Preexposure to cocaine attenuates aversions induced by both cocaine and fluoxetine: Implications for the basis of cocaine-induced conditioned taste aversions

3,4-Methylenedioxypyrovalerone (MDPV)-induced conditioned taste avoidance in the F344/N and LEW rat strains

“…For example, transgenic mice with SERT deletions display attenuated acquisition of cocaine-induced taste avoidance compared to wild-type and DAT knockout mice (Jones et al, 2010), although it should be noted that NET knockouts also produced significant attenuation of avoidance, precluding a solitary role of 5-HT in this behavioral effect. Additionally, Serafine et al (2010) reported that animals exposed to cocaine prior to taste avoidance conditioning with fluoxetine (a selective 5-HT reuptake inhibitor) displayed attenuated fluoxetine-induced taste avoidance, suggesting some adaptation to their common aversive effects (see Braveman, 1975; Cappell et al, 1975; for a review see Simpson and Riley, 2001). It should be noted that fluoxetine preexposure had no impact on cocaine-induced taste avoidance, although as noted by the authors, it is possible this was a dose-dependent effect.…”

Exposure to nicotine during periadolescence or early adulthood alters aversive and physiological effects induced by ethanol

“…Although the mechanism underlying the US preexposure effect (either with the same or different drugs) is not fully characterized, for some drugs, e.g., alcohol, nicotine and morphine, it is thought that changes to the drug during preexposure impact the effects of that (or a different drug) at conditioning, weakening its ability to induce aversions (Barker and Johns, 1978, Berman and Cannon, 1974, Hunt et al , 1985, Iwamoto and Williamson, 1984, Simpson and Riley, 2005). The impact of preexposure in the cross-drug design is generally thought to be the result of the development of tolerance to common aversive effects shared by the drugs, presumably due to some common mechanism of action (Riley and Simpson, 2001: Serafine and Riley 2009: Serafine and Riley 2010). It is interesting to note that the cross-drug preexposure effect has been previously reported with nicotine and alcohol (Kunin et al , 1999).…”

Dopamine mediates cocaine-induced conditioned taste aversions as demonstrated with cross-drug preexposure to GBR 12909

“…Since preexposure can result in either effect, it is necessary to use doses during conditioning that induce intermediate aversions (to detect potentiation or attenuation). In this context, cocaine has been reported to induce intermediate aversions at a dose of 18 mg/kg (Freeman et al, 2005; Serafine and Riley, 2009; 2010). Therefore, this dose was used during conditioning in the present experiment.…”

“…This prediction is based on work utilizing the cross-drug preexposure preparation (De Beun et al, 1996; Gommans et al, 1998; Serafine and Riley, 2009) in which exposure to one compound is given prior to aversion conditioning with another. Under such conditions, aversions to the second compound are often weakened, an effect commonly interpreted as being due to cross tolerance (or adaptation) to the shared aversion-inducing effects of the two drugs (Berman and Cannon, 1974; Jones et al, 2009; LeBlanc and Cappell, 1974; Simpson and Riley, 2005; Serafine and Riley, 2009; 2010; for reviews and alternative interpretations, see Cappell and LeBlanc, 1977; Randich and LoLordo, 1979; Riley and Simpson, 2001). In one of the first demonstrations of the use of this procedure for investigations of common stimulus properties, De Beun and colleagues (1993) reported that CTAs induced by the selective serotonin (5-HT) agonist 8-OHDPAT were blocked by preexposure to compounds that also had 5-HT agonist activity (for the same receptor subtype, e.g., 5-HT 1A ; see De Beun et al, 1993).…”

“…Given that these compounds (ipsapirone, buspirone, RU-24969, sertraline, d-amphetamine, LSD, metergoline and idazoxane) were effective in blocking 8-OHDPAT-induced CTAs, De Beun and colleagues concluded that cross-drug preexposure could be used to assess the commonalities in aversion-inducing mechanism between different compounds (De Beun et al, 1993). Since this demonstration, several other investigations have also utilized this procedure to examine common mechanisms in the aversive effects of various compounds (see De Beun et al, 1996; Gommans et al, 1998; Jones et al, 2009; Kayir et al, 2008; Olivier et al, 1999; Van Hest et al, 1992; Serafine and Riley, 2009; 2010). …”