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A Mechanism Linking Two Known Vulnerability Factors for Alcohol Abuse: Heightened Alcohol Stimulation and Low Striatal Dopamine D2 Receptors.

Abstract：

:Alcohol produces both stimulant and sedative effects in humans and rodents. In humans, alcohol abuse disorder is associated with a higher stimulant and lower sedative responses to alcohol. Here, we show that this association is conserved in mice and demonstrate a causal link with another liability factor: low expression of striatal dopamine D2 receptors (D2Rs). Using transgenic mouse lines, we find that the selective loss of D2Rs on striatal medium spiny neurons enhances sensitivity to ethanol stimulation and generates resilience to ethanol sedation. These mice also display higher preference and escalation of ethanol drinking, which continues despite adverse outcomes. We find that striatal D1R activation is required for ethanol stimulation and that this signaling is enhanced in mice with low striatal D2Rs. These data demonstrate a link between two vulnerability factors for alcohol abuse and offer evidence for a mechanism in which low striatal D2Rs trigger D1R hypersensitivity, ultimately leading to compulsive-like drinking.

journal_name

Cell Rep

journal_title

Cell reports

authors

Bocarsly ME,da Silva E Silva D,Kolb V,Luderman KD,Shashikiran S,Rubinstein M,Sibley DR,Dobbs LK,Alvarez VA

doi

10.1016/j.celrep.2019.09.059

subject

Has Abstract

pub_date

2019-10-29 00:00:00

pages

1147-1163.e5

issue

5

issn

2211-1247

pii

S2211-1247(19)31256-2

journal_volume

29

pub_type

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