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Chunk #36 — RESULTS — Medication by OPRM1 and DAT genotypes — Alcohol Stimulation and Sedation

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Naltrexone modification of drinking effects in a subacute treatment and bar-lab paradigm: influence of OPRM1 and dopamine transporter (SLC6A3) genes.
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There was no three-way interaction between medication group, OPRM1 genotype and DAT genotype on post alcohol priming drink stimulation (F(1,75)=1.52, p=0.22). Although, there was no significant two-way interaction (F(1,79)=0.021, p=0.89) of genotypes (figure 2) there was a main effect of OPRM1 genotype (F(1,79)=5.13, p= 0.028) and a main effect of DAT genotype (f (1,79)= 0.032) on alcohol stimulation, such that those subjects with OPRM1 asn40asn had more stimulation than asp40 subjects and those with at least one DAT 9 VNTR had more stimulation compared to those with no DAT 9 VNTR (i.e. 10/10 genotype). Of interest, the most alcohol stimulation was observed in those with both the OPRM1 asn40asn genotype and having at least one DAT VNTR 9, the same group that had the lowest drinking while on naltrexone during the 5-day natural observation period. There were no significant interactions of medication by the two genotypes or main effects of genotype on alcohol induced sedation.