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Conversely, cFos+ immunostaining in other cerebellar regions seems to be unrelated to CS+ preference but to other aspects of the conditioning procedure. At the prefrontal cortex, cFos expression seemed to be related to cocaine administration rather than to its ability to establish conditioned preference. The present results suggest that as it has been observed in some clinical studies, the cerebellum RVX-208 might be an important and largely overlooked part of the neural circuits involved in generating, maintaining and/or retrieving drug memories. Several processes underlie motivational alterations in drug-seeking and drug-taking behaviour. Indeed, conditioned reinforcement, incentive motivation, behavioural sensitization and maladaptive stimulus-response learning, all contribute to orientating BMS-777607 cost the response towards drug-related stimuli (Kalivas & Volkow 2005; Hyman, Malenka & Nestler 2006; Everitt et?al. 2008; Robinson & Berridge 2008; Koob & Volkow 2010). Specifically, Pavlovian conditioning tunes the motivational impact of drug-associated stimuli by strengthening the memory of drug-related cues and, thus, boosting the importance of stimuli and contexts that enclose drug seeking and taking (Everitt & Robbins 2005). Drug-associated cues and contexts guide drug-seeking and have an important effect on drug intake, gaining progressively more control over an individual's behaviour as some of them transit through successive behavioural stages towards habitual consumption and ultimately reaching the addicted state. Because of the relevance for drug seeking and taking, there has been a growing interest in identifying the neural circuits and molecular mechanisms underlying the formation, maintenance and retrieval of drug-related selleck products memories. It has been argued that Pavlovian and instrumental conditioned memories are controlled and stored by dopamine (DA)�Cglutamate interactions into the nucleus accumbens, basolateral amygdala, hippocampus and prefrontal cortex (Bower & Parson 2003). Chronic drug abuse produces a re-organization of these prefronto�Cstriatal�Climbic networks via their effects on neurotransmitter systems (Nestler 2005), neuronal morphology (Nestler 2005) and functional interactions within and between neuronal assemblies that belong to this circuitry (Belin & Everitt 2008; Noori, Spanagel & Hansson 2012). Over the past decades, it has become clear that the cerebellum constitutes functional loop circuits with different brain areas previously involved in drug effects and addictive behaviour such as prefrontal and associative non-motor cortices, the basal ganglia (Bostan, Dum & Strick 2010) and limbic system (Heath et?al. 1978). Remarkably, several cerebellar regions have bidirectional connections with the prefrontal and sensorimotor cortices (Dum & Strick 2003; Kelly & Strick 2003), and the striatum (Hoshi et?al. 2005; Bostan et?al. 2010).
