http://www.cnr.it/ontology/cnr/individuo/prodotto/ID14829
CB1 cannabinoid receptors and on-demand defense against excitotoxicity. (Articolo in rivista)
- Type
- Label
- CB1 cannabinoid receptors and on-demand defense against excitotoxicity. (Articolo in rivista) (literal)
- Anno
- 2003-01-01T00:00:00+01:00 (literal)
- Alternative label
Marsicano G, Goodenough S, Monory K, Hermann H, Eder M, Cannich A, Azad SC, Cascio MG, Gutierrez SO, van der Stelt M, Lopez-Rodriguez ML, Casanova E, Schutz G, Zieglgansberger W, Di Marzo V, Behl C, Lutz B. (2003)
CB1 cannabinoid receptors and on-demand defense against excitotoxicity.
in Science (N. Y., N.Y.)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Marsicano G, Goodenough S, Monory K, Hermann H, Eder M, Cannich A, Azad SC, Cascio MG, Gutierrez SO, van der Stelt M, Lopez-Rodriguez ML, Casanova E, Schutz G, Zieglgansberger W, Di Marzo V, Behl C, Lutz B. (literal)
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- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
- Cascio M.G. contratto di collaborazione presso ICB; van Der Stelt M. assegnisti ICB (literal)
- Note
- ISI Web of Science (WOS) (literal)
- Titolo
- CB1 cannabinoid receptors and on-demand defense against excitotoxicity. (literal)
- Abstract
- Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protective mechanisms could not be triggered in mutant mice. The endogenous cannabinoid system thus provides on-demand protection against acute excitotoxicity in central nervous system neurons.
(literal)
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