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Molecular and cellular mechanisms of cocaine addiction

Although addicts are aware of the negative health, social and economic consequences of their drug abuse, they continue to compulsively seek and use illicit drugs. This begs the question “ why can’t addicts just quit?” One response to this question is that drugs of abuse changes the brain in such a way that addicts lose control over their ability to stop drug use.

Figure 1. 2 (taken from Volkow et al., 2003) shows a schematic of how drugs of abuse affect different brain circuits. The compulsive use of illicit drugs such as cocaine is thought to induce neuroadaptations in brain regions associated with reward-related learning and memory processes. These changes cause a)a) hyper-sensitization to cues associated with drugtaking, b) impulsive decision making and c) aberrant habit-like learned behaviors somuch so that even exposure to adverse consequences do not sway addicts away from drug seeking and taking (Thomas et al., 2008).

Drugs of abuse affect the same neural pathways involved in motivation, processing of rewards and decision making. The mesolimbic dopamine system which comprises of the ventral tegmental area (VTA), the nucleus accumbens (NAC), the PFC, hippocampus, amygdala and the bed nucleus of the stria terminalis is generally considered the reward pathway. The rewarding effect of psychostimulants is dependent on the balance between their influence on dopamine (DA), norepinephrine (NE) and 5-hydroxytryptamine (5-HT; serotonin) transmission; the increase in synaptic DA is thought to be the antecedent for their reinforcing and addictive properties of the drugs (Di Chiarra, 2000; Wise, 1994). While the overall effect of drugs of abuse in the mesolimbic system is increased levels of catecholamines in the synapse, individual psychostimulants may achieve this effect in different ways. Cocaine exerts its effects by increasing extracellular monoamine (DA, 5-HT and NE) concentrations by blocking the reuptake of monoamines from the synapse (Rotham et al., 2001).

Critically important to reinforcing drug use is cocaine’s ability to bind to and block the pre-synaptic dopamine transporter (Wise, 1984). This blockade results in an accumulation of synaptic dopamine which in turn enhances dopaminergic signaling through increased activation of postsynaptic dopamine receptors. The neurobiological effects of drugs of abuse on the reward circuitry have been extensively studied. However, what is less clear is why following extended periods of abstinence users remain susceptible to relapse. To this end, relapse remains the primary obstacle to the effective treatment of drug abuse (Stewart, 2000).

An individual’s susceptibility to relapse is governed by both genetic and non-genetic factors (Kendler et al., 2003). Studies have implicated that repeated drug use “ hijacks” the neural circuitry involved in learning and memory. This hypothesis has emerged from observations where drug-associated cues evoke drug memory, which induces craving during abstinence and precipitates relapse (Robins et al., 2008).

A number of studies have addressed the problem of relapse to cocaine seeking induced by drug cues, priming injections and stress using rodent models in conditioned place preference and self-administration paradigms (Erb et al., 1998; Erb and Stewart, 1999; Itzhak and Martin, 2002; Lu et al., 2002; Shaham et al., 2003; Wang et al.

, 2000). Although the same behavioral phenotype is observed, cocaine priming and stress induced reinstatement of drug seeking seem to be mediated by different neural mechanisms (Aguilar et al., 2009). For example, Sanchez and colleagues (2003) demonstrated that the D1 agonist SKF 81297 attenuated stress inducedbut did not affect cocaine-induced reinstatement.

Furthermore, Kreibich and 5 Blendy (2004) demonstrated that different patterns of phosphorylated cAMP response element-binding protein (pCREB) activation in discrete brain regions were observed in stress-induced versus cocaine-induced reinstatement. Thus, a thorough understanding of how elements that precipitate relapse impact brain physiology and neurochemistry is necessary for combating addiction. Specifically, an understanding of how these druginduced changes affect learning and memory processes will be of valuable importance.

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