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Accumulation of N‐Arachidonoylethanolamine (Anandamide) into Cerebellar Granule Cells Occurs via Facilitated Diffusion

Abstract: N‐Arachidonoylethanolamine (anandamide, AEA) is a putative endogenous ligand of the cannabinoid receptor. Intact cerebellar granule neurons in primary culture rapidly accumulate AEA. [3H]AEA accumulation by cerebellar granule cells is dependent on incubation time (t1/2 of 2.6 ± 0.8 min at 37°C) and temperature. The accumulation of AEA is saturable and has an apparent Km of 41 ± 15 µM and a Vmax of 0.61 ± 0.04 nmol/min/106 cells. [3H]AEA accumulation by cerebellar granule cells is significantly reduced by 200 µM phloretin (57.4 ± 4% of control) in a noncompetitive manner. [3H]AEA accumulation is not inhibited by either ouabain or removal of extracellular sodium. [3H]AEA accumulation is fairly selective for AEA among other naturally occurring N‐acylethanolamines; only N‐oleoylethanolamine significantly inhibited [3H]AEA accumulation at a concentration of 10 µM. The ethanolamides of palmitic acid and linolenic acid were inactive at 10 µM. N‐Arachidonoylbenzylamine and N‐arachidonoylpropylamine, but not arachidonic acid, 15‐hydroxy‐AEA, or 12‐hydroxy‐AEA, compete for AEA accumulation. When cells are preloaded with [3H]AEA, temperature‐dependent efflux occurs with a half‐life of 1.9 ± 1.0 min. Phloretin does not inhibit [3H]AEA efflux from cells. These results suggest that AEA is accumulated by cerebellar granule cells by a protein‐mediated transport process that has the characteristics of facilitated diffusion.