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Kainate Induces Mobilization of Synaptic Vesicles at the Growth Cone through the Activation of Protein Kinase A inglese (Articolo in rivista)

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Kainate Induces Mobilization of Synaptic Vesicles at the Growth Cone through the Activation of Protein Kinase A inglese (Articolo in rivista) (literal)

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Giuliana Gelsomino1,7, Elisabetta Menna1, Flavia Antonucci1, Simona Rodighiero4, Loredana Riganti1, Christophe Mulle5, Fabio Benfenati2, Flavia Valtorta3, Claudia Verderio1 and Michela Matteoli1,6 (2013)
Kainate Induces Mobilization of Synaptic Vesicles at the Growth Cone through the Activation of Protein Kinase A inglese
in Cerebral cortex (N. Y. N. Y., 1991)
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Giuliana Gelsomino1,7, Elisabetta Menna1, Flavia Antonucci1, Simona Rodighiero4, Loredana Riganti1, Christophe Mulle5, Fabio Benfenati2, Flavia Valtorta3, Claudia Verderio1 and Michela Matteoli1,6 (literal)

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1 Department of Medical Pharmacology and Consiglio Nazionale delle Ricerche (CNR) Institute of Neuroscience, University of Milano, 20129 Milano, Italy 2 Department of Neuroscience and Brain Technologies, The Italian Institute of Technology and Dipartimento di Medicina Sperimentale, University of Genova, 16163 Genova, Italy 3 San Raffaele Scientific Institute, Vita-Salute University, 20132 Milano, Italy 4 Fondazione Filarete, 20139 Milano, Italy 5 Interdisciplinary Institute for Neuroscience, University of Bordeaux, CNRS UMR 5297, F-33000 Bordeaux, France 6 Istituto Clinico Humanitas, Istituto di ricovero e cura a carattere scientifico (IRCCS), 20089 Rozzano, Italy 7 Current address: CNR, Institute of Molecular Bioimaging and Physiology, 20090 Segrate, Milano, Italy (literal)

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Kainate Induces Mobilization of Synaptic Vesicles at the Growth Cone through the Activation of Protein Kinase A inglese (literal)

Abstract

Activation of protein kinase A (PKA) pathway at presynaptic terminals plays a crucial role in the supply of synaptic vesicles (SVs) from the reserve pool, affecting the steady-state level of activity and the reconstitution of the readily releasable pool after intense stimulation. However, the identity of the stimuli activating this pathway is undefined. Using fluorescence resonance energy transfer and molecular genetic, we show that kainate, through the activation of presynaptic kainate receptors, induces PKA activation and enhances synapsin I phosphorylation at PKA-specific residues. This leads to a dispersion of synapsin I immunoreactivity, which is accompanied by a PKA-dependent increase in the rate of SV recycling at the growth cone and by an enhanced miniature excitatory postsynaptic currents frequency in mature networks. Selective activation of this pathway is induced by the native neurotransmitter glutamate, when applied in the high nanomolar range. These data identify glutamate, specifically acting on KARs, as one of the stimuli able to induce phosphorylation of synapsin at PKA sites, both at the axonal growth cone and at the mature synapse, thus increasing SV availability and contributing to plasticity phenomena. (literal)

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