Narakidonoylethanolamiini

N-arachidonoylethanolamine, commonly known as anandamide, is an endogenous lipid neurotransmitter that belongs to the endocannabinoid system. It is an amide formed from arachidonic acid and ethanolamine and is produced on demand in various tissues, especially in the brain.

Anandamide primarily signals through cannabinoid receptors, with high affinity for CB1 receptors in the central nervous system and lower affinity for CB2 receptors in the immune system. It can also activate other targets, such as the TRPV1 receptor. In neurons, its release from postsynaptic cells can suppress the release of other neurotransmitters via retrograde signaling, modulating synaptic transmission.

Rapid inactivation constrains anandamide signaling. It is mainly hydrolyzed by the enzyme fatty acid amide hydrolase (FAAH) into arachidonic acid and ethanolamine. This short half-life contributes to tight temporal control of endocannabinoid signaling. Inhibitors of FAAH have been explored to enhance anandamide signaling for potential analgesic and anxiolytic effects.

Physiological roles attributed to anandamide include modulation of pain, appetite, mood, and memory, as well as possible neuroprotective and anti-inflammatory effects. It is broadly distributed in tissues, with particularly high concentrations in the brain, and participates in multiple neural and systemic processes.

Discovery and naming: Anandamide was described in 1992 by researchers including Raphael Mechoulam and colleagues. The name combines “ananda” (Sanskrit for bliss) with ethanolamine, reflecting its structure and proposed function as an endocannabinoid messenger.