◽  
Author(s):  
Yann Humeau ◽  
Frédéric Doussau ◽  
Francesco Vitiello ◽  
Paul Greengard ◽  
Fabio Benfenati ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Neuronal Activity ◽  
Short Term ◽  
Short Term Plasticity ◽  
Vesicle Pools

scholarly journals ELKS1 localizes the synaptic vesicle priming protein bMunc13-2 to a specific subset of active zones

2017 ◽  
Vol 216 (4) ◽  
pp. 1143-1161 ◽  
Author(s):  
Hiroshi Kawabe ◽  
Miso Mitkovski ◽  
Pascal S. Kaeser ◽  
Johannes Hirrlinger ◽  
Felipe Opazo ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Hippocampal Neurons ◽  
Short Term ◽  
Network Characteristics ◽  
Short Term Plasticity ◽  
Neuronal Synapses ◽  
Specific Subset ◽  
Specific Proteins ◽  
Active Zones ◽  
Essential Function

Presynaptic active zones (AZs) are unique subcellular structures at neuronal synapses, which contain a network of specific proteins that control synaptic vesicle (SV) tethering, priming, and fusion. Munc13s are core AZ proteins with an essential function in SV priming. In hippocampal neurons, two different Munc13s—Munc13-1 and bMunc13-2—mediate opposite forms of presynaptic short-term plasticity and thus differentially affect neuronal network characteristics. We found that most presynapses of cortical and hippocampal neurons contain only Munc13-1, whereas ∼10% contain both Munc13-1 and bMunc13-2. Whereas the presynaptic recruitment and activation of Munc13-1 depends on Rab3-interacting proteins (RIMs), we demonstrate here that bMunc13-2 is recruited to synapses by the AZ protein ELKS1, but not ELKS2, and that this recruitment determines basal SV priming and short-term plasticity. Thus, synapse-specific interactions of different Munc13 isoforms with ELKS1 or RIMs are key determinants of the molecular and functional heterogeneity of presynaptic AZs.

scholarly journals TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis

2021 ◽  
Author(s):  
Zhong-Jiao Jiang ◽  
Wenping Li ◽  
Li-Hua Yao ◽  
Brian S. Grewe ◽  
Andrea McGinley ◽  
...  
Keyword(s):  
Nervous System ◽  
Synaptic Vesicle ◽  
Neuronal Death ◽  
Physiological Role ◽  
Neuroendocrine Cells ◽  
Short Term ◽  
Widespread Distribution ◽  
Short Term Plasticity ◽  
Inhibitory Synaptic Transmission

AbstractTRPM7 contributes to a variety of physiological and pathological processes in many tissues and cells. With a widespread distribution in the nervous system, TRPM7 is involved in animal behaviors and neuronal death induced by ischemia. However, the physiological role of TRPM7 in CNS neuron remains unclear. Here, we identify endocytic defects in neuroendocrine cells and neurons from TRPM7 knockout (KO) mice, indicating a role of TRPM7 in synaptic vesicle endocytosis. Our experiments further pinpoint the importance of TRPM7 as an ion channel in synaptic vesicle endocytosis. Ca2+ imaging detects a defect in presynaptic Ca2+ dynamics in TRPM7 KO neuron, suggesting an importance of Ca2+ influx via TRPM7 in synaptic vesicle endocytosis. Moreover, the short-term depression is enhanced in both excitatory and inhibitory synaptic transmission from TRPM7 KO mice. Taking together, our data suggests that Ca2+ influx via TRPM7 may be critical for short-term plasticity of synaptic strength by regulating synaptic vesicle endocytosis in neurons.

scholarly journals TRPM7 is critical for short-term synaptic depression by regulating synaptic vesicle endocytosis

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Zhong-Jiao Jiang ◽  
Wenping Li ◽  
Li-Hua Yao ◽  
Badeia Saed ◽  
Yan Rao ◽  
...  
Keyword(s):  
Nervous System ◽  
Synaptic Vesicle ◽  
Neuronal Death ◽  
Physiological Role ◽  
Neuroendocrine Cells ◽  
Short Term ◽  
Widespread Distribution ◽  
Short Term Plasticity ◽  
Inhibitory Synaptic Transmission

TRPM7 contributes to a variety of physiological and pathological processes in many tissues and cells. With a widespread distribution in the nervous system, TRPM7 is involved in animal behaviors and neuronal death induced by ischemia. However, the physiological role of TRPM7 in CNS neuron remains unclear. Here, we identify endocytic defects in neuroendocrine cells and neurons from TRPM7 knockout (KO) mice, indicating a role of TRPM7 in synaptic vesicle endocytosis. Our experiments further pinpoint the importance of TRPM7 as an ion channel in synaptic vesicle endocytosis. Ca2+ imaging detects a defect in presynaptic Ca2+ dynamics in TRPM7 KO neuron, suggesting an importance of Ca2+ influx via TRPM7 in synaptic vesicle endocytosis. Moreover, the short-term depression is enhanced in both excitatory and inhibitory synaptic transmission from TRPM7 KO mice. Taken together, our data suggests that Ca2+ influx via TRPM7 may be critical for short-term plasticity of synaptic strength by regulating synaptic vesicle endocytosis in neurons.

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