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A dual-Ca2+-sensor model for neurotransmitter release in a central synapse
Jianyuan Sun1, Zhiping P Pang, Dengkui Qin
1Department of Neuroscience, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. Jianyuan.Sun@UTSouthwestern.edu
Nature
|November 30, 2007
Summary
Asynchronous neurotransmitter release, previously enigmatic, is now quantitatively described. Deleting synaptotagmin 2 (Syt2) isolates asynchronous release, revealing its distinct calcium dynamics and role in vesicle pool depletion.
Area of Science:
- Neuroscience
- Synaptic Transmission
- Calcium Signaling
Background:
- Synchronous neurotransmitter release is well-understood.
- The nature and mechanisms of asynchronous release remain largely unknown.
- Investigating asynchronous release is crucial for a complete understanding of synaptic function.
Purpose of the Study:
- To quantitatively describe asynchronous neurotransmitter release.
- To elucidate the calcium (Ca2+) dependence of asynchronous release.
- To propose a model explaining both synchronous and asynchronous release.
Main Methods:
- Utilized genetically modified mice lacking synaptotagmin 2 (Syt2) to isolate asynchronous release.
- Employed photolysis of caged calcium (Ca2+) to precisely control presynaptic calcium levels.
- Quantified calcium cooperativity and affinity for both release types.
Main Results:
- Asynchronous release exhibits a Ca2+ cooperativity of ~2 and affinity of ~44 μM.
- Synchronous release shows Ca2+ cooperativity of ~5 and affinity of ~38 μM.
- Asynchronous release empties the readily releasable vesicle pool during sustained Ca2+ elevation.
Conclusions:
- Asynchronous release is physiologically relevant, especially at lower Ca2+ concentrations.
- A dual Ca2+ sensor model can quantitatively explain both release modes.
- This study provides a framework for understanding presynaptic calcium dynamics and neurotransmitter release.
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