Abstract
A shared pathology among many neurological and neurodegenerative disorders is neuronal loss. Cannabinoids have been shown to be neuroprotective in multiple systems. However, both agonists and antagonists of the CB(1) cannabinoid receptor are neuroprotective, but the mechanisms responsible for these actions remain unclear. Recently a CB(1) receptor interacting protein, CRIP1a, was identified and found to alter CB(1) activity. Here we show that in an assay of glutamate neurotoxicity in primary neuronal cortical cultures CRIP1a disrupts agonist-induced neuroprotection and confers antagonist-induced neuroprotection.
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Benzoxazines / pharmacology
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Blotting, Western
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Cannabinoid Receptor Agonists*
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Cannabinoid Receptor Antagonists*
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Carrier Proteins / pharmacology*
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Cell Count
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Cell Survival / drug effects
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Cells, Cultured
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Cerebral Cortex / cytology
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Cerebral Cortex / drug effects
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Excitatory Amino Acids / toxicity*
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Genetic Vectors
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Glutamic Acid / toxicity*
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Immunohistochemistry
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Lentivirus / genetics
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Morpholines / pharmacology
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Naphthalenes / pharmacology
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Neuroprotective Agents*
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Piperidines / pharmacology
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Plasmids / genetics
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Pyrazoles / pharmacology
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Rats
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Rats, Long-Evans
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Real-Time Polymerase Chain Reaction
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Receptor, Cannabinoid, CB1 / biosynthesis
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Rimonabant
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Synapsins / metabolism
Substances
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Benzoxazines
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Cannabinoid Receptor Agonists
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Cannabinoid Receptor Antagonists
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Carrier Proteins
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Cnrip1 protein, rat
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Excitatory Amino Acids
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Morpholines
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Naphthalenes
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Neuroprotective Agents
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Piperidines
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Pyrazoles
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Receptor, Cannabinoid, CB1
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Synapsins
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Glutamic Acid
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(3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanone
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Rimonabant