Most recently, a series of studies has indicated that the SP/NK1R system is involved in alcohol-related behaviors. For example, NK1R knockout mice do not exhibit conditioned place preference for alcohol and consume less alcohol in voluntary two bottle choice drinking (George et al., 2008; Thorsell et al., 2010). NK1R antagonist administration in wild-type mice also decreases alcohol consumption (Thorsell et al., 2010), as does microRNA silencing of NK1R expression (Baek et al., 2010). Additionally, the NK1R knockout mice fail to escalate their alcohol consumption following repeated cycles of deprivation, suggesting that the SP/NK1R may mediate neuroadaptations that contribute to escalation (Thorsell et al., 2010).
