Background

Animal models of binge drinking (BD) are crucial for clarifying the neurobiological and psychobiological mechanisms underlying this harmful behavior [see Jeanblanc et al. (2019) for a review]. Considerable advances have been made by forcibly administering ethanol (Becker and Lopez, 2016), employing operant paradigms (Simms et al., 2010), developing strains with a genetic predisposition to ethanol (Colombo et al., 2014), or using self-administration models in Wistar rats where ethanol is presented in an intermittent and temporally restricted fashion (Salguero et al, 2020; Ruiz-Leyva et al, 2020). These animal models, however, do not always mimic the contextual variables surrounding human drinking behaviors or fail to achieve pharmacologically relevant blood ethanol concentrations within the proposed time frame for this type of consumption. Moreover, alcohol use is driven by several factors. For instance, it has been observed that the induction of aversive states in conjunction with ethanol availability generally leads to an increase in ethanol consumption and favors the development of psychiatric diseases—including alcohol use disorders (AUD)—via epigenetic changes [for a review, see Pucci et al. (2019)]. In addition, the induction of frustration and anxiety (Díaz-Morán et al., 2013a and 2013b; Sabariego et al, 2013; Kawasaki et al., 2017; Jiménez-García et al., 2019) is associated with increases in ethanol consumption as a coping strategy (Ramirez-Castillo et al., 2019). Paradoxically, exposure to appetitive stimuli (i.e., food) also enhances ethanol consumption. Seminal studies showed that concurrent access to food and ethanol enhanced drinking behaviors in animals (Mello and Mendelson, 1971; Meisch and Thompson, 1972). In this respect, both substance use disorders (including AUD) and BD appear to be comorbid (or at least closely related) with binge eating (BE) (Ferriter and Ray; 2011; Munn-Chernoff et al., 2020). Conceptually, BE involves ingestion of large amounts of palatable (sugary and/or fatty) food in a short period of time, associated with a feeling of loss of control [see Dingemans et al. (2017) for a review].

The present protocol aims to serve as a guide for researchers interested in the study of the interaction of binge-like behaviors and should help replicability efforts. It is also an improvement over the models described above. An exhaustive description of the novel animal model of BE-BD interaction originally developed by Ruiz-Leyva et al. (2022) is presented. Here, the self-administration model induced remarkably high levels of absolute ethanol consumption (approximately 5 g/kg/90 min) and ethanol preference (80%–90%), much greater than those reported by other preclinical models. For instance, rats exposed to intermittent access to 20% ethanol in a two-bottle-choice procedure achieved 9–10 g/kg, yet they did that in a 24 h period, whereas those tested in the drinking-in-the-dark-multiple-scheduled access rarely exceed 5–6.5 g/kg/day. In this model, food-deprived rats are briefly exposed to a measurable amount of highly palatable sugary pellets immediately followed by a two-bottle-choice test (ethanol vs. water). Here, the authors reported dramatic and specific increases in ethanol intake as the BE behavior develops, leading to pharmacologically relevant blood ethanol concentrations. In addition, ethanol consumption turned compulsive by the last sessions and sensitive to naltrexone administration.