Loose Coupling Between Ca2+ Channels and Release Sensors at a Plastic Hippocampal Synapse

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Science  07 Feb 2014:
Vol. 343, Issue 6171, pp. 665-670
DOI: 10.1126/science.1244811

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From Channel to Sensor

The coupling between voltage-activated calcium channels and calcium sensors of exocytosis on synaptic vesicles is a key factor that determines the timing and efficiency of transmitter release. It is still largely unclear how tight this coupling is at mature synapses in the central nervous system. Vyleta and Jonas (p. 665) found that mossy fiber boutons contain high concentrations of endogenous calcium buffers that normally limit the amount of calcium that reaches the calcium sensor responsible for neurotransmitter release. As a consequence, the calcium signal available to trigger release is small for the initial action potential. However, after high-frequency stimulation, the endogenous calcium buffer binds calcium and is less able to buffer calcium entry, which allows more calcium to reach the calcium sensor, increasing neurotransmitter release and synaptic facilitation.


The distance between Ca2+ channels and release sensors determines the speed and efficacy of synaptic transmission. Tight “nanodomain” channel-sensor coupling initiates transmitter release at synapses in the mature brain, whereas loose “microdomain” coupling appears restricted to early developmental stages. To probe the coupling configuration at a plastic synapse in the mature central nervous system, we performed paired recordings between mossy fiber terminals and CA3 pyramidal neurons in rat hippocampus. Millimolar concentrations of both the fast Ca2+ chelator BAPTA [1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid] and the slow chelator EGTA efficiently suppressed transmitter release, indicating loose coupling between Ca2+ channels and release sensors. Loose coupling enabled the control of initial release probability by fast endogenous Ca2+ buffers and the generation of facilitation by buffer saturation. Thus, loose coupling provides the molecular framework for presynaptic plasticity.

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