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. Author manuscript; available in PMC: 2011 Aug 1.
Published in final edited form as: Mol Biosyst. 2010 Apr 14;6(8):1411–1418. doi: 10.1039/c000237b

Figure 7. In situ NAE release from NAPE in primary neuron cultures from mice lacking GDE1 and NAPE-PLD.

Figure 7

(A) Time-dependence of NAE release in the presence or absence of the FAAH inhibitor PF-3845. NAE release in the absence of neurons was negligible on this timescale (not shown). (B) Assays conducted in primary neurons for 6 hours in the presence of PF-3845. Comparison of wild-type neurons to neurons from GDE1(−/−) or NAPE-PLD(−/−) mice reveals no impairment in the ability to release NAE from NAPE in situ. (C) Comparison of NAPE-PLD(−/−) neurons to GDE1(−/−)/NAPE-PLD(−/−) neurons reveals wild-type levels of NAE release in GDE1(−/−)/NAPE-PLD(−/−) neurons. (D) NAE release from 14C-NAPE or an ether-linked (non-hydrolyzable) NAPE analogue in neurons from GDE1(−/−)/NAPE-PLD(−/−) mice reveals the necessity of de-acylation prior to NAE release. These data represent single experiments performed in triplicate, representative of multiple experiments. *, p < 0.05.