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151 results on '"Pittaluga, ANNA MARIA"'

1. Unveiling Niaprazine's Potential: Behavioral Insights into a Re-Emerging Anxiolytic Agent.

Author

Trebesova, Hanna, Monaco, Martina, Baldassari, Sara, Ailuno, Giorgia, Lancellotti, Edilio, Caviglioli, Gabriele, Pittaluga, Anna Maria, and Grilli, Massimo

Subjects
MAZE tests, TRANQUILIZING drugs, NERVE endings, DRINKING water, PHYSIOLOGICAL stress
Abstract

Ongoing global research actions seek to comprehensively understand the adverse impact of stress and anxiety on the physical and mental health of both human beings and animals. Niaprazine (NIA) is a chemical compound that belongs to the class of piperazine derivatives. This compound has recently gained renewed attention due to its potential therapeutic properties for treating certain conditions such as anxiety. Despite its potential benefits, the behavioral effects of NIA have not been thoroughly investigated. This study aimed to examine NIA's potential as an anti-anxiety and anti-stress agent. After administering either vehicle or NIA in their drinking water to mice for 14 days, we conducted behavioral analyses using the Marble Burying Test and the Elevated Plus Maze test. NIA-treated mice spend more time in the open arms and bury fewer marbles. Moreover, a stability study confirmed the linear relationship between NIA concentration and its response across concentrations encompassing the NIA mother solution and the NIA solutions administered to mice. Also, a preliminary synaptic toxicity analysis showed no direct damage to cortical nerve endings. Here, we show that NIA can modulate anxiety-related behaviors without significantly impacting exploratory activity or adverse effects. Our work describes new findings that contribute to the research on safer and more tolerable anxiety management options. [ABSTRACT FROM AUTHOR]

Published
2024
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5. The promnesic effects of Tilia tomentosa bud extracts on old male mice

Author

Trebesova, Hanna, Orlandi, Valentina, Olivero, Guendalina, Turrini, Federica, Dario, Donno, Gabriele, Beccaro, Boggia, Raffaella, Pittaluga, ANNA MARIA, and Grilli, Massimo

Subjects
nutraceuticals, Tilia tomentosa, behavioural analysis, synaptosomes, CNS, CNS, synaptosomes, nutraceuticals, behavioural analysis, Tilia tomentosa, neuropharmacology, neuropharmacology
Published
2022

6. GLI EFFETTI ANSIOLITICI E PROMNESICI DEGLI ESTRATTI DI TILIA TOMENTOSA: UNO STUDIO PRECLINICO

Author

Trebesova, Hanna, Orlandi, Valentina, Sabrina, Gandolfo, Olivero, Guendalina, Turrini, Federica, Dario, Donno, Beccaro, Gabriele, Boggia, Raffaella, Pittaluga, ANNA MARIA, and Grilli, Massimo

Subjects
neurofarmacologia, Nutraceutica, fitoterapia, SNC, test comportamentali, sinaptosomi, neurofarmacologia, Nutraceutica, test comportamentali, sinaptosomi, fitoterapia, SNC
Published
2022

21. Characterization data of water-soluble hydrophilic and amphiphilic dendrimers prodrugs for delivering bioactive chemical entities otherwise non soluble

Author

Alfei, Silvana, Spallarossa, Andrea, Catena, Silvia, Turrini, Federica, Zuccari, Guendalina, Pittaluga, ANNA MARIA, and Boggia, Raffaella

Subjects
remarkable healthy properties, antioxidant power, water-solubility, natural products, cationic polyester-based dendrimers, hydrophilic and amphiphilic dendrimeric drug formulations, cationic polyester-based dendrimers, hydrophilic and amphiphilic dendrimeric drug formulations, natural products, remarkable healthy properties, water-solubility, improved bioavailability, protracted drug release profile, buffer capacity, antioxidant power, buffer capacity, improved bioavailability, protracted drug release profile
Published
2019

23. Non-PAMAM amino acids-modified dendrimers nanoparticles for enhancing water-solubility of insoluble bioactive molecules: our state of the art

Author

Alfei, Silvana, Spallarossa, Andrea, Catena, Silvia, Turrini, Federica, Zuccari, Guendalina, Pittaluga, ANNA MARIA, and Boggia, Raffaella

Subjects
remarkable healthy properties, antioxidant power, water-solubility, natural products, cationic polyester-based dendrimers, hydrophilic and amphiphilic dendrimeric drug formulations, cationic polyester-based dendrimers, hydrophilic and amphiphilic dendrimeric drug formulations, natural products, remarkable healthy properties, water-solubility, improved bioavailability, protracted drug release profile, buffer capacity, antioxidant power, buffer capacity, improved bioavailability, protracted drug release profile
Published
2019

30. Antibodies Against the NH2-Terminus of the GluA Subunits Affect the AMPA-Evoked Releasing Activity: The Role of Complement.

Author

Cisani, Francesca, Olivero, Guendalina, Usai, Cesare, Van Camp, Gilles, Maccari, Stefania, Morley-Fletcher, Sara, and Pittaluga, Anna Maria

Subjects
WESTERN immunoblotting, NERVE endings, IMMUNOGLOBULINS, SYNAPTOSOMES, COMPLEMENT activation
Abstract

Antibodies recognizing the amino-terminal domain of receptor subunit proteins modify the receptor efficiency to controlling transmitter release in isolated nerve endings (e.g., synaptosomes) indirectly confirming their presence in these particles but also allowing to speculate on their subunit composition. Western blot analysis and confocal microscopy unveiled the presence of the GluA1, GluA2, GluA3, and GluA4 receptor subunits in cortical synaptosomes. Functional studies confirmed the presence of presynaptic release-regulating AMPA autoreceptors in these terminals, whose activation releases [3H]D-aspartate ([3H]D-Asp, here used as a marker of glutamate) in a NBQX-dependent manner. The AMPA autoreceptors traffic in a constitutive manner, since entrapping synaptosomes with the pep2-SVKI peptide (which interferes with the GluA2-GRIP1/PICK1 interaction) amplified the AMPA-evoked releasing activity, while the inactive pep2-SVKE peptide was devoid of activity. Incubation of synaptosomes with antibodies recognizing the NH2 terminus of the GluA2 and the GluA3 subunits increased, although to a different extent, the GluA2 and 3 densities in synaptosomal membranes, also amplifying the AMPA-evoked glutamate release in a NBQX-dependent fashion. We then analyzed the releasing activity of complement (1:300) from both treated and untreated synaptosomes and found that the complement-induced overflow occurred in a DL-t-BOA-sensitive, NBQX-insensitive fashion. We hypothesized that anti-GluA/GluA complexes in neuronal membranes could trigger the classic pathway of activation of the complement, modifying its releasing activity. Accordingly, the complement-evoked release of [3H]D-Asp from antiGluA2 and anti-GluA3 antibody treated synaptosomes was significantly increased when compared to untreated terminals and facilitation was prevented by omitting the C1q component of the immunocomplex. Antibodies recognizing the NH2 terminus of the GluA1 or the GluA4 subunits failed to affect both the AMPA and the complement-evoked tritium overflow. Our results suggest the presence of GluA2/GluA3-containing release-regulating AMPA autoreceptors in cortical synaptosomes. Incubation of synaptosomes with commercial anti-GluA2 or anti-GluA3 antibodies amplifies the AMPA-evoked exocytosis of glutamate through a complement-independent pathway, involving an excessive insertion of AMPA autoreceptors in plasma membranes but also affects the complement-dependent releasing activity, by promoting the classic pathway of activation of the immunocomplex. Both events could be relevant to the development of autoimmune diseases typified by an overproduction of anti-GluA subunits. [ABSTRACT FROM AUTHOR]

Published
2021
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37. Presynaptic, release‐regulating mGlu2‐preferring and mGlu3‐preferring autoreceptors in CNS: pharmacological profiles and functional roles in demyelinating disease

Author

DI PRISCO, Silvia, Merega, Elisa, Bonfiglio, Tommaso, Olivero, Guendalina, Cervetto, Chiara, Grilli, Massimo, Usai, Cesare, Marchi, Mario, and Pittaluga, ANNA MARIA

Subjects
Central Nervous System, Male, Presynaptic Terminals, acute administration, Receptors, Metabotropic Glutamate, LY541850, Bridged Bicyclo Compounds, Mice, Structure-Activity Relationship, NAAG, EAE mice, LY341495, LY379268, cortex, glutamate exocytosis, mGlu2/3 autoreceptors, spinal cord, Animals, Autoreceptors, Dose-Response Relationship, Drug, Dipeptides, Research Papers, Amino Acids, Dicarboxylic, Mice, Inbred C57BL, Female, Demyelinating Diseases, Synaptosomes
Abstract

Presynaptic, release-regulating metabotropic glutamate 2 and 3 (mGlu2/3) autoreceptors exist in the CNS. They represent suitable targets for therapeutic approaches to central diseases that are typified by hyperglutamatergicity. The availability of specific ligands able to differentiate between mGlu2 and mGlu3 subunits allows us to further characterize these autoreceptors. In this study we investigated the pharmacological profile of mGlu2/3 receptors in selected CNS regions and evaluated their functions in mice with experimental autoimmune encephalomyelitis (EAE).The comparative analysis of presynaptic mGlu2/3 autoreceptors was performed by determining the effect of selective mGlu2/3 receptor agonist(s) and antagonist(s) on the release of [(3)H]-D-aspartate from cortical and spinal cord synaptosomes in superfusion. In EAE mice, mGlu2/3 autoreceptor-mediated release functions were investigated and effects of in vivo LY379268 administration on impaired glutamate release examined ex vivo.Western blot analysis and confocal microscopy confirmed the presence of presynaptic mGlu2/3 receptor proteins. Cortical synaptosomes possessed LY541850-sensitive, NAAG-insensitive autoreceptors having low affinity for LY379268, while LY541850-insensitive, NAAG-sensitive autoreceptors with high affinity for LY379268 existed in spinal cord terminals. In EAE mice, mGlu2/3 autoreceptors completely lost their inhibitory activity in cortical, but not in spinal cord synaptosomes. In vivo LY379268 administration restored the glutamate exocytosis capability in spinal cord but not in cortical terminals in EAE mice.We propose the existence of mGlu2-preferring and mGlu3-preferring autoreceptors in mouse cortex and spinal cord respectively. The mGlu3 -preferring autoreceptors could represent a target for new pharmacological approaches for treating demyelinating diseases.

Published
2016

45. Pharmacological characterization of NMDA-like receptors in the single-celled organism Paramecium primaurelia

Author

Ramoino, Paola, Candiani, Simona, Pittaluga, Anna Maria, Usai, Cesare, Gallus, Lorenzo, Ferrando, Sara, Milanese, Marco, Faimali, Marco, and Bonanno, Giambattista

Subjects
pharmacology, Swimming behaviour, NMDA receptor, Glutamatergic NMDA system, Ciliated protozoa
Abstract

Paramecium primaurelia is a unicellular eukaryote that moves in freshwater by ciliary beating and responds to environmental stimuli by altering motile behaviour. The movements of the cilia are controlled by the electrical changes of the cell membrane: when the intraciliary Ca2+ concentration associated with plasma membrane depolarization increases, the ciliary beating reverses its direction, and consequently the swimming direction changes. The ciliary reversal duration is correlated with the amount of Ca2+ influx. Here, we evaluated the effects due to the activation or blockade of N-methyl-D-aspartic acid (NMDA) receptors on swimming behaviour in Paramecium. Paramecia normally swim forward, drawing almost linear tracks. We observed that the simultaneous administration of NMDA and glycine induced a partial ciliary reversal (PaCR) leading to a continuous spiral-like swim. Furthermore, the duration of continuous ciliary reversal (CCR), triggered by high external KCl concentrations, was longer in NMDA+glycine-treated cells. NMDA action required the presence of Ca2+, as the normal forward swimming was restored when the ion was omitted from the extracellular milieu. The PaCR and the enhancement of CCR duration significantly decreased when the antagonists of the glutamate site D-AP5 or CGS19755, the NMDA channel blocker MK-801 or the glycine site antagonist DCKA was added. The action of NMDA+glycine was also abolished by Zn2+ or ifenprodil, the GluN2A and the GluN2B NMDA-containing subunit blockers, respectively. Searches of the Paramecium genome database currently available indicate that the NMDA-like receptor with ligand-binding characteristics of an NMDA receptor-like complex, purified from rat brain synaptic membranes and found in some metazoan genomes, is also present in Paramecium. These results provide evidence that functional NMDA receptors similar to those typical of mammalian neuronal cells are present in the single-celled organism Paramecium and thus suggest that the glutamatergic NMDA system is a phylogenetically old behaviour-controlling mechanism.

Published
2014

49. Acute desipramine restores presynaptic cortical defects in murine experimental autoimmune encephalomyelitis by suppressing central CCL5 overproduction

Author

DI PRISCO, Silvia, Merega, Elisa, Lanfranco, M, Casazza, Simona, Uccelli, Antonio, and Pittaluga, ANNA MARIA

Subjects
Cerebral Cortex, Mice, Inbred C57BL, Mice, Encephalomyelitis, Autoimmune, Experimental, Desipramine, Presynaptic Terminals, Animals, Female, Antidepressive Agents, Tricyclic, Chemokine CCL5, Research Papers, Drug Administration Schedule
Abstract

Altered glutamate exocytosis and cAMP production in cortical terminals of experimental autoimmune encephalomyelitis (EAE) mice occur at the early stage of disease (13 days post-immunization, d.p.i.). Neuronal defects were paralleled by overexpression of the central chemokine CCL5 (also known as RANTES), suggesting it has a role in presynaptic impairments. We propose that drugs able to restore CCL5 content to physiological levels could also restore presynaptic defects. Because of its efficacy in controlling CCL5 overexpression, desipramine (DMI) appeared to be a suitable candidate to test our hypothesis.Control and EAE mice at 13 d.p.i. were acutely or chronically administered DMI and monitored for behaviour and clinical scores. Noradrenaline and glutamate release, cAMP, CCL5 and TNF-α production were quantified in cortical synaptosomes and homogenates. Peripheral cytokine production was also determined.Noradrenaline exocytosis and α₂ -adrenoeceptor-mediated activity were unmodified in EAE mice at 13 d.p.i. when compared with control. Acute, but not chronic, DMI reduced CCL5 levels in cortical homogenates of EAE mice at 13 d.p.i., but did not affect peripheral IL-17 and TNF-α contents or CCL5 plasma levels. Acute DMI caused a long-lasting restoration of glutamate exocytosis, restored endogenous cAMP production and impeded the shift from inhibition to facilitation of the CCL5-mediated control of glutamate exocytosis. Finally, DMI ameliorated anxiety-related behaviour but not motor activity or severity of clinical signs.We propose DMI as an add-on therapy to normalize neuropsychiatric symptoms in multiple sclerosis patients at the early stage of the disease.

Published
2013

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