scholarly journals Correction: LKB1 Regulates Mitochondria-Dependent Presynaptic Calcium Clearance and Neurotransmitter Release Properties at Excitatory Synapses along Cortical Axons

PLoS Biology ◽  
2018 ◽  
Vol 16 (9) ◽  
pp. e3000040 ◽  
Author(s):  
Seok-Kyu Kwon ◽  
Richard Sando ◽  
Tommy L. Lewis ◽  
Yusuke Hirabayashi ◽  
Anton Maximov ◽  
...  
Keyword(s):  
Neurotransmitter Release ◽  
Excitatory Synapses ◽  
Calcium Clearance ◽  
Presynaptic Calcium

scholarly journals LKB1 Regulates Mitochondria-Dependent Presynaptic Calcium Clearance and Neurotransmitter Release Properties at Excitatory Synapses along Cortical Axons

PLoS Biology ◽  
2016 ◽  
Vol 14 (7) ◽  
pp. e1002516 ◽  
Author(s):  
Seok-Kyu Kwon ◽  
Richard Sando ◽  
Tommy L. Lewis ◽  
Yusuke Hirabayashi ◽  
Anton Maximov ◽  
...  
Keyword(s):  
Neurotransmitter Release ◽  
Excitatory Synapses ◽  
Calcium Clearance ◽  
Presynaptic Calcium

Presynaptic calcium signals during neurotransmitter release: Detection with fluorescent indicators and other calcium chelators

1992 ◽  
Vol 86 (1-3) ◽  
pp. 129-134 ◽  
Author(s):  
GJ Augustine ◽  
EM Adler ◽  
MP Charlton ◽  
M Hans ◽  
D Swandulla ◽  
...  
Keyword(s):  
Neurotransmitter Release ◽  
Calcium Signals ◽  
Fluorescent Indicators ◽  
Presynaptic Calcium

scholarly journals Homeostatic synaptic depression is achieved through a regulated decrease in presynaptic calcium channel abundance

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Michael A Gaviño ◽  
Kevin J Ford ◽  
Santiago Archila ◽  
Graeme W Davis
Keyword(s):  
Synaptic Plasticity ◽  
Neuromuscular Junction ◽  
Action Potential ◽  
Calcium Channel ◽  
Neurotransmitter Release ◽  
Calcium Influx ◽  
Homeostatic Synaptic Plasticity ◽  
Action Potential Waveform ◽  
Presynaptic Calcium ◽  
Potential Waveform

Homeostatic signaling stabilizes synaptic transmission at the neuromuscular junction (NMJ) of Drosophila, mice, and human. It is believed that homeostatic signaling at the NMJ is bi-directional and considerable progress has been made identifying mechanisms underlying the homeostatic potentiation of neurotransmitter release. However, very little is understood mechanistically about the opposing process, homeostatic depression, and how bi-directional plasticity is achieved. Here, we show that homeostatic potentiation and depression can be simultaneously induced, demonstrating true bi-directional plasticity. Next, we show that mutations that block homeostatic potentiation do not alter homeostatic depression, demonstrating that these are genetically separable processes. Finally, we show that homeostatic depression is achieved by decreased presynaptic calcium channel abundance and calcium influx, changes that are independent of the presynaptic action potential waveform. Thus, we identify a novel mechanism of homeostatic synaptic plasticity and propose a model that can account for the observed bi-directional, homeostatic control of presynaptic neurotransmitter release.

scholarly journals Single calcium channel nanodomains drive presynaptic calcium entry at lamprey reticulospinal presynaptic terminals

2021 ◽  
Author(s):  
S Ramachandran ◽  
S Rodgriguez ◽  
M Potcoava ◽  
S Alford
Keyword(s):  
Active Zone ◽  
Neurotransmitter Release ◽  
Action Potentials ◽  
Information Transfer ◽  
Single Channel ◽  
Light Sheet ◽  
Stochastic Variation ◽  
Presynaptic Terminals ◽  
Light Sheet Microscopy ◽  
Presynaptic Calcium

AbstractSynchronous neurotransmission is central to efficient information transfer in neural circuits, requiring precise coupling between action potentials, Ca2+ entry and neurotransmitter release. However, determinations of Ca2+ requirements for release, which may originate from entry through single voltage-gated Ca2+ channels, remain largely unexplored in simple active zone synapses common in the nervous system. Understanding these requirements is key to addressing Ca2+ channel and synaptic dysfunction underlying numerous neurological and neuropsychiatric disorders. Here, we present single channel analysis of evoked active zone Ca2+ entry, using cell-attached patch clamp and lattice light sheet microscopy over active zones at single central lamprey reticulospinal presynaptic terminals. Our findings show a small pool (mean of 23) of Ca2+ channels at each terminal, comprising subtypes N-type (CaV2.2), P/Q-type (CaV2.1) and R-type (CaV2.3), available to gate neurotransmitter release. Significantly, of this pool only 1-6 (mean of 4) channels open upon depolarization. High temporal fidelity lattice light sheet imaging reveals AP-evoked Ca2+ transients exhibiting quantal amplitude variations between action potentials and stochastic variation of precise locations of Ca2+ entry within the active zone. Further, Ca2+ channel numbers at each active zone correlate to the number of presynaptic primed synaptic vesicles. Together, our findings indicate 1:1 association of Ca2+ channels with primed vesicles, suggesting Ca2+ entry via as few as one channel may trigger neurotransmitter release.

scholarly journals Postsynaptic Neuroligin-1 Mediates Presynaptic Endocytosis During Neuronal Activity

2021 ◽  
Vol 14 ◽  
Author(s):  
Jiaqi Keith Luo ◽  
Holly Melland ◽  
Jess Nithianantharajah ◽  
Sarah L. Gordon
Keyword(s):  
Ampa Receptors ◽  
Neurotransmitter Release ◽  
Synaptic Vesicles ◽  
High Fidelity ◽  
Excitatory Synapses ◽  
Synaptic Efficacy ◽  
Molecular Architecture ◽  
Adhesion Protein ◽  
Presynaptic Nerve Terminal ◽  
Presynaptic Release

Fast, high-fidelity neurotransmission and synaptic efficacy requires tightly regulated coordination of pre- and postsynaptic compartments and alignment of presynaptic release sites with postsynaptic receptor nanodomains. Neuroligin-1 (Nlgn1) is a postsynaptic cell-adhesion protein exclusively localised to excitatory synapses that is crucial for coordinating the transsynaptic alignment of presynaptic release sites with postsynaptic AMPA receptors as well as postsynaptic transmission and plasticity. However, little is understood about whether the postsynaptic machinery can mediate the molecular architecture and activity of the presynaptic nerve terminal, and thus it remains unclear whether there are presynaptic contributions to Nlgn1-dependent control of signalling and plasticity. Here, we employed a presynaptic reporter of neurotransmitter release and synaptic vesicle dynamics, synaptophysin-pHluorin (sypHy), to directly assess the presynaptic impact of loss of Nlgn1. We show that lack of Nlgn1 had no effect on the size of the readily releasable or entire recycling pool of synaptic vesicles, nor did it impact exocytosis. However, we observed significant changes in the retrieval of synaptic vesicles by compensatory endocytosis, specifically during activity. Our data extends growing evidence that synaptic adhesion molecules critical for forming transsynaptic scaffolds are also important for regulating activity-induced endocytosis at the presynapse.

scholarly journals Presynaptic Calcium Channels

2019 ◽  
Vol 20 (9) ◽  
pp. 2217 ◽  
Author(s):  
Sumiko Mochida
Keyword(s):  
Neurotransmitter Release ◽  
Synaptic Vesicles ◽  
Neuronal Firing ◽  
Regulatory Proteins ◽  
Channel Modulation ◽  
Signaling Complex ◽  
Presynaptic Plasticity ◽  
Presynaptic Calcium ◽  
Ca2 Channels ◽  
Α1 Subunit

Presynaptic Ca2+ entry occurs through voltage-gated Ca2+ (CaV) channels which are activated by membrane depolarization. Depolarization accompanies neuronal firing and elevation of Ca2+ triggers neurotransmitter release from synaptic vesicles. For synchronization of efficient neurotransmitter release, synaptic vesicles are targeted by presynaptic Ca2+ channels forming a large signaling complex in the active zone. The presynaptic CaV2 channel gene family (comprising CaV2.1, CaV2.2, and CaV2.3 isoforms) encode the pore-forming α1 subunit. The cytoplasmic regions are responsible for channel modulation by interacting with regulatory proteins. This article overviews modulation of the activity of CaV2.1 and CaV2.2 channels in the control of synaptic strength and presynaptic plasticity.

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