At the behavioural level, endocannabinoids have been experimentally determined to mediate the effects of stress on two behavioural processes. One common behavioural response to stress in animals and humans is an increase in the consumption of addictive substances or a relapse following a period of abstinence. In mice which have had several weeks access to an ethanol solution, exposure to a foot shock stress resulted in a dramatic increase in ethanol consumption over the following 24 h period following stress (Racz et al., 2003); in mice lacking the CB1 receptor, stress did not promote ethanol consumption (Racz et al., 2003). This data suggest that stress-induced mobilization of endocannabinoid signaling mediates an increase in ethanol consumption, a finding which is consistent with the fact that facilitation of endocannabinoid neurotransmission, in and of itself, promotes ethanol consumption (Blednov et al., 2007; Hansson et al., 2007).
