Aspirin-triggered lipoxin induces CB1-dependent catalepsy in mice
| Autor: | Fabrício A. Pamplona, Octávio Menezes-de-Lima, Reinaldo N. Takahashi |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Male
Cannabinoid receptor Polyunsaturated Alkamides medicine.medical_treatment Models Neurological Arachidonic Acids Pharmacology Catalepsy chemistry.chemical_compound Mice Piperidines Receptor Cannabinoid CB1 medicine Animals Cyclooxygenase Inhibitors Receptors Lipoxin Lipoxin Arachidonate 5-Lipoxygenase Aspirin General Neuroscience Antagonist Anandamide medicine.disease Endocannabinoid system Lipoxins Eicosanoid chemistry Biochemistry Pyrazoles lipids (amino acids peptides and proteins) Cannabinoid Rimonabant Central Nervous System Agents Endocannabinoids |
| Zdroj: | Neuroscience letters. 470(1) |
| ISSN: | 1872-7972 |
| Popis: | Evidence are that inhibition of cyclooxygenase 2 (COX-2) enhances endocannabinoid signaling, indicating a crosstalk between these two eicosanoid pathways. Aspirin, a non-selective COX inhibitor, acetylates COX-2 with generation of a lipoxygenase (LOX) substrate, whose end product is the 15-epi-lipoxin A(4) (15-epi-LXA(4)), an aspirin-triggered lipoxin. Our objective was to investigate whether 15-epi-LXA(4) would potentiate in vivo effects of the endocannabinoid anandamide (AEA). Catalepsy was selected as a behavioral parameter and tested 5 min after AEA injection in all experiments. AEA induced dose-dependent (200 pmol/2 microl, i.c.v.) catalepsy. A sub-dose of AEA (10 pmol/2 microl, i.c.v.) was potentiated by aspirin (300 mg/kg, p.o.) via a 5-LOX-dependent step. The cataleptic effect induced by the interaction between sub-doses of 15-epi-LXA(4) (0.01 pmol/2 microl, i.c.v.) and AEA (10 pmol/2 microl, i.c.v.) was prevented by the cannabinoid CB(1) receptors antagonist SR141716A (1mg/kg, i.p.), but not by the antagonist of lipoxin ALX receptors Boc-2 (10 microg/kg, i.p.). While previous studies have shown that COX inhibition itself may enhance endocannabinoid effects, here we add another piece of evidence revealing that a LOX-derivative produced in consequence of COX-2 acetylation participates in this process. |
| Databáze: | OpenAIRE |
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