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26 results on '"Bolognesi, Paolo"'

4. Improved Design-Oriented Analytical Modelling of Switched Reluctance Machines Based on Fröhlich-Kennelly Equations

Author

Rocca, Roberto, De Donato, Giulio, Bolognesi, Paolo, Boccaletti, Chiara, and Capponi, Fabio Giulii

Abstract

The need to reduce computational burden in the preliminary design stage of switched reluctance machines is fostering the interest in design-oriented analytical modelling. To this end, this work proposes a novel design-oriented analytical model that comprises two main parts, each of them containing an original scientific contribution: 1) a new interpolation technique for the flux loci based on 2${\text{nd}}$-order Fröhlich-Kennelly equations, and 2) an analytical model that calculates flux linkage in partial overlap and saturated conditions. The model is validated against finite element analyses of four switched reluctance machines and the experimental results of a physical prototype. Finally, an in-depth discussion on the use, accuracy and limitations of proposed analytical model is provided.

Published
2024
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22. Olanzapine, but not clozapine, increases glutamate release in the prefrontal cortex of freely moving mice by inhibiting D-aspartate oxidase activity

Author

Sacchi, Silvia, primary, Novellis, Vito De, additional, Paolone, Giovanna, additional, Nuzzo, Tommaso, additional, Iannotta, Monica, additional, Belardo, Carmela, additional, Squillace, Marta, additional, Bolognesi, Paolo, additional, Rosini, Elena, additional, Motta, Zoraide, additional, Frassineti, Martina, additional, Bertolino, Alessandro, additional, Pollegioni, Loredano, additional, Morari, Michele, additional, Maione, Sabatino, additional, Errico, Francesco, additional, and Usiello, Alessandro, additional

Published
2017
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26. Leucine-rich repeat kinase 2 (LRRK2) inhibitors differentially modulate glutamate release and Serine935 LRRK2 phosphorylation in striatal and cerebrocortical synaptosomes.

Author

Mercatelli D, Bolognesi P, Frassineti M, Pisanò CA, Longo F, Shimshek DR, and Morari M

Subjects
Animals, Corpus Striatum drug effects, Corpus Striatum metabolism, Dopamine metabolism, Exocytosis, Gene Knock-In Techniques, Glutamic Acid metabolism, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 antagonists & inhibitors, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 chemistry, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 genetics, Male, Mice, Phosphorylation, Serine metabolism, Synaptosomes drug effects, Synaptosomes metabolism, Visual Cortex drug effects, Visual Cortex metabolism, Aminopyridines pharmacology, Benzamides pharmacology, Benzodiazepinones pharmacology, Corpus Striatum cytology, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 metabolism, Pyrimidines pharmacology, Visual Cortex cytology
Abstract

Mutations in leucine-rich repeat kinase 2 ( LRRK2 ) gene have been pathogenically linked to Parkinson's disease, and pharmacological inhibition of LRRK2 is being pursued to tackle nigro-striatal dopaminergic neurodegeneration. However, LRRK2 kinase inhibitors may have manifold actions, affecting not only pathological mechanisms in dopaminergic neurons but also physiological functions in nondopaminergic neurons. Therefore, we investigated whether LRRK2 kinase inhibitors differentially modulate dopamine and glutamate release from the mouse striatum and cerebral cortex. Spontaneous and KCl-evoked [ 3 H]-dopamine and glutamate release from superfused synaptosomes obtained from wild-type and LRRK2 knock-out, kinase-dead or G2019S knock-in mice was measured. Two structurally unrelated inhibitors, LRRK2-IN-1 and GSK2578215A, were tested. LRRK2, phosphoSerine1292 and phosphoSerine935 LRRK2 levels were measured in all genotypes, and target engagement was evaluated by monitoring phosphoSerine935 LRRK2. LRRK2-IN-1 inhibited striatal glutamate but not dopamine release; GSK2578215A inhibited striatal dopamine and cortical glutamate but enhanced striatal glutamate release. LRRK2-IN-1 reduced striatal and cortical phosphoSerine935 levels whereas GSK2578215A inhibited only the former. Neither LRRK2 inhibitor affected neurotransmitter release in LRRK2 knock-out and kinase-dead mice; however, they facilitated dopamine without affecting striatal glutamate in G2019S knock-in mice. GSK2578215A inhibited cortical glutamate release in G2019S knock-in mice. We conclude that LRRK2-IN-1 and GSK2578215A modulate exocytosis by blocking LRRK2 kinase activity, although their effects vary depending on the nerve terminal examined. The G2019S mutation unravels a dopamine-promoting action of LRRK2 inhibitors while blunting their effects on glutamate release, which highlights their positive potential for the treatment of PD, especially of LRRK2 mutation carriers., Competing Interests: DRS is employed by Novartis Pharma. All other Authors declare no competing interests.

Published
2019
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