Brain mechanisms of high-strength alcohol seeking
Lead Research Organisation:
University of Sussex
Department Name: Sch of Psychology
Abstract
In the last 15 years, there have been serious concerns over the abuse of low-cost, 'super-strength' alcoholic beverages, such as beer that contain over 7.5% alcohol. Such high alcohol levels dramatically increase the risk for alcohol addiction.
Environmental signals or 'cues' associated with alcohol intake, such as being in a pub or a beer logo, trigger cravings for alcohol that may lead to excessive drinking and relapse in humans, and alcohol seeking in laboratory animals. The nucleus accumbens (NAc), and its projections to the hypothalamus and ventral tegmental area, is a key brain area involved in cue-controlled drug and natural reward seeking. In our BBSRC-funded studies, we have shown that drug and natural reward cues activate sparse sets of neurons called 'neuronal ensembles' in this brain area (e.g. Ziminski et al. 2017; PMID: 28213443).
To date, whether increased alcohol content in beverages alters the magnitude and duration of neurobehavioural reactivity to these cues has not been fully elucidated. Using mice, the first aim of this proposed project is to determine whether cues (e.g. alcohol drinking context, alcohol-delivery tone) associated with high-alcohol (9%) compared to normal alcohol (4%) content beer provokes more robust and persistent forms of alcohol seeking. Focussing on the NAc and related regions, the second aim is to combine immunohistochemical characterisation, and in vivo methods, such as fibre photometry and optogenetics, to reveal these mechanisms, in particular the role that inhibitory interneurons play in regulating neuronal ensemble activity during cue-controlled seeking of high-strengh beer.
Alcohol use is the most prevalent and harmful of all substance abuse disorders. Their promotion through advertisements that act as alcohol cues is of concern, and alcohol-related negative health consequences burden the NHS. Thus, understanding the mechanisms that control reactivity to high-strength alcohol cues will have significant economic and societal impact.
Environmental signals or 'cues' associated with alcohol intake, such as being in a pub or a beer logo, trigger cravings for alcohol that may lead to excessive drinking and relapse in humans, and alcohol seeking in laboratory animals. The nucleus accumbens (NAc), and its projections to the hypothalamus and ventral tegmental area, is a key brain area involved in cue-controlled drug and natural reward seeking. In our BBSRC-funded studies, we have shown that drug and natural reward cues activate sparse sets of neurons called 'neuronal ensembles' in this brain area (e.g. Ziminski et al. 2017; PMID: 28213443).
To date, whether increased alcohol content in beverages alters the magnitude and duration of neurobehavioural reactivity to these cues has not been fully elucidated. Using mice, the first aim of this proposed project is to determine whether cues (e.g. alcohol drinking context, alcohol-delivery tone) associated with high-alcohol (9%) compared to normal alcohol (4%) content beer provokes more robust and persistent forms of alcohol seeking. Focussing on the NAc and related regions, the second aim is to combine immunohistochemical characterisation, and in vivo methods, such as fibre photometry and optogenetics, to reveal these mechanisms, in particular the role that inhibitory interneurons play in regulating neuronal ensemble activity during cue-controlled seeking of high-strengh beer.
Alcohol use is the most prevalent and harmful of all substance abuse disorders. Their promotion through advertisements that act as alcohol cues is of concern, and alcohol-related negative health consequences burden the NHS. Thus, understanding the mechanisms that control reactivity to high-strength alcohol cues will have significant economic and societal impact.
Organisations
People |
ORCID iD |
| Eisuke Koya (Primary Supervisor) |
Studentship Projects
| Project Reference | Relationship | Related To | Start | End | Student Name |
|---|---|---|---|---|---|
| BB/T008768/1 | 30/09/2020 | 29/09/2028 | |||
| 2618520 | Studentship | BB/T008768/1 | 30/09/2021 | 29/09/2025 |