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Addiction in general, though this paper will focus on alcohol specifically, is characterized by a chronic relapse state that embodies key elements, such as the compulsion to seek out and use the drug, the inability to control the amount used, and a negative emotional state when the substance cannot be accessed (Gilpin and Koob, 2008). Alcohol consumption evolves from impulsive to compulsive through repeated binging, withdrawal, and craving cycles, which cause neuroadaptations (Cui et al., 2013; Koob, 2013).
Research on the neurobiology of addiction has focused on the positive reinforcing effects and the activation of the mesocorticolimbic dopamine circuit being the sole motivator. The mesolimbic system (the primary reward circuit) projects from the ventral tegmental area (VTA) to the nucleus accumbens (NAcc) and utilizes dopamine as its main neurotransmitter (Gilpin and Koob 2008). This circuit helps shape incentive salience, better known as the “wanting” or “desire” for alcohol (Robinson & Berridge, 1993; Berridge, 2007). Oral ethanol self-administration is reduced by the administration of dopamine and NMDA receptor antagonists into the nucleus accumbens (Rassnick 1992). Weiss et al measured dopamine levels in the extracellular fluid of the NAcc and showed alcohol ingestion or even the anticipation of alcohol causes an increase in dopamine (Weiss et al. 1993).
However, Rassnick also demonstrated that positive reinforcement alone does not motivate alcohol consumption while using a 6-hydroxydopamine (6-OHDA)-induced lesions of the mesolimbic dopamine system did not block alcohol self administration (Rassnick et al. 1993). Even in the presence of administered methylphenidate, subjects experiencing alcohol withdrawal show lowered levels of dopamine by 50-70%, as compared to controls; withdrawal causes decreases in dopamine function and the neuroadaptations that lead to a hypodopaminergic state during withdrawal (Karkhanis 2015 CIE ethanol exposure reduces presynaptic DOPAMINE NEUROTRANSMISSION IN THE MOUSE NUCLEUS ACCUMBENS; Volkow et al. 2007 Profound decreases in dopamine release in striatum in detoxified alcoholics: possible orbitofrontal involvement.). In the early stages of alcohol use and abuse, positive reinforcement acts as the main motivating factor in alcohol-drinking behavior. However, at some point chronic alcohol exposure causes a shift from alcohol use to alcohol dependence that parallels the switch from positive reinforcement to a mixture of both positive and negative as the motivating factor behind alcohol use; this is caused by neural changes, or plasticity, that chronic alcohol exposure elicits (Gilpin and Koob, 2008).
There are three widely recognized stages of alcohol use that overlap and ultimately contribute to the progressive transition from alcohol use to alcohol dependence. They are: 1) binge and intoxication, 2) withdrawal and negative affect, and 3) pre-occupation and anticipation, better known as craving (Volkow et al., 2016). Neuroadaptations within the addiction circuitry and the progressive transition from alcohol use to dependence hinge on the repeated cycling of these three stages.
Three phenomena contribute to the progression of alcohol use disorders and the shift from positive reinforcement to both positive and negative reinforcement as motivators for alcohol use. They are sensitization, tolerance, and withdrawal. Drug sensitization, which is the opposite of tolerance, refers to the individuals increased stimulus that occurs when the same amount of substance is taken as before; this leads to the cue-induced craving. When it takes more alcohol to achieve the same level of intoxication, as a smaller amount used to, then the subject has developed a tolerance. Withdrawal is the outward presentation of neural changes and happens when adverse effects occur in the absence of the substance, such as insomnia, delirium tremors, anxiety, and seizures. As these elements of addiction repeat, the disease progresses and spirals more out of control (Gilpin 2008)
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