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CB1 Cannabinoid Receptors and On-Demand Defense against Excitotoxicity
Science (American Association for the Advancement of Science), 2003-10, Vol.302 (5642), p.84-88
2003

Details

Autor(en) / Beteiligte
Titel
CB1 Cannabinoid Receptors and On-Demand Defense against Excitotoxicity
Ist Teil von
  • Science (American Association for the Advancement of Science), 2003-10, Vol.302 (5642), p.84-88
Ort / Verlag
Washington, DC: American Association for the Advancement of Science
Erscheinungsjahr
2003
Link zum Volltext
Quelle
American Association for the Advancement of Science
Beschreibungen/Notizen
  • 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 intemeurons. 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.
Sprache
Englisch
Identifikatoren
ISSN: 0036-8075
eISSN: 1095-9203
DOI: 10.1126/science.1088208
Titel-ID: cdi_proquest_miscellaneous_75745009
Format
–
Schlagworte
Animals, Arachidonic Acids - metabolism, Arachidonic Acids - pharmacology, Biological and medical sciences, Brain, Brain - drug effects, Brain - metabolism, Brain-Derived Neurotrophic Factor - genetics, Brain-Derived Neurotrophic Factor - metabolism, Cannabinoids, Cannabinoids - metabolism, Convulsions & seizures, Endocannabinoids, Epilepsy - metabolism, Epilepsy - physiopathology, Excitatory Amino Acid Agonists - pharmacology, Excitatory Postsynaptic Potentials, Forebrain, Furans - pharmacology, gamma-Aminobutyric Acid - metabolism, Gene Expression Regulation - drug effects, Genes, Immediate-Early, Genotypes, Glutamic Acid - metabolism, Glycerides - metabolism, Hippocampus, Hippocampus - drug effects, Hippocampus - metabolism, In Vitro Techniques, Kainic Acid - pharmacology, Male, Medical sciences, Messenger RNA, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Mitogen-Activated Protein Kinases - metabolism, Mutation, Nervous system, Neurons, Neurons - drug effects, Neurons - metabolism, Neurons - physiology, Neuropharmacology, Neuroprotective agent, Neuroprotective Agents - metabolism, Neuroscience, Pharmacology. Drug treatments, Physiological aspects, Piperidines - pharmacology, Polyunsaturated Alkamides, Prosencephalon - drug effects, Prosencephalon - metabolism, Pyrazoles - pharmacology, Receptors, Receptors, Cannabinoid, Receptors, Drug - antagonists & inhibitors, Receptors, Drug - genetics, Receptors, Drug - metabolism, Seizures, Signal Transduction

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