Translation of neuropeptide-mediated effects into clinical treatments has typically proven difficult. However, recent data showing that the opioid agonist/partial agonist buprenorphine reduces alcohol intake in msP rats via activation of NOP receptors (Ciccocioppo et al., 2007) not only confirm a possible link between N/OFQ and excessive alcohol consumption, but suggest a possible path toward clinical applications. Buprenorphine has long been in clinical use for the treatment of pain (Picard et al., 1997) and management of heroin dependence (Johnson et al., 2000; Kakko et al., 2003). Our findings with buprenorphine provide “proof of concept” for the feasibility of targeting central NOP receptors via peripheral drug administration to suppress excessive alcohol intake. In addition, as reported in clinical studies, in heroin addicts, buprenorphine given at doses higher than those needed to occupy opioid receptors is beneficial in controlling cocaine addiction (Montoya et al., 2004): another study showed that in heroin addicts, it not only lowers opiate consumption, but also decreases alcohol intake (Kakko et al., 2003).
