scholarly journals Acetylcholine-Induced Inhibition of Presynaptic Calcium Signals and Transmitter Release in the Frog Neuromuscular Junction

2016 ◽  
Vol 7 ◽  
Author(s):  
Eduard Khaziev ◽  
Dmitry Samigullin ◽  
Nikita Zhilyakov ◽  
Nijaz Fatikhov ◽  
Ellya Bukharaeva ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Transmitter Release ◽  
Frog Neuromuscular Junction ◽  
Calcium Signals ◽  
Presynaptic Calcium

scholarly journals Transmitter release is evoked with low probability predominately by calcium flux through single channel openings at the frog neuromuscular junction

2015 ◽  
Vol 113 (7) ◽  
pp. 2480-2489 ◽  
Author(s):  
Fujun Luo ◽  
Markus Dittrich ◽  
Soyoun Cho ◽  
Joel R. Stiles ◽  
Stephen D. Meriney
Keyword(s):  
Neuromuscular Junction ◽  
Calcium Channels ◽  
Calcium Channel ◽  
Calcium Ions ◽  
Transmitter Release ◽  
Synaptic Vesicles ◽  
Vesicle Fusion ◽  
Frog Neuromuscular Junction ◽  
Low Probability ◽  
Presynaptic Calcium

The quantitative relationship between presynaptic calcium influx and transmitter release critically depends on the spatial coupling of presynaptic calcium channels to synaptic vesicles. When there is a close association between calcium channels and synaptic vesicles, the flux through a single open calcium channel may be sufficient to trigger transmitter release. With increasing spatial distance, however, a larger number of open calcium channels might be required to contribute sufficient calcium ions to trigger vesicle fusion. Here we used a combination of pharmacological calcium channel block, high-resolution calcium imaging, postsynaptic recording, and 3D Monte Carlo reaction-diffusion simulations in the adult frog neuromuscular junction, to show that release of individual synaptic vesicles is predominately triggered by calcium ions entering the nerve terminal through the nearest open calcium channel. Furthermore, calcium ion flux through this channel has a low probability of triggering synaptic vesicle fusion (∼6%), even when multiple channels open in a single active zone. These mechanisms work to control the rare triggering of vesicle fusion in the frog neuromuscular junction from each of the tens of thousands of individual release sites at this large model synapse.

Intraterminal Ca2+ and Spontaneous Transmitter Release at the Frog Neuromuscular Junction

2001 ◽  
Vol 85 (1) ◽  
pp. 287-294 ◽  
Author(s):  
J. K. Angleson ◽  
W. J. Betz
Keyword(s):  
Neuromuscular Junction ◽  
Phorbol Ester ◽  
Intracellular Recording ◽  
Transmitter Release ◽  
The Other ◽  
Nerve Terminals ◽  
Frog Neuromuscular Junction ◽  
Tetraacetic Acid ◽  
Ratiometric Imaging ◽  
The Relationship

We investigated the relationship between intraterminal Ca2+concentration ([Ca2+]i) and the frequency of miniature end plate potentials (MEPPs) at the frog neuromuscular junction by use of ratiometric imaging of fura-2-loaded nerve terminals and intracellular recording of MEPPs. Elevation of extracellular [KCl] over the range of 2–20 mM resulted in increases in [Ca2+]i and MEPP frequency. Loading terminals with the fast and slow Ca2+-buffers bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid-acetoxymethyl (BAPTA-AM) and EGTA-AM resulted in equivalent reductions in the KCl-dependent increases in MEPP frequency. The [Ca2+]i dependence of MEPP frequency determined by elevation of [Ca2+]i due to application of 0.1–10 μM ionomycin was similar to that determined when [Ca2+]i was raised by increasing extracellular KCl. Measurements in 10 mM extracellular KCl revealed that application of the phorbol ester phorbol 12 myristate 13-acetetate (PMA) caused an increase in MEPP frequency while the inactive analogue, 4α-PMA, did not. PMA application also caused an increase in [Ca2+]i. The relationship between [Ca2+]i and MEPP frequency in PMA was the same as was determined by the other methods of raising [Ca2+]i. Under all conditions tested, our data revealed a low [Ca2+]i threshold for activation of transmitter release and are consistent with a K d for [Ca2+]i on the order of 1 μM.

Sign in / Sign up

Export Citation Format

Share Document