Allosteric modulation of the presynaptic Ca2+ sensor for vesicle fusion

Xuelin Lou, Volker Scheuss and Ralf Schneggenburger ()
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Xuelin Lou: Max-Planck-Institut für biophysikalische Chemie
Volker Scheuss: Max-Planck-Institut für biophysikalische Chemie
Ralf Schneggenburger: Max-Planck-Institut für biophysikalische Chemie

Nature, 2005, vol. 435, issue 7041, 497-501

Abstract: Abstract Neurotransmitter release is triggered by an increase in the cytosolic Ca2+ concentration ([Ca2+]i), but it is unknown whether the Ca2+-sensitivity of vesicle fusion is modulated during synaptic plasticity. We investigated whether the potentiation of neurotransmitter release by phorbol esters1,2,3, which target presynaptic protein kinase C (PKC)/munc-13 signalling cascades4,5,6, exerts a direct effect on the Ca2+-sensitivity of vesicle fusion. Using direct presynaptic Ca2+-manipulation and Ca2+ uncaging at a giant presynaptic terminal, the calyx of Held, we show that phorbol esters potentiate transmitter release by increasing the apparent Ca2+-sensitivity of vesicle fusion. Phorbol esters potentiate Ca2+-evoked release as well as the spontaneous release rate. We explain both effects by an increased fusion ‘willingness’ in a new allosteric model of Ca2+-activation of vesicle fusion. In agreement with an allosteric mechanism, we observe that the classically high Ca2+ cooperativity in triggering vesicle fusion (∼ 4) is gradually reduced below 3 µM [Ca2+]i, reaching a value of

Date: 2005
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DOI: 10.1038/nature03568

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