Abstract：
:Neurotransmitter release can be synchronous and occur within milliseconds of action potential invasion, or asynchronous and persist for tens of milliseconds. The molecular determinants of release kinetics remain poorly understood. It has been hypothesized that asynchronous release dominates when fast Synaptotagmin isoforms are far from calcium channels or when specialized sensors, such as Synaptotagmin 7, are abundant. Here we test these hypotheses for GABAergic projections onto neurons of the inferior olive, where release in different subnuclei ranges from synchronous to asynchronous. Surprisingly, neither of the leading hypotheses accounts for release kinetics. Instead, we find that rapid Synaptotagmin isoforms are abundant in subnuclei with synchronous release but absent where release is asynchronous. Viral expression of Synaptotagmin 1 transforms asynchronous synapses into synchronous ones. Thus, the nervous system controls levels of fast Synaptotagmin isoforms to regulate release kinetics and thereby controls the ability of synapses to encode spike rates or precise timing.
journal_name
Neuronjournal_title
Neuronauthors
Turecek J,Regehr WGdoi
10.1016/j.neuron.2019.01.013subject
Has Abstractpub_date
2019-03-06 00:00:00pages
938-949.e4issue
5eissn
0896-6273issn
1097-4199pii
S0896-6273(19)30014-5journal_volume
101pub_type
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