10 results on '"Cavasinni, Francesca"'
Search Results
2. Abnormal activity of the Na/Ca exchanger enhances glutamate transmission in experimental autoimmune encephalomyelitis
- Author
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Rossi, Silvia, De Chiara, Valentina, Furlan, Roberto, Musella, Alessandra, Cavasinni, Francesca, Muzio, Luca, Bernardi, Giorgio, Martino, Gianvito, and Centonze, Diego
- Published
- 2010
- Full Text
- View/download PDF
3. Cxcl10 enhances blood cells migration in the sub-ventricular zone of mice affected by experimental autoimmune encephalomyelitis
- Author
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Muzio, Luca, Cavasinni, Francesca, Marinaro, Cinzia, Bergamaschi, Andrea, Bergami, Alessandra, Porcheri, Cristina, Cerri, Federica, Dina, Giorgia, Quattrini, Angelo, Comi, Giancarlo, Furlan, Roberto, and Martino, Gianvito
- Published
- 2010
- Full Text
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4. Persistent inflammation alters the function of the endogenous brain stem cell compartment
- Author
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Pluchino, Stefano, Muzio, Luca, Imitola, Jaime, Deleidi, Michela, Alfaro-Cervello, Clara, Salani, Giuliana, Porcheri, Cristina, Brambilla, Elena, Cavasinni, Francesca, Bergamaschi, Andrea, Garcia-Verdugo, Jose Manuel, Comi, Giancarlo, Khoury, Samia J., and Martino, Gianvito
- Published
- 2008
5. Brain-Derived Neurotrophic Factor Controls Cannabinoid CB1 Receptor Function in the Striatum.
- Author
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De Chiara, Valentina, Angelucci, Francesco, Rossi, Silvia, Musella, Alessandra, Cavasinni, Francesca, Cantarella, Cristina, Mataluni, Giorgia, Sacchetti, Lucia, Napolitano, Francesco, Castelli, Maura, Caltagirone, Carlo, Bernardi, Giorgio, Maccarrone, Mauro, Usiello, Alessandro, and Centonze, Diego
- Subjects
BRAIN ,NEUROTROPHINS ,EMOTIONS ,GABA ,CHOLESTEROL metabolism ,DOPAMINE ,LABORATORY mice - Abstract
The role of brain-derived neurotrophic factor (BDNF) in emotional processes suggests an interaction with the endocannabinoid system. Here, we addressed the functional interplay between BDNF and cannabinoid CB
1 receptors (CB1 Rs) in the striatum, a brain area in which both BDNF and CB1 s play a role in the emotional consequences of stress and of rewarding experiences. BDNF potently inhibited CB1 R function in the striatum, through a mechanism mediated by altered cholesterol metabolism and membrane lipid raft function. The effect of BDNF was restricted to CB1 Rs controlling GABA-mediated IPSCs (CB1 R(GABA) ), whereas CB1 Rs modulating glutamate transmission and GABAB receptors were not affected. The action of BDNF on CB1 R(GABA) function was tyrosine kinase dependent and was complete even after receptor sensitization with cocaine or environmental manipulations activating the dopamine (DA)-dependent reward system. In mice lacking one copy of the BDNF gene (BDNF+/- ), CB1 R(GABA) responses were potentiated and were preserved from the action of haloperidol, a DA D2 receptor (D2 R) antagonist able to fully abolish CB1 R(GABA) function in rewarded animals. Haloperidol also enhanced BDNF levels in the striatum, suggesting that this neurotrophin may act as a downstream effector of D2 Rs in the modulation of cannabinoid signaling. Accordingly, 5 d cocaine exposure both reduced striatal BDNF levels and increased CB1 R(GABA) activity, through a mechanism dependent on D2 Rs. The present study identifies a novel mechanism of CB1 R regulation mediated by BDNF and cholesterol metabolism and provides some evidence that DA D2 R-dependent modulation of striatal CB1 R activity is mediated by this neurotrophin. [ABSTRACT FROM AUTHOR]- Published
- 2010
- Full Text
- View/download PDF
6. Voluntary Exercise and Sucrose Consumption Enhance Cannabinoid CB1 Receptor Sensitivity in the Striatum.
- Author
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De Chiara, Valentina, Errico, Francesco, Musella, Alessandra, Rossi, Silvia, Mataluni, Giorgia, Sacchetti, Lucia, Siracusano, Alberto, Castelli, Maura, Cavasinni, Francesca, Bernardi, Giorgio, Usiello, Alessandro, and Centonze, Diego
- Subjects
SUCROSE ,SYNAPSES ,NEURAL transmission ,GABA ,NEURAL circuitry - Abstract
The endogenous cannabinoid system is involved in the regulation of the central reward pathway. Running wheel and sucrose consumption have rewarding and reinforcing properties in rodents, and share many neurochemical and behavioral characteristics with drug addiction. In this study, we investigated whether running wheel or sucrose consumption altered the sensitivity of striatal synapses to the activation of cannabinoid CB1 receptors. We found that cannabinoid CB1 receptor-mediated presynaptic control of striatal inhibitory postsynaptic currents was remarkably potentiated after these environmental manipulations. In contrast, the sensitivity of glutamate synapses to CB1 receptor stimulation was unaltered, as well as that of GABA synapses to the stimulation of presynaptic GABAB receptors. The sensitization of cannabinoid CB1 receptor-mediated responses was slowly reversible after the discontinuation of running wheel or sucrose consumption, and was also detectable following the mobilization of endocannabinoids by metabotropic glutamate receptor 5 stimulation. Finally, we found that the upregulation of cannabinoid transmission induced by wheel running or sucrose had a crucial role in the protective effects of these environmental manipulations against the motor and synaptic consequences of stress. [ABSTRACT FROM AUTHOR]
- Published
- 2010
- Full Text
- View/download PDF
7. Inflammation Triggers Synaptic Alteration and Degeneration in Experimental Autoimmune Encephalomyelitis.
- Author
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Centonze, Diego, Muzio, Luca, Rossi, Silvia, Cavasinni, Francesca, De Chiara, Valentina, Bergami, Alessandra, Musella, Alessandra, D'Amelio, Marcello, Cavallucci, Virve, Martorana, Alessandro, Bergamaschi, Andrea, Cencioni, Maria Teresa, Diamantini, Adamo, Butti, Erica, Comi, Giancarlo, Bernardi, Giorgio, Cecconi, Francesco, Battistini, Luca, Furlan, Roberto, and Martino, Gianvito
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CENTRAL nervous system diseases ,ENCEPHALOMYELITIS ,TUMOR necrosis factors ,CYTOKINES ,VIRUS diseases - Abstract
Neurodegeneration is the irremediable pathological event occurring during chronic inflammatory diseases of the CNS. Here we show that, in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, inflammation is capable in enhancing glutamate transmission in the striatum and in promoting synaptic degeneration and dendritic spine loss. These alterations occur early in the disease course, are independent of demyelination, and are strongly associated with massive release of tumor necrosis factor-α from activated microglia. CNS invasion by myelin-specific blood-borne immune cells is the triggering event, and the downregulation of the early gene Arc/Arg3.1, leading to the abnormal expression and phosphorylation of AMPA-receptors, represents a culminating step in this cascade of neurodegenerative events. Accordingly, EAE-induced synaptopathy subsided during pharmacological blockade of AMPA receptors. Our data establish a link between neuroinflammation and synaptic degeneration and calls for early neuroprotective therapies in chronic inflammatory diseases of the CNS. [ABSTRACT FROM AUTHOR]
- Published
- 2009
- Full Text
- View/download PDF
8. Exercise attenuates the clinical, synaptic and dendritic abnormalities of experimental autoimmune encephalomyelitis
- Author
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Rossi, Silvia, Furlan, Roberto, De Chiara, Valentina, Musella, Alessandra, Lo Giudice, Temistocle, Mataluni, Giorgia, Cavasinni, Francesca, Cantarella, Cristina, Bernardi, Giorgio, Muzio, Luca, Martorana, Alessandro, Martino, Gianvito, and Centonze, Diego
- Subjects
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EXERCISE & psychology , *ALLERGIC encephalomyelitis , *NEURAL transmission , *NEURODEGENERATION , *DENDRITIC cells , *NEUROLOGICAL disorders , *MEDICAL model - Abstract
Abstract: Voluntary exercise is beneficial in models of primarily neurodegenerative disorders. Whether exercise also affects inflammatory neurodegeneration is unknown. In the present study, we evaluated the clinical, synaptic and neuropathological effects of voluntary wheel running in mice with myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. Exercising EAE mice exhibited less severe neurological deficits compared to control EAE animals. The sensitivity of striatal GABA synapses to the stimulation of cannabinoid CB1 receptors was dramatically downregulated following EAE induction, and was rescued by exercise in EAE mice with access to a running wheel. Finally, we found that exercise was able to contrast dendritic spine loss induced by EAE in striatal neurons, although the degree of inflammatory response was similar in the two experimental groups. Our work suggests that life style and experiences can impact the clinical course of inflammatory neurodegenerative diseases by affecting their synaptic bases. [Copyright &y& Elsevier]
- Published
- 2009
- Full Text
- View/download PDF
9. Preservation of striatal cannabinoid CB1 receptor function correlates with the antianxiety effects of fatty acid amide hydrolase inhibition.
- Author
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Rossi S, De Chiara V, Musella A, Sacchetti L, Cantarella C, Castelli M, Cavasinni F, Motta C, Studer V, Bernardi G, Cravatt BF, Maccarrone M, Usiello A, and Centonze D
- Subjects
- Animals, Mice, Amidohydrolases antagonists & inhibitors, Anti-Anxiety Agents pharmacology, Corpus Striatum physiopathology, Enzyme Inhibitors pharmacology, Receptor, Cannabinoid, CB1 physiology
- Abstract
The endocannabinoid anandamide (AEA) plays a crucial role in emotional control, and inhibition of its degradation by the fatty acid amide hydrolase (FAAH) has a potent antianxiety effect. The mechanism by which the magnification of AEA activity reduces anxiety is still largely undetermined. By using FAAH mutant mice and both intraperitoneal and intracerebroventricular administration of the FAAH inhibitor (3'-(aminocarbonyl)[1,1'-biphenyl]-3-yl)-cyclohexylcarbamate (URB597), we found that enhanced AEA signaling reversed, via central cannabinoid CB1 receptors (CB1Rs), the anxious phenotype of mice exposed to social defeat stress. This behavioral effect was associated with preserved activity of CB1Rs regulating GABA transmission in the striatum, whereas these receptors were dramatically down-regulated by stress in control animals. The hypothalamic-pituitary-adrenal (HPA) axis was not involved in the antistress effects of FAAH inhibition, although the HPA axis is a biological target of endogenous AEA. We also provided some physiological indications that striatal CB1Rs regulating GABA synapses are not the receptor targets of FAAH inhibition, which rather resulted in the stimulation of striatal CB1Rs regulating glutamate transmission. Collectively, our findings suggest that preservation of cannabinoid CB1 receptor function within the striatum is a possible synaptic correlate of the antianxiety effects of FAAH inhibition.
- Published
- 2010
- Full Text
- View/download PDF
10. Brain-derived neurotrophic factor controls cannabinoid CB1 receptor function in the striatum.
- Author
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De Chiara V, Angelucci F, Rossi S, Musella A, Cavasinni F, Cantarella C, Mataluni G, Sacchetti L, Napolitano F, Castelli M, Caltagirone C, Bernardi G, Maccarrone M, Usiello A, and Centonze D
- Subjects
- Animals, Behavior, Animal drug effects, Brain-Derived Neurotrophic Factor deficiency, Brain-Derived Neurotrophic Factor metabolism, Cholesterol metabolism, Cocaine pharmacology, Corpus Striatum cytology, Dopamine Antagonists pharmacology, Dopamine Uptake Inhibitors pharmacology, Dronabinol analogs & derivatives, Dronabinol pharmacology, Enzyme Inhibitors pharmacology, Excitatory Amino Acid Antagonists pharmacology, GABA Agents pharmacology, Haloperidol pharmacology, In Vitro Techniques, Inhibitory Postsynaptic Potentials drug effects, Inhibitory Postsynaptic Potentials physiology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Patch-Clamp Techniques methods, Phenols pharmacology, Piperidines pharmacology, Pyrazoles pharmacology, Reward, beta-Cyclodextrins pharmacology, Brain-Derived Neurotrophic Factor pharmacology, Neurons drug effects, Neurons metabolism, Receptor, Cannabinoid, CB1 metabolism
- Abstract
The role of brain-derived neurotrophic factor (BDNF) in emotional processes suggests an interaction with the endocannabinoid system. Here, we addressed the functional interplay between BDNF and cannabinoid CB(1) receptors (CB(1)Rs) in the striatum, a brain area in which both BDNF and CB(1)s play a role in the emotional consequences of stress and of rewarding experiences. BDNF potently inhibited CB(1)R function in the striatum, through a mechanism mediated by altered cholesterol metabolism and membrane lipid raft function. The effect of BDNF was restricted to CB(1)Rs controlling GABA-mediated IPSCs (CB(1)R(GABA)), whereas CB(1)Rs modulating glutamate transmission and GABA(B) receptors were not affected. The action of BDNF on CB(1)R(GABA) function was tyrosine kinase dependent and was complete even after receptor sensitization with cocaine or environmental manipulations activating the dopamine (DA)-dependent reward system. In mice lacking one copy of the BDNF gene (BDNF(+/-)), CB(1)R(GABA) responses were potentiated and were preserved from the action of haloperidol, a DA D(2) receptor (D(2)R) antagonist able to fully abolish CB(1)R(GABA) function in rewarded animals. Haloperidol also enhanced BDNF levels in the striatum, suggesting that this neurotrophin may act as a downstream effector of D(2)Rs in the modulation of cannabinoid signaling. Accordingly, 5 d cocaine exposure both reduced striatal BDNF levels and increased CB(1)R(GABA) activity, through a mechanism dependent on D(2)Rs. The present study identifies a novel mechanism of CB(1)R regulation mediated by BDNF and cholesterol metabolism and provides some evidence that DA D(2)R-dependent modulation of striatal CB(1)R activity is mediated by this neurotrophin.
- Published
- 2010
- Full Text
- View/download PDF
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