The number of neurotransmitter-filled vesicles released into the synaptic cleft with each action potential dictates the reliability of synaptic transmission. Variability of this fundamental property provides diversity of synaptic function across brain regions, but the source of this variability is unclear. The prevailing view is that release of a single (univesicular release, UVR) or multiple vesicles (multivesicular release, MVR) reflects variability in vesicle release probability, a notion that is well-supported by the calcium-dependence of release mode. However, using mouse brain slices, we now demonstrate that the number of vesicles released is regulated by the size of the readily-releasable pool, upstream of vesicle release probability. Our results point to a model wherein protein kinase A and its vesicle-associated target, synapsin, dynamically control release site occupancy to dictate the number of vesicles released without altering release probability. Together these findings define molecular mechanisms that control MVR and functional diversity of synaptic signaling.

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It is well known that a beam splitter (BS) can be used as a source of photon quantum entanglement. This is due to the fact that the statistics of photons changes at the output ports of the BS. Usually, quantum entanglement and photon statistics take into account the constancy of the reflection coefficient R or the transmission coefficient T of the BS, where $$R + T = 1$$ R + T = 1 . It has recently been shown that if BS is used in the form of coupled waveguides, the coefficients R and T will depend on the photon frequencies. In this paper, it is shown that the quantum entanglement and statistics of photons at the output ports of a BS can change significantly if a BS is used in the form of coupled waveguides, where the coefficients R and T are frequency-dependent.

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