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Does cellular uptake and diffusion (trafficking) of anandamide mediate its antidepressant activity on prefrontal cortex neurons?
My hypothesis is that anandamide trafficking by intracellular CB1 activation may modulate the activity of the GPR55 receptor and induce neuronal differentiation in prefrontal cortex neurons.
The endogenous fatty acid anandamide (AEA) is a partial agonist at cannabinoid CB1 receptors and has been reported to be a full agonist at the recombinant vanilloid receptor, VR1.
Anandamide is a partial agonist of CB1 receptors in sensory neurons: QuoteThe endogenous fatty acid anandamide (AEA) is a partial agonist at cannabinoid CB1 receptors and has been reported to be a full agonist at the recombinant vanilloid receptor, VR1.http://www.ncbi.nlm.nih.gov/pubmed/12359623
In addition to it's short half-life, rapid hydrolysis and extensive catabolism by FAAH, anandamide displays extremely poor affinity to CB1 receptors - have you reviewed the Ki values? This is precisely why methanandamide was synthesized as a pharmacologic replacement.
How does retrograde anandamide signaling affect FAAH metabolism?http://www.ncbi.nlm.nih.gov/pubmed/12770562
Anandamide is metabolized by FAAH.
Taken together the results demonstrate that anandamide mobilizes Ca2+ from a caffeine-sensitive intracellular Ca2+ store that functionally overlaps in part with the internal stores mobilized by histamine.
Quote from: exothermic on 05/07/2016 03:47:39Anandamide is metabolized by FAAH.Is caffeine a pharmacological FAAH inhibitor? I'm interested in understanding how retrograde anandamide signaling is diffused via caffeine, possibly blocking FAAH activity on-demand.
CaffeineCo-administering caffeine and cannabis has a long history. Bell  claimed that oral administration of hashish with coffee increased the effects of cannabis, and at the same time diminished its duration. He proposed a pharmacokinetic mechanismócoffee promoted more rapid absorption of hashish.Caffeine and theophylline are antagonists of adenosine receptors. Adenosine receptors are tonically activated by adenosine, their endogenous ligand. Rodent studies indicate that A1-subtype adenosine receptors tonically inhibit CB1 activity . Thus the antagonism of A1 receptors by caffeine and theophylline enhances eCB system function (e.g., activation of CB1 by 2-AG). Caffeine potentiated CB1-mediated activity stimulated by THC and WIN-55,212 in hippocampus slices .