Abstract
Using a variety of animal models that simulate key features of the alcohol use disorder (AUD), remarkable progress has been made in identifying neurochemical targets that may contribute to the development of alcohol addiction. In this search, the dopamine (DA) and norepinephrine (NE) systems have been long thought to play a leading role in comparison with other brain systems. However, just recent development and application of optogenetic approaches into the alcohol research field provided opportunity to identify neuronal circuits and specific patterns of neurotransmission that govern the key components of ethanol-addictive behaviors. This critical review summarizes earlier findings, which initially disclosed catecholamine substrates of ethanol actions in the brain and shows how the latest methodologies help us to reveal the significance of DA and NE release changes. Specifically, we focused on recent optogenetic investigations aimed to reveal cause-effect relationships between ethanol-drinking (seeking and taking) behaviors and catecholamine dynamics in distinct brain pathways. These studies gain the knowledge that is needed for the better understanding addiction mechanisms and, therefore, for development of more effective AUD treatments. Based on the reviewed findings, new messages for researches were indicated, which may have broad applications beyond the field of alcohol addiction.
Highlights
Alcohol use disorder (AUD) is a problematic pattern of alcohol use, which is widely spread among adult population in the world and for the most part accompanied by co-occurring psychiatric disorders, e.g., drug use disorders, major depressive disorders, specific phobias, and antisocial and borderline personality disorders (Kranzler and Soyka, 2018), and results in serious health and socioeconomic problems in our society (Substance Abuse and Mental Health Services Administration (Samhsa), 2019; Tucker et al, 2020)
The functioning of dopamine (DA) and norepinephrine (NE) systems seems to be altered by ethanol more than others and, they were the main targets in the field of alcohol research
Over the past several decades the development and use of translational animal models has resulted in notable progress in our understanding of ethanol and stress induced effects on synaptic transmission, especially on DA and NE systems. More importantly, these findings provided critical insights into some of the neural circuits that are involved in ethanol addiction-related behaviors, which include the ventral tegmental area (VTA)— nucleus accumbens (NAc) and locus coeruleus (LC)—prefrontal cortex and basolateral amygdala pathways (Vena et al, 2020; Ye et al, 2020)
Summary
Alcohol use disorder (AUD) is a problematic pattern of alcohol use, which is widely spread among adult population in the world and for the most part accompanied by co-occurring psychiatric disorders, e.g., drug use disorders, major depressive disorders, specific phobias, and antisocial and borderline personality disorders (Kranzler and Soyka, 2018), and results in serious health and socioeconomic problems in our society (Substance Abuse and Mental Health Services Administration (Samhsa), 2019; Tucker et al, 2020). Noradrenergic afferents from the LC to the ventral tegmental area (VTA) have been shown to modulate DA neuron firing and extracellular DA concentrations in the nucleus accumbens (NAc), caudate, and prefrontal cortex (Mejias-Aponte, 2016), likely via activation of α1-adrenoreceptors (Rommelfanger et al, 2009). It has been observed in both preclinical and clinical studies that selective antagonists of α1-adrenoreceptors and agonists α2-adrenoreceptors alter ethanol- seeking and consumption (Haass-Koffler et al, 2018). Drugs designed to reduce central NE activity appear to decrease motivation to ethanol and drinking behaviors in rodents, ethanol-preferring animals (Haass-Koffler et al, 2018)
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