scholarly journals Mechanisms of short‐term plasticity at neuromuscular active zones of Drosophila

HFSP Journal ◽  
2010 ◽  
Vol 4 (2) ◽  
pp. 72-84 ◽  
Author(s):  
Stefan Hallermann ◽  
Manfred Heckmann ◽  
Robert J. Kittel
Keyword(s):  
Short Term ◽  
Short Term Plasticity ◽  
Active Zones

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 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 Subcortical short‐term plasticity elicited by deep brain stimulation

2021 ◽  
Author(s):  
Mohammad Z. Awad ◽  
Ryan J. Vaden ◽  
Zachary T. Irwin ◽  
Christopher L. Gonzalez ◽  
Sarah Black ◽  
...  
Keyword(s):  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Short Term ◽  
Short Term Plasticity ◽  
Deep Brain

scholarly journals Author Correction: Presynaptic endoplasmic reticulum regulates short-term plasticity in hippocampal synapses

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Nishant Singh ◽  
Thomas Bartol ◽  
Herbert Levine ◽  
Terrence Sejnowski ◽  
Suhita Nadkarni
Keyword(s):  
Endoplasmic Reticulum ◽  
Short Term ◽  
Short Term Plasticity ◽  
Hippocampal Synapses

scholarly journals Unc13A and Unc13B contribute to the decoding of distinct sensory information in Drosophila

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Atefeh Pooryasin ◽  
Marta Maglione ◽  
Marco Schubert ◽  
Tanja Matkovic-Rachid ◽  
Sayed-mohammad Hasheminasab ◽  
...  
Keyword(s):  
Sensory Information ◽  
Projection Neuron ◽  
Physical Distance ◽  
Neural Decoding ◽  
Short Term ◽  
Short Term Plasticity ◽  
Appetitive Stimuli ◽  
Excitatory Projection ◽  
Direct Genetic Evidence ◽  
Nanoscale Level

AbstractThe physical distance between presynaptic Ca2+ channels and the Ca2+ sensors triggering the release of neurotransmitter-containing vesicles regulates short-term plasticity (STP). While STP is highly diversified across synapse types, the computational and behavioral relevance of this diversity remains unclear. In the Drosophila brain, at nanoscale level, we can distinguish distinct coupling distances between Ca2+ channels and the (m)unc13 family priming factors, Unc13A and Unc13B. Importantly, coupling distance defines release components with distinct STP characteristics. Here, we show that while Unc13A and Unc13B both contribute to synaptic signalling, they play distinct roles in neural decoding of olfactory information at excitatory projection neuron (ePN) output synapses. Unc13A clusters closer to Ca2+ channels than Unc13B, specifically promoting fast phasic signal transfer. Reduction of Unc13A in ePNs attenuates responses to both aversive and appetitive stimuli, while reduction of Unc13B provokes a general shift towards appetitive values. Collectively, we provide direct genetic evidence that release components of distinct nanoscopic coupling distances differentially control STP to play distinct roles in neural decoding of sensory information.

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