Anandamide Uptake Did Not by Itself Prove a Dedicated Membrane Transporter
A compound increasing anandamide without inhibiting FAAH does not, by itself, identify a dedicated anandamide membrane transporter. A supplied review describes competing interpretations of this pharmacological observation.
The transporter hypothesis had indirect support
Pava and Woodward explain that proponents cited compounds increasing anandamide without blocking its principal hydrolytic enzyme, FAAH. Such results suggested another process might regulate uptake or removal, but did not identify that process molecularly.
An alternative mechanism remained plausible
The review describes critics arguing that passive diffusion could account for uptake and noting the absence of an identified gene or specific molecular mechanism in that historical evidence base. The disagreement concerned the explanation for an observation, rather than whether anandamide could enter cells.
Describe the evidence at the level it resolves
An uptake effect, an enzyme effect and identification of a transport protein are different findings. Naming a compound a transport inhibitor should not make the existence or identity of its proposed target seem settled. This is the review’s 2012 account of the debate, not a claim that all subsequent research remains unchanged. It also concerns endogenous anandamide handling, not transport of THC in a forensic specimen.
Related reading: Alcohol–Endocannabinoid Reviews Need to Keep Stages of Dependence Separate.
Research cited
Pava MJ, Woodward JJ. A Review of the Interactions between Alcohol and the Endocannabinoid System: Implications for Alcohol Dependence and Future Directions for Research (2012). The experiments discussed here are described through this supplied review.
