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Fabio Benfenati

Researcher at Istituto Italiano di Tecnologia

Publications -  424
Citations -  24243

Fabio Benfenati is an academic researcher from Istituto Italiano di Tecnologia. The author has contributed to research in topics: Synapsin & Synapsin I. The author has an hindex of 77, co-authored 406 publications receiving 21422 citations. Previous affiliations of Fabio Benfenati include University of Padua & University of Modena and Reggio Emilia.

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Study of the conformation of DARPP-32, a dopamine- and cAMP-regulated phosphoprotein, by fluorescence spectroscopy.

TL;DR: Findings indicate that DARPP-32 contains at least two distinct domains and that phosphorylation has no dramatic effects on its conformation.
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Biocompatibility of a Magnetic Tunnel Junction Sensor Array for the Detection of Neuronal Signals in Culture

TL;DR: This study presents the first biomagnetic chip based on magnetic tunnel junction (MTJ) technology for cell culture studies and shows the biocompatibility of these sensors, paving the way to the development of high performing biomagnetic sensing technology for the electrophysiology of in vitro systems, in analogy with Multi Electrode Arrays.
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Neuronal hyperactivity causes Na+/H+ exchanger-induced extracellular acidification at active synapses.

TL;DR: A novel extracellular pH-indicator that is sensitive to acidic shifts reveals that neuronal hyperactivity causes acidic shifts that are localized to active synapses and generated by the Na+/H+ exchanger.
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TBC1D24 regulates axonal outgrowth and membrane trafficking at the growth cone in rodent and human neurons.

TL;DR: The data reveal that alterations of membrane trafficking at the growth cone induced by TBC1D24 loss of function cause axonal and excitability defects, which correlate with the disease severity and highlight an important role for TBC 1D24 in connectivity during brain development.
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Exocytosis regulates trafficking of GABA and glycine heterotransporters in spinal cord glutamatergic synapses: a mechanism for the excessive heterotransporter-induced release of glutamate in experimental amyotrophic lateral sclerosis.

TL;DR: It can be hypothesized that the excessive GAT-1 and GlyT-1/2 heterotransporter-mediated Glu release, in the spinal cord of SOD1(G93A) mice, is due to the heterotranporter over-expression at the nerve terminal membrane, promoted by thecessive Glu exocytosis.