P
Pietro Baldelli
Researcher at University of Genoa
Publications - 97
Citations - 4591
Pietro Baldelli is an academic researcher from University of Genoa. The author has contributed to research in topics: Neurotransmission & Synapsin. The author has an hindex of 40, co-authored 92 publications receiving 3932 citations. Previous affiliations of Pietro Baldelli include Istituto Italiano di Tecnologia & University of Turin.
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Journal ArticleDOI
The synapsins: Key actors of synapse function and plasticity
TL;DR: A comprehensive description of the molecular basis ofsynapsin function is given, as well as an overview of the more recent evidence linking mutations in the synapsin proteins to the onset of severe central nervous system diseases such as epilepsy and schizophrenia.
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Acute stress increases depolarization-evoked glutamate release in the rat prefrontal/frontal cortex: the dampening action of antidepressants.
Laura Musazzi,Marco Milanese,Pasqualina Farisello,Simona Zappettini,Daniela Tardito,V.S. Barbiero,Tiziana Bonifacino,Alessandra Mallei,Pietro Baldelli,Giorgio Racagni,Maurizio Raiteri,Fabio Benfenati,Giambattista Bonanno,Maurizio Popoli +13 more
TL;DR: Patch-clamp recordings of pyramidal neurons in the prefrontal cortex revealed that stress increased glutamatergic transmission through both pre- and postsynaptic mechanisms, and that antidepressants may normalize it by reducing release probability.
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SYN1 loss-of-function mutations in autism and partial epilepsy cause impaired synaptic function
Anna Fassio,Lysanne Patry,Sonia Congia,Franco Onofri,Amélie Piton,Julie Gauthier,Davide Pozzi,Mirko Messa,Enrico Defranchi,Manuela Fadda,Anna Corradi,Pietro Baldelli,Line Lapointe,Judith St-Onge,Caroline Meloche,Laurent Mottron,Flavia Valtorta,Dang Khoa Nguyen,Guy A. Rouleau,Fabio Benfenati,Patrick Cossette +20 more
TL;DR: It is demonstrated that SYN1 is a novel predisposing gene to ASDs, in addition to epilepsy, and the hypothesis that a disturbance of synaptic homeostasis underlies the pathogenesis of both diseases is strengthened.
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Lack of Synapsin I Reduces the Readily Releasable Pool of Synaptic Vesicles at Central Inhibitory Synapses
TL;DR: The deletion of SYN1 did not affect paired-pulse depression or post-tetanic potentation, but was associated with a moderate increase of synaptic depression evoked by trains of action potentials, which became apparent at high stimulation frequencies and was accompanied by a slow down of recovery from depression.
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Protein kinase A-mediated synapsin I phosphorylation is a central modulator of Ca2+-dependent synaptic activity.
Andrea Menegon,Dario Bonanomi,Chiara Albertinazzi,Francesco Lotti,Giuliana Ferrari,Hung-Teh Kao,Fabio Benfenati,Pietro Baldelli,Flavia Valtorta +8 more
TL;DR: Data define a hierarchical crosstalk between cAMP- and CaM-dependent cascades and point to synapsin as a major effector of PKA in the modulation of activity-dependent SV exocytosis, which is primarily caused by calmodulin-dependent activation of cAMP pathways rather than by direct activation of CaM kinases.