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N-Arachidonoyl dopamine
N-Arachidonoyl dopamine
General
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Chiral rotation [α]D
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Dipole moment ? D
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Except where noted otherwise, data are given for
materials in their standard state (at 25 °C, 100 kPa)
Infobox disclaimer and references


N-Arachidonoyl dopamine (NADA) is an endocannabinoid that acts as an agonist of the CB1 receptor[1] and the transient receptor potential V1 (TRPV1) 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 50nM. The high potency makes it the putative endogenous TRPV1 agonist.[2]

See also[]

References[]

  1. Ralevic V (July 2003). Cannabinoid modulation of peripheral autonomic and sensory neurotransmission. European Journal of Pharmacology 472 (1–2): 1–21.
  2. Huang SM, Bisogno T, Trevisani M, Al-Hayani A, De Petrocellis L, Fezza F, Tognetto M, Petros TJ, Krey JF, Chu CJ, Miller JD, Davies SN, Geppetti P, Walker JM, Di Marzo V (June 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.

External links[]


Cannabinoids edit

{Anandamide} {CBD} {CBDV} {CBN} {CBV} {CP 55,940} {HU-210} {Nabilone} {Rimonabant} {THC} {THCV} {WIN 55,212-2} {URB597}


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