11 results on '"Sala, Mariaelvina"'
Search Results
2. Linking NMDA Receptor Synaptic Retention to Synaptic Plasticity and Cognition
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Franchini, Luca, Stanic, Jennifer, Ponzoni, Luisa, Mellone, Manuela, Carrano, Nicolò, Musardo, Stefano, Zianni, Elisa, Olivero, Guendalina, Marcello, Elena, Pittaluga, Anna, Sala, Mariaelvina, Bellone, Camilla, Racca, Claudia, Di Luca, Monica, and Gardoni, Fabrizio
- Subjects
Molecular Interaction ,Molecular Neuroscience ,Neuroscience ,nervous system ,musculoskeletal, neural, and ocular physiology ,lcsh:Q ,lcsh:Science ,Article ,ddc:616.8 - Abstract
Summary NMDA receptor (NMDAR) subunit composition plays a pivotal role in synaptic plasticity at excitatory synapses. Still, the mechanisms responsible for the synaptic retention of NMDARs following induction of plasticity need to be fully elucidated. Rabphilin3A (Rph3A) is involved in the stabilization of NMDARs at synapses through the formation of a complex with GluN2A and PSD-95. Here we used different protocols to induce synaptic plasticity in the presence or absence of agents modulating Rph3A function. The use of Forskolin/Rolipram/Picrotoxin cocktail to induce chemical LTP led to synaptic accumulation of Rph3A and formation of synaptic GluN2A/Rph3A complex. Notably, Rph3A silencing or use of peptides interfering with the GluN2A/Rph3A complex blocked LTP induction. Moreover, in vivo disruption of GluN2A/Rph3A complex led to a profound alteration of spatial memory. Overall, our results demonstrate a molecular mechanism needed for NMDAR stabilization at synapses after plasticity induction and to trigger downstream signaling events necessary for cognitive behavior., Graphical Abstract, Highlights • LTP induces trafficking of Rph3A at synapses and formation of GluN2A/Rph3A complex • Disruption of Rph3A/GluN2A complex leads to LTP impairment • Rph3A/GluN2A complex is needed for modifications of dendritic spines induced by LTP • Disruption of Rph3A/GluN2A complex leads to spatial memory impairment, Molecular Interaction; Neuroscience; Molecular Neuroscience
- Published
- 2019
3. Electronic nicotine delivery systems (ENDS): A convenient means of smoking?
- Author
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Sala M and Gotti C
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- Humans, Electronic Nicotine Delivery Systems, Cigarette Smoking, Smoking Cessation
- Abstract
Electronic nicotine delivery systems (ENDS), which are becoming increasingly popular in many parts of the world, have recently become more sophisticated in terms of their more active content and better controlled vaporisation. This review begins by describing how cigarette smoking led to the development of ENDS as a means of combatting nicotine addiction. ENDS are usually categorised as belonging to one of only three main generations, but a fourth has been added in order to differentiate the latest, most powerful, most advanced and innovative that have improved heating efficiency. Descriptions of the principal substances contained in ENDS are followed by considerations concerning the risk of toxicity due to the presence of albeit low concentrations of such a variety of compounds inhaled over a long time, and the increasingly widespread use of ENDS as a means of smoking illicit drugs. We also review the most widely used pharmacotherapeutic approaches to smoking cessation, and recent epidemiological data showing that ENDS can help some people to stop smoking. However, in order to ensure their appropriate regulation, there is a need for higher-quality evidence concerning the health effects and safety of ENDS, and their effectiveness in discouraging tobacco smoking., Competing Interests: Declaration of Competing Interest None., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)
- Published
- 2023
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4. Deletion of calcineurin from astrocytes reproduces proteome signature of Alzheimer's disease and epilepsy and predisposes to seizures.
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Tapella L, Dematteis G, Ruffinatti FA, Ponzoni L, Fiordaliso F, Corbelli A, Albanese E, Pistolato B, Pagano J, Barberis E, Marengo E, Balducci C, Forloni G, Verpelli C, Sala C, Distasi C, Sala M, Manfredi M, Genazzani AA, and Lim D
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- Animals, Astrocytes, Calcineurin, Mice, Neuroinflammatory Diseases, Proteome, Proteomics, Seizures genetics, Alzheimer Disease genetics, Epilepsy genetics
- Abstract
Calcineurin (CaN), acting downstream of intracellular calcium signals, orchestrates cellular remodeling in many cellular types. In astrocytes, major homeostatic players in the central nervous system (CNS), CaN is involved in neuroinflammation and gliosis, while its role in healthy CNS or in early neuro-pathogenesis is poorly understood. Here we report that in mice with conditional deletion of CaN in GFAP-expressing astrocytes (astroglial calcineurin KO, ACN-KO), at 1 month of age, transcription was largely unchanged, while the proteome was deranged in the hippocampus and cerebellum. Gene ontology analysis revealed overrepresentation of annotations related to myelin sheath, mitochondria, ribosome and cytoskeleton. Over-represented pathways were related to protein synthesis, oxidative phosphorylation, mTOR and neurological disorders, including Alzheimer's disease (AD) and seizure disorder. Comparison with published proteomic datasets showed significant overlap with the proteome of a familial AD mouse model and of human subjects with drug-resistant seizures. ACN-KO mice showed no alterations of motor activity, equilibrium, anxiety or depressive state. However, in Barnes maze ACN-KO mice learned the task but adopted serial search strategy. Strikingly, beginning from about 5 months of age ACN-KO mice developed spontaneous tonic-clonic seizures with an inflammatory signature of epileptic brains. Altogether, our data suggest that the deletion of astroglial CaN produces features of neurological disorders and predisposes mice to seizures. We suggest that calcineurin in astrocytes may serve as a novel Ca
2+ -sensitive switch which regulates protein expression and homeostasis in the central nervous system., (Copyright © 2021 Elsevier Ltd. All rights reserved.)- Published
- 2021
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5. Persistent cognitive and affective alterations at late withdrawal stages after long-term intermittent exposure to tobacco smoke or electronic cigarette vapour: Behavioural changes and their neurochemical correlates.
- Author
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Ponzoni L, Braida D, Carboni L, Moretti M, Viani P, Clementi F, Zoli M, Gotti C, and Sala M
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- Affect physiology, Animals, Cigarette Smoking metabolism, Cognition physiology, E-Cigarette Vapor administration & dosage, Hippocampus chemistry, Hippocampus drug effects, Hippocampus metabolism, Inhalation Exposure adverse effects, Male, Maze Learning drug effects, Maze Learning physiology, Mice, Mice, Inbred BALB C, Recognition, Psychology drug effects, Recognition, Psychology physiology, Substance Withdrawal Syndrome psychology, Affect drug effects, Cigarette Smoking adverse effects, Cognition drug effects, E-Cigarette Vapor adverse effects, Substance Withdrawal Syndrome metabolism, Tobacco Smoke Pollution adverse effects
- Abstract
Smoking cessation induces a withdrawal syndrome associated with anxiety, depression, and impaired neurocognitive functions, but much less is known about the withdrawal of e-cigarettes (e-CIG). We investigated in Balb/c mice the behavioural and neurochemical effects of withdrawal for up to 90 days after seven weeks' intermittent exposure to e-CIG vapour or cigarette smoke (CIG). The withdrawal of e-CIG and CIG induced early behavioural alterations such as spatial memory deficits (spatial object recognition task), increased anxiety (elevated plus maze test) and compulsive-like behaviour (marble burying test) that persisted for 60-90 days. Notably, attention-related (virtual object recognition task) and depression-like behaviours (tail suspension and sucrose preference tests) appeared only 15-30 days after withdrawal and persisted for as long as up to 90 days. At hippocampal level, the withdrawal-induced changes in the levels of AMPA receptor GluA1 and GluA2/3 subunits, PSD 95 protein, corticotropin-releasing factor (Crf) and Crf receptor 1 (CrfR1) mRNA were biphasic: AMPA receptor subunit and PSD95 protein levels initially remained unchanged and decreased after 60-90 days, whereas Crf/CrfR1 mRNA levels initially increased and then markedly decreased after 60 days. These late reductions correlated with the behavioural impairments, particularly the appearance of depression-like behaviours. Our findings show that major behavioural and neurochemical alterations persist or even first appear late after the withdrawal of chronic CIG smoke or e-CIG vapour exposure, and underline importance of conducting similar studies of humans, including e-CIG vapers., Competing Interests: Declaration of Competing Interest The authors declare no competing financial interest, (Copyright © 2020 Elsevier Ltd. All rights reserved.)
- Published
- 2020
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6. Increased sensitivity to Δ 9 -THC-induced rewarding effects after seven-week exposure to electronic and tobacco cigarettes in mice.
- Author
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Ponzoni L, Moretti M, Braida D, Zoli M, Clementi F, Viani P, Sala M, and Gotti C
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- Animals, Cyclohexanols metabolism, Guanosine 5'-O-(3-Thiotriphosphate) metabolism, Male, Mice, Nucleus Accumbens metabolism, Proto-Oncogene Proteins c-fos metabolism, Radioligand Assay, Receptors, AMPA metabolism, Sulfur Radioisotopes metabolism, Tobacco Use Cessation Devices adverse effects, Tritium metabolism, Conditioning, Psychological drug effects, Dronabinol pharmacology, Electronic Nicotine Delivery Systems, Tobacco Products adverse effects
- Abstract
Cigarette (CIG) smoking often precedes the use of illegal drugs. Electronic-cigarettes (e-CIGs) have been promoted as a means of stopping smoking and reducing the harmful effects of CIGs on the population. However, although e-CIGs eliminate some of the morbidity associated with combustible tobacco, they are still nicotine-delivery devices. In order to study whether the nicotine delivered via e-CIG acts as "a gateway drug" to the use of cannabis, we analysed the behavioural and molecular effects of 7 weeks' pre-exposure to air (AIR), e-CIGs or CIGs on addiction-related conditioned place preference (CPP) in mice using a sub-threshold (0.01 mg/kg) dose of delta-9-tetrahydrocannabinol (Δ
9 -THC), the principal psychoactive constituent of cannabis. After 8 and 66 days of withdrawal, this Δ9 -THC dose was ineffective in inducing CPP in mice pre-exposed to pump-driven AIR, but very effective in mice pre-exposed to e-CIGs or CIGs. Exposure to e-CIGs or CIGs increases the expression of ΔFosB in the nucleus accumbens (NAc), which remains high during short-term e-CIG or CIG withdrawal and long-term CIG withdrawal and is not influenced by treatment with Δ9 -THC. At the end of e-CIG or CIG exposure and during withdrawal, the mice also had a higher AMPA receptors GluA1/GluA2-3 ratio in the NAc. Chronic nicotine exposure increases sensitivity to rewarding effects of Δ9 -THC in mice and produces long-lasting neurobiological changes regardless of the delivery method (CIG vs. e-CIG). The exposure to passive tobacco smoke or e-CIG vapours can similarly increase vulnerability to the effects of cannabis and possibly other drugs of abuse., (Copyright © 2019. Published by Elsevier B.V.)- Published
- 2019
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7. Spontaneous object and movement representations in 4-month-old human infants and albino Swiss mice.
- Author
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Langus A, Saksida A, Braida D, Martucci R, Sala M, and Nespor M
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- Animals, Female, Humans, Infant, Male, Mice, Neuropsychological Tests, Cognition physiology, Movement physiology, Pattern Recognition, Visual physiology, Visual Perception physiology
- Abstract
Can young infants decompose visual events into independent representations of objects and movements? Previous studies suggest that human infants may be born with the notion of objects but there is little evidence for movement representations during the first months of life. We devised a novel Rapid Visual Recognition Procedure to test whether the nervous system is innately disposed for the conceptual decomposition of visual events. We show that 4-month-old infants can spontaneously build object and movement representations and recognize these in partially matching test events. Also albino Swiss mice that were tested on a comparable procedure could spontaneously build detailed mental representations of moving objects. Our results dissociate the ability to conceptually decompose physical events into objects and spatio-temporal relations from various types of human and non-human specific experience, and suggest that the nervous system is genetically predisposed to anticipate the representation of objects and movements in both humans and non-human species., (Copyright © 2015 Elsevier B.V. All rights reserved.)
- Published
- 2015
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8. Learning about oxytocin: pharmacologic and behavioral issues.
- Author
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Chini B, Leonzino M, Braida D, and Sala M
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- Animals, Brain drug effects, Brain physiology, Humans, Learning physiology, Memory physiology, Learning drug effects, Memory drug effects, Oxytocin pharmacology, Psychotropic Drugs pharmacology
- Abstract
Despite the accumulating evidence suggesting that the neuropeptide oxytocin (OT) plays a role in neuropsychiatric disorders characterized by social dysfunction, the influence of OT on the nonsocial aspects of learning and memory have been less investigated. To foster research in this area, we review the effects of OT on learning and memory in animal models and humans. In healthy animal models, OT improves memory consolidation and extinction, but only if given at a low dose immediately after the acquisition phase. On the contrary, OT effects in healthy humans have been inconsistent; although, in this case, OT was always given before the acquisition phase and no dose-response curves have ever been drawn up. Interestingly, a specific impairment in the reversal of learning has been found in mice devoid of OT receptors and OT has been demonstrated to enhance fear extinction in rodents. All together, these data suggest that OT plays a role in elementary forms of behavioral flexibility and adaptive responses and support its therapeutic potential in neuropsychiatric disorders characterized by cognitive inflexibility and/or impairment (autism, schizophrenia, Alzheimer's disease, Parkinson disease, stroke, posttraumatic stress disorder). Accordingly, OT has been shown to improve cognitive flexibility in OT receptor-deficient mice, and scattered findings indicate that intranasal OT has positive effects on the memory of patients with schizophrenia or posttraumatic stress disorders. Further studies of the therapeutic potential of OT as an enhancer of learning and memory are warranted., (© 2013 Society of Biological Psychiatry Published by Society of Biological Psychiatry All rights reserved.)
- Published
- 2014
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9. Pharmacologic rescue of impaired cognitive flexibility, social deficits, increased aggression, and seizure susceptibility in oxytocin receptor null mice: a neurobehavioral model of autism.
- Author
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Sala M, Braida D, Lentini D, Busnelli M, Bulgheroni E, Capurro V, Finardi A, Donzelli A, Pattini L, Rubino T, Parolaro D, Nishimori K, Parenti M, and Chini B
- Subjects
- Aggression physiology, Analysis of Variance, Animals, Arginine Vasopressin metabolism, Autistic Disorder, Autoradiography, Cells, Cultured, Cognition physiology, Disease Models, Animal, Hippocampus cytology, Hippocampus drug effects, Hippocampus metabolism, Immunohistochemistry, Male, Mice, Mice, Knockout, Neurons cytology, Neurons drug effects, Neurons metabolism, Oxytocin metabolism, Seizures genetics, Aggression drug effects, Arginine Vasopressin pharmacology, Cognition drug effects, Oxytocin pharmacology, Receptors, Oxytocin genetics, Seizures physiopathology, Social Behavior
- Abstract
Background: Oxytocin (OT) has been suggested as a treatment to improve social behavior in autistic patients. Accordingly, the OT (Oxt(-/-)) and the OT receptor null mice (Oxtr(-/-)) display autistic-like deficits in social behavior, increased aggression, and reduced ultrasonic vocalization., Methods: Oxtr(-/-) mice were characterized for general health, sociability, social novelty, cognitive flexibility, aggression, and seizure susceptibility. Because vasopressin (AVP) and OT cooperate in controlling social behavior, learning, and aggression, they were tested for possible rescue of the impaired behaviors. Primary hyppocampal cultures from Oxtr(+/+) and Oxtr(-/-) mouse embryos were established to investigate the balance between gamma-aminobutyric acid (GABA) and glutamate synapses and the expression levels of OT and AVP (V1a) receptors were determined by autoradiography., Results: Oxtr(-/-) mice display two additional, highly relevant, phenotypic characteristics: 1) a resistance to change in a learned pattern of behavior, comparable to restricted interests and repetitive behavior in autism, and 2) an increased susceptibility to seizures, a frequent and clinically relevant symptom of autism. We also show that intracerebral administration of both OT and AVP lowers aggression and fully reverts social and learning defects by acting on V1a receptors and that seizure susceptibility is antagonized by peripherally administered OT. Finally, we detect a decreased ratio of GABA-ergic versus total presynapses in hippocampal neurons of Oxtr(-/-) mice., Conclusions: Autistic-like symptoms are rescued on administration of AVP and OT to young Oxtr(-/-) adult animals. The Oxtr(-/-) mouse is thus instrumental to investigate the neurochemical and synaptic abnormalities underlying autistic-like disturbances and to test new strategies of pharmacologic intervention., (Copyright © 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)
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- 2011
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10. Involvement of kappa-opioid and endocannabinoid system on Salvinorin A-induced reward.
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Braida D, Limonta V, Capurro V, Fadda P, Rubino T, Mascia P, Zani A, Gori E, Fratta W, Parolaro D, and Sala M
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- Analysis of Variance, Animals, Behavior, Animal drug effects, Cannabinoid Receptor Modulators antagonists & inhibitors, Diterpenes, Clerodane, Dopamine metabolism, Dose-Response Relationship, Drug, Drug Administration Routes, Drug Interactions, Male, Microdialysis methods, Motor Activity drug effects, Naltrexone analogs & derivatives, Naltrexone pharmacology, Narcotic Antagonists pharmacology, Piperidines pharmacology, Pyrazoles pharmacology, Rats, Rats, Wistar, Rimonabant, Self Administration, Antioxidants pharmacology, Cannabinoid Receptor Modulators physiology, Conditioning, Operant drug effects, Diterpenes pharmacology, Endocannabinoids, Receptors, Opioid, kappa physiology, Reward
- Abstract
Background: The recreational drug, Salvinorin A, derived from the plant of Salvia divinorum, is a potent and selective kappa-opioid receptor agonist. The abuse of selective k-agonists is a novel phenomenon, the mechanism of which is not fully understood., Methods: We investigated salvinorin A given SC on the conditioned place preference (.05-160 microg/kg) and intracerebroventricular (ICV) self-administration (.01-1 microg/infusion) paradigms, in Wistar rats., Results: The present results demonstrate the rewarding effects of Salvinorin A in a range of doses between .1 and 40 microg/kg SC for conditioned place preference test and .1-.5 microg/infusion for ICV self-administration. Highest doses (160 microg/kg for conditioned place preference test and 1 microg/infusion for ICV self-administration) were aversive. The rewarding effect was antagonized by intraperitoneal (IP) pretreatment with the cannabinoid CB(1) receptor antagonist, rimonabant [N-piperidino-5-(4-chlorophenyl)1-(2,4-dichloro phenyl)-4 methyl pyrazole 3-carboxamide] (1 mg/kg), and the kappa-opioid receptor antagonist, nor-binaltorphimine (nor-BNI) (10 mg/kg). In the shell of nucleus accumbens, dopamine extracellular levels were increased after administration of salvinorin A (40 microg/kg SC), reaching a maximum value of about 150%., Conclusions: These data provide the demonstration of the rewarding effects of Salvinorin A through an interaction between kappa-opioid and (endo)cannabinoid system in rats.
- Published
- 2008
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11. Endocannabinoids and 3,4-methylenedioxymethamphetamine (MDMA) interaction.
- Author
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Sala M and Braida D
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- Animals, Cannabis, Drug Interactions, Humans, Neurotoxicity Syndromes physiopathology, Reinforcement, Psychology, Reward, Cannabinoid Receptor Modulators pharmacology, Endocannabinoids, Hallucinogens pharmacology, N-Methyl-3,4-methylenedioxyamphetamine pharmacology
- Published
- 2005
- Full Text
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