The mature forms of the G118/D40-hMOPR stably expressed in CHO cells had a shorter half-life than those of the A118/N40-hMOPR (Fig. 6), but their precursors had similar half-lives and turnover rates, suggesting that the G118/D40-hMOPR may have lower expression levels. However, the impact of A118G/A112G on MOPR level is not uniform and our results obtained in CHO cells appears to be applicable to brain regions or cell lines that showed decreased MOPR levels, but no those that did not. In vivo, A112G knock-in mice (G/G mice) has lower MOPR protein level in the thalamus and in the whole brain than wildtype mice (A/A mice) [18]. In contrast, in the striatum and hippocampus, G/G mice and A/A mice had similar levels of MOPR (manuscript in preparation). In addition, in the humanized G118-h/mMOPR and A118-h/mMOPR mice, no genotype differences in MOPR densities were observed in the striatum and the ventral tegmental area [19]. Moreover, in the human carriers of the G118 allele, the number of [3H]DAMGO binding sites was unaffected in the secondary somatosensory area and the ventral posterior part of the
