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 lateral thalamic tissue, compared with the homozygous A118 carriers [35]. It is noteworthy, however, that in this study 86% of the human carriers of the G118 allele were heterozygotes [35]. Recently smokers heterozygous for the G118 allele have been shown to have lower levels of MOPR binding potential as measured by 11C-carfentanil in certain unilateral or bilateral brain regions, such as the amygdala, thalamus, and anterior cingulate cortex, compared to those homozygous for the A118 allele. In contrast, no differences were observed in other areas including the ventral striatum/nucleus accumbens and caudate [36]. In vitro, A118G mutation of the hMOPR decreased receptor expression in stably transfected HEK293 [37,38] and AV-12 cells [38] or transiently transfected CHO cells [39], as revealed by [3H]DAMGO binding and/or immunoblotting, but did not change protein expression of the hMOPR in transiently transfected COS [40], HEK293 and AV-12 cells [38]. Thus, the A118G/A112G SNP either decreases or does not change expression of MOPR in different brain
