Site-specific synapsin I phosphorylation participates in the expression of post-tetanic potentiation and its enhancement by BDNF

Pierluigi Valente, Silvia Casagrande, Thierry Nieus, Anne M J Verstegen, Flavia Valtorta, Fabio Benfenati, Pietro Baldelli

Research output: Contribution to journalArticlepeer-review

Abstract

A large amount of experimental evidence has highlighted the rapid changes in synaptic efficacy induced by high-frequency stimulation andBDNFat central excitatory synapses.Weclarified the quantal mechanisms and the involvement of Synapsin I (SynI) phosphorylation in the expression of post-tetanic potentiation (PTP) and in its modulation by BDNF in mouse glutamatergic autapses.Wefound that PTP is associated with an elevation in the probability of release and a concomitant increase in the size of the readily releasable pool (RRP). The latter component was virtually absent in SynI knock-out (KO) neurons, which indeed displayed impaired PTP. PTP was fully rescued by the expression of wild-type SynI, but not of its dephosphomimetic mutants in the phosphorylation sites for cAMP-dependent protein kinase and Ca2+/calmodulin-dependent protein kinases I/II. BDNF potently enhanced PTP through a further increase in the RRP size, which was missing in SynI KO neurons. In these neurons, the BDNF-induced PTP enhancement was rescued by the expression of wild-type SynI, but not of its dephosphomimetic mutant at the mitogen-dependent protein kinase sites. The results indicate that the increase in RRP size necessary for the full expression of PTP, and its sensitivity to BDNF, involve phosphorylation of SynI at distinct sites, thus implicating SynI as an essential downstream effector for the expression of PTP and for its enhancement by BDNF.

Original languageEnglish
Pages (from-to)5868-5879
Number of pages12
JournalJournal of Neuroscience
Volume32
Issue number17
DOIs
Publication statusPublished - Apr 25 2012

ASJC Scopus subject areas

  • Neuroscience(all)

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