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Turecek, Josef

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Turecek

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Josef

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Turecek, Josef

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2015 - 20172

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Author's Publications: search.filters.isAuthorOfPublication.5a2d1c97-13b4-43b7-adce-f6cc115c0296

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    The calcium sensor synaptotagmin 7 is required for synaptic facilitation
    (2015) Jackman, Skyler L.; Turecek, Josef; Belinsky, Justine E.; Regehr, Wade
    It has been known for over 70 years that synaptic strength is dynamically regulated in a use-dependent manner1. At synapses with a low initial release probability, closely spaced presynaptic action potentials can result in facilitation, a short-term form of enhancement where each subsequent action potential evokes greater neurotransmitter release2. Facilitation can enhance neurotransmitter release manyfold and profoundly influence information transfer across synapses3, but the underlying mechanism remains a mystery. Among the proposed mechanisms is that a specialized calcium sensor for facilitation transiently increases the probability of release2,4 and is distinct from the fast sensors that mediate rapid neurotransmitter release. Yet such a sensor has never been identified, and its very existence has been disputed5,6. Here we show that synaptotagmin 7 (syt7) is a calcium sensor that is required for facilitation at multiple central synapses. In syt7 knockout mice, facilitation is eliminated even though the initial probability of release and presynaptic residual calcium signals are unaltered. Expression of wild-type syt7 in presynaptic neurons restored facilitation, whereas expression of a mutated syt7 with a calcium-insensitive C2A domain did not. By revealing the role of syt7 in synaptic facilitation, these results resolve a longstanding debate about a widespread form of short-term plasticity, and will enable future studies that may lead to a deeper understanding of the functional importance of facilitation.
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    Synaptotagmin 7 confers frequency invariance onto specialized depressing synapses
    (2017) Turecek, Josef; Jackman, Skyler L.; Regehr, Wade
    At most synapses in the brain, short-term plasticity dynamically modulates synaptic strength. Rapid frequency-dependent changes in synaptic strength play critical roles in sensory adaptation, gain control and many other neural computations1,2. However, some auditory, vestibular and cerebellar synapses maintain constant strength over a wide range of firing frequencies3–5, and as a result efficiently encode firing rates. Despite its apparent simplicity, frequency-invariant transmission is difficult to achieve because of inherent synaptic nonlinearities6. Here we study frequency-invariant transmission at Purkinje cell to deep cerebellar nuclear (PC to DCN) synapses and vestibular synapses. Prolonged activation of these synapses leads to initial depression, which is followed by steady-state responses that are frequency invariant for their physiological activity range. We find that Synaptotagmin 7 (Syt7), a recently identified calcium sensor for short-term facilitation7, is present at both synapses. It was unclear why a sensor for facilitation would be present at these and other depressing synapses. We find that at PC and vestibular synapses, Syt7 supports a hidden component of facilitation that can be unmasked in wildtype animals but is absent in Syt7 knockout animals. In wildtype mice, facilitation increases with firing frequency and counteracts depression to produce frequency-invariant transmission. In Syt7 knockout mice, PC and vestibular synapses exhibit conventional use-dependent depression, weakening to a greater extent as the firing frequency is increased. Presynaptic rescue of Syt7 expression restores both facilitation and frequency-invariant transmission. Our results identify a function for Syt7 at synapses that exhibit overall depression, and demonstrate that facilitation plays an unexpected and important role in producing frequency-invariant transmission.