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Chunk #11 — 3. A118G and drug dependence — 3.1. Alcohol

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OPRM1 SNP (A118G): involvement in disease development, treatment response, and animal models.
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Alcohol has been shown to affect a wide variety of transmitter systems; however, the rewarding and reinforcing aspects of alcohol intake seem to be mediated by the opioid system (Gianoulakis, 2004; Oswald and Wand, 2004). Indeed, acute alcohol administration has been shown to cause β-endorphin release measured in the plasma (Gianoulakis and Barcomb, 1987) or in reward-related brain regions (Rasmussen et al., 1998). MOPRs appear critical for mediating alcohol effects as MOPR knock-out mice show reduced ethanol intake and reward (Hall et al., 2001; Roberts et al., 2000). Likewise, antagonism of the receptor by naloxone in rats (Reid et al., 1986) and naltrexone in humans (O’Malley et al., 1992; Volpicelli et al., 1992) has been shown to reduce alcohol intake.