Reinstatement of extinguished cocaine-taking behavior by cocaine and caffeine

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Abstract

Interactions between caffeine and cocaine have been demonstrated in a number of behavioral paradigms. The present study was undertaken in an attempt to determine whether caffeine could reinstate extinguished cocaine-taking behavior in rats. Experienced self-administering rats were first put through extinction training. The rats were then given an injection of either saline, cocaine (5.0, 10.0, or20.0 mg/kg), or caffeine (5.0, 10.0, 20.0, 40.0 mg/kg). Both cocaine and caffeine induced a dose-dependent increase in the number of responses made on the previously cocaine-associated lever. These results confirm findings that the originally self-administered drug can serve as a prime to reinstate drug-taking behavior, and that nondopaminergic agonists can also provide an effective prime to reinstate responding. Potential mechanisms for these effects are discussed.

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Cited by (74)

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    Broadly, these results are consistent with the majority of the literature showing a sex difference where females self-administer more cocaine than males (see Anker and Carroll, 2011). Reinstatement of cocaine-seeking after a CAF priming injection has been well-established (Regier et al., 2014; Weerts and Griffiths, 2003; Green and Schenk, 2002; Schenk et al., 1996; Worley et al., 1994), yet sex-specific effects of CAF as a priming agent have not been studied. The present study was the first to show that females had enhanced responding, compared to males, on the cocaine-associated lever after a priming injection of CAF (5 mg/kg).

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    Within the striatum, postsynaptic adenosine receptor subtypes co-localize with specific dopamine receptor subtypes in the medium spiny neurons where they appear to antagonize postsynaptic dopamine signaling (Bertran-Gonzalez et al., 2009; Ferre et al., 1994a, 1994b, 1999; Gines et al., 2000; Hakansson et al., 2006; Svenningsson et al., 1998). Emergent findings show that A1 and A2A receptors may play a critical role in regulating cocaine-induced behavioral responses (Bachtell and Self, 2009; Filip et al., 2006; Green and Schenk, 2002; Knapp et al., 2001; O'Neill et al., 2012; Poleszak and Malec, 2002b; Worley et al., 1994). Most relevant is a recent study demonstrating that systemic administration of an A2A agonist decreased, while administration of an A2A antagonist increased, cocaine-induced locomotor sensitization in rats (Filip et al., 2006).

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    More importantly, despite limited success demonstrating primary reinforcement by caffeine (Atkinson and Enslen, 1976) there have been several studies demonstrating that caffeine increases the reinforcing effects of other drugs. Caffeine administration increases alcohol drinking (Kunin et al., 2000), cocaine self-administration (Schenk et al., 1994), and reinstates extinguished cocaine-seeking behavior (Green and Schenk, 2002; Worley et al., 1994). Prior exposure to caffeine also increases the psychomotor stimulant effects of amphetamine (Palmatier et al., 2003; Simola et al., 2006), nicotine (Celik et al., 2006; Palmatier et al., 2003) and cocaine (Schenk et al., 1994) as well as the primary reinforcing effects of cocaine (Horger et al., 1991) and nicotine (Jones and Griffiths, 2003; Shoaib et al., 1999).

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