N-arachidonoyl-dopamine, or NADA is a agonist (activator) of the CB1 receptors [1] and the Transient Receptor potential V1 ion channel. Its discovery was described in 2002 by an academic research group from Italy and the USA. It was found in the brain of rats, with especially high concentrations in the hippocampus, cerebellum and striatum. It activates the TRPV1 channel with an EC50 of approximately of 50 nM. The high potency makes it the putative endogenous TRPV1 agonist.[2]
References
- ^
Ralevic V. (2003). "Cannabinoid modulation of peripheral autonomic and sensory neurotransmission". European journal of pharmacology. 472 (1–2): 1–21. doi:10.1016/S0014-2999(03)01813-2. PMID 12860468.
{{cite journal}}: Unknown parameter|month=ignored (help) - ^ Huang SM, Bisogno T, Trevisani M; et al. (2002). "An endogenous capsaicin-like substance with high potency at recombinant and native vanilloid VR1 receptors". Proceedings of the National Academy of Sciences of the United States of America. 99 (12): 8400–5. doi:10.1073/pnas.122196999. PMC 123079. PMID 12060783.
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External links
- General information about NADA.