期刊
NEUROPHARMACOLOGY
卷 202, 期 -, 页码 -出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuropharm.2021.108856
关键词
Alcohol; Extended amygdala; Central amygdala; Bed nucleus of stria terminalis; Nucleus accumbens; Ventral tegmental area; Addiction
资金
- National Institute of Health [R01 AA023305, U01 AA028709]
- United States (U.S.) Department of Veterans Affairs, Biomedical Laboratory Research and Development Service [I01 BX003451]
Alcohol dependence is characterized by a shift in motivation from positive reinforcement to negative reinforcement, involving neural adaptations in VTA and extended amygdala, particularly in chronic alcohol responses. The exact mechanisms of this transition are not fully understood, but preclinical models play a significant role in studying this phenomenon.
Alcohol dependence is characterized by a shift in motivation to consume alcohol from positive reinforcement (i. e., increased likelihood of future alcohol drinking based on its rewarding effects) to negative reinforcement (i.e., increased likelihood of future alcohol drinking based on alcohol-induced reductions in negative affective symptoms, including but not limited to those experienced during alcohol withdrawal). The neural adaptations that occur during this transition are not entirely understood. Mesolimbic reinforcement circuitry (i.e., ventral tegmental area [VTA] neurons) is activated during early stages of alcohol use, and may be involved in the recruitment of brain stress circuitry (i.e., extended amygdala) during the transition to alcohol dependence, after chronic periods of high-dose alcohol exposure. Here, we review the literature regarding the role of canonical brain reinforcement (VTA) and brain stress (extended amygdala) systems, and the connections between them, in acute, sub-chronic, and chronic alcohol response. Particular emphasis is placed on preclinical models of alcohol use.
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