reveal that the N40D substitution destroys an N′-terminal glycosylation site and reduces the surface expression for MORs (Ray et al., 2011; Wang, Huang, Ung, Blendy, & Liu-Chen, 2012; Wang, Huang, Blendy, & Liu-Chen, 2014; Halikere et al., 2019). However, another study using a humanized mouse model of MOR N40D is not in complete agreement with this finding (Bilbao et al., 2015). Thus, to gain insight into mechanisms underlying drug abuse, it is imperative to understand how the D40 variant impacts MOR signaling and synaptic function in human neuronal context.
