A dual-Ca2+-sensor model for neurotransmitter release in a central synapse

Jianyuan Sun (), Zhiping P. Pang, Dengkui Qin, Abigail T. Fahim, Roberto Adachi and Thomas C. Südhof ()
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Jianyuan Sun: Departments of Neuroscience and,
Zhiping P. Pang: Departments of Neuroscience and,
Dengkui Qin: Departments of Neuroscience and,
Abigail T. Fahim: The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA
Roberto Adachi: The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA
Thomas C. Südhof: Departments of Neuroscience and,

Nature, 2007, vol. 450, issue 7170, 676-682

Abstract: Abstract Ca2+-triggered synchronous neurotransmitter release is well described, but asynchronous release—in fact, its very existence—remains enigmatic. Here we report a quantitative description of asynchronous neurotransmitter release in calyx-of-Held synapses. We show that deletion of synaptotagmin 2 (Syt2) in mice selectively abolishes synchronous release, allowing us to study pure asynchronous release in isolation. Using photolysis experiments of caged Ca2+, we demonstrate that asynchronous release displays a Ca2+ cooperativity of ∼2 with a Ca2+ affinity of ∼44 μM, in contrast to synchronous release, which exhibits a Ca2+ cooperativity of ∼5 with a Ca2+ affinity of ∼38 μM. Our results reveal that release triggered in wild-type synapses at low Ca2+ concentrations is physiologically asynchronous, and that asynchronous release completely empties the readily releasable pool of vesicles during sustained elevations of Ca2+. We propose a dual-Ca2+-sensor model of release that quantitatively describes the contributions of synchronous and asynchronous release under conditions of different presynaptic Ca2+ dynamics.

Date: 2007
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DOI: 10.1038/nature06308

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