Now it is widely agreed that alcohol directly affects the activity of various neuronal proteins and especially neurotransmitter receptors (Heilig and Egli 2006). In acute intoxicating effects of alcohol consumption largely because of changes in the activity of several neurotransmitter receptors. Some of these effects, such as alcohol-induced increases in the release of dopamine, serotonin and endogenous opioids, are strongly involved in the reinforcing properties of alcohol and in the development of alcohol dependence. The mesocorticolimbic dopamine system is the major dopaminergic pathway involved in alcohol addiction. With chronic alcohol consumption, neuroadaptations develop in order to oppose the acute effects of alcohol and reestablish normal neuronal cell function. Alcohol-induced neuroadaptations generally are in the opposite direction to the acute effects of alcohol on neurotransmitter systems and contribute to the maintenance of alcohol abuse. For example, whereas acute alcohol potentiates the GABAergic system and inhibits the glutamatergic neurotransmission, resulting in an overall inhibition of brain activity, the chronic consumption of alcohol leads to a GABAergic downregulation and a glutamatergic upregulation by multiple mechanisms. However, it needs to stress that that alcoholism is a complex heterogeneous disease (Cloninger 1987, Lesch et al. 2003, Cardoso et al. 2006, Reulbach et al. 2007) and many neurotransmitter systems that are affected by alcohol suggest that no single agent produces a consistent robust treatment effect (Tambour and Quertemont 2007). Therefore no doubt that a psychobiological model of three pathways for alcohol craving (reward, relief and obsessive craving) and therapeutic implications particularly in the field of anticraving drug therapy were hypothesized (Verheul et al. 1999, Addolorato et al. 2005). First, craving is a dopaminergic/opioidergic dysregulation (deficit of opioids/endorphines, hypersensitivity to the reinforcing effects of alcohol) and naltrexone (nonspecific opioid receptor antagonist) could be used for reward craving. Second, craving is a GABAergic/glutamatergic dysregulation (dysregulation of glutamate with neuronal overexcitability, hypersensitivity to the sedative effects of alcohol) and acamprosate (functional NMDA antagonist) or baclofen (GABA_B agonist) could be of value against relief craving. Third, craving is a serotoninergic dysregulation (deficit of serotonin) and selective serotonin reuptake inhibitors (SSRI), ondansetron (5-HT₃ antagonist) or topiramate (normothymic agent) can show clinical efficacy. Concluding, it seems that personalized therapy could be more specific for different subtypes alcohol-dependent patients with different craving neuromechanisms.

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