F
Felice Nava
Researcher at University of Cagliari
Publications - 97
Citations - 3098
Felice Nava is an academic researcher from University of Cagliari. The author has contributed to research in topics: Schottky barrier & Schottky diode. The author has an hindex of 27, co-authored 92 publications receiving 2890 citations. Previous affiliations of Felice Nava include University of California, Irvine & University of Messina.
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Journal ArticleDOI
An anorexic lipid mediator regulated by feeding
F. Rodríguez de Fonseca,Miguel Navarro,Raquel Gómez,Leticia Escuredo,Felice Nava,Jin Fu,Eric Murillo-Rodríguez,Andrea Giuffrida,Jesse LoVerme,Silvana Gaetani,Satish Kathuria,Christine M. Gall,Daniele Piomelli +12 more
TL;DR: It is shown that, in rats, food deprivation markedly reduces OEA biosynthesis in the small intestine, and results indicate that OEA is a lipid mediator involved in the peripheral regulation of feeding.
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A Peripheral Mechanism for CB1 Cannabinoid Receptor-Dependent Modulation of Feeding
Raquel Gómez,Miguel Navarro,Belen Ferrer,José Carlos Menéndez Gregono G. Trigo,Ainhoa Bilbao,Ignacio del Arco,Andrea Cippitelli,Felice Nava,Daniele Piomelli,Fernando Rodríguez de Fonseca +9 more
TL;DR: An unexpected role for peripheral CB1 receptors in the regulation of feeding is revealed and Capsaicin deafferentation abolished the peripheral effects of both cannabinoid agonists and antagonists, suggesting that these agents modulate food intake by acting onCB1 receptors located on capsaicin-sensitive sensory terminals.
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Elevated circulating levels of anandamide after administration of the transport inhibitor, AM404
Andrea Giuffrida,Fernando Rodríguez de Fonseca,Felice Nava,Patrick Loubet-Lescoulié,Daniele Piomelli +4 more
TL;DR: Results are consistent with the hypothesis that AM404 inhibits anandamide inactivation in vivo, and potentiates several responses elicited by administration of exogenousAnandamide.
Journal ArticleDOI
D2 dopamine receptors enable Δ9-tetrahydrocannabinol induced memory impairment and reduction of hippocampal extracellular acetylcholine concentration.
TL;DR: The findings suggest that impairment of working memory and inhibition of hippocampal extracellular acetylcholine concentration are mediated by the concomitant activation of D2 dopamine and CB1 cannabinoid receptors, and that D 2 dopamine receptor antagonists may be useful in the treatment of the cognitive deficits induced by marijuana.
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Effects of chronic Δ9-tetrahydrocannabinol treatment on hippocampal extracellular acetylcholine concentration and alternation performance in the T-maze
TL;DR: Findings confirm the proposition that CB(1) cannabinoid receptors mediate the negative effects induced by Delta(9)-THC both on hippocampal extracellular acetylcholine concentration and correct alternation tasks in the T-maze, and indicate that these effects may be differentiated.