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Long-lasting microbial dysbiosis and altered enteric neurotransmitters in adult rats following adolescent binge ethanol exposure.

ABSTRACT: Human alcoholism and ethanol exposure of adult mice cause acute microbial dysbiosis. Adolescent binge drinking is common, but the effect of adolescent ethanol exposure on the adult microbiome and enteric neurotransmitters has not been studied. In the current study, male Wistar rats received adolescent intermittent ethanol (AIE) treatment, and fecal samples were collected on postnatal day (P)54 and P95 for bacterial 16S rRNA amplicon sequencing. Cecal tissue was collected on P95 for analysis of innate immune and neurotransmitter marker expression. At the genus level, AIE treatment altered the relative abundance of several microbes, including decreased relative abundance of Dehalobacterium and CF231 (a member of the Paraprevotellaceae family) that persisted into adulthood. Across aging, the relative abundance of several microbes was altered in both control- and AIE-treated rats. At P95, AIE exposure was associated with increased cecal serotonin levels and reduced choline acetyltransferase gene expression. Taxonomic shifts at P54 and at P95 suggest that AIE causes both immediate and lasting microbial dysbiosis. The lasting microbial dysbiosis was accompanied by alterations of enteric neurotransmitters.

SUBMITTER: Vetreno RP

PROVIDER: S-EPMC7319904 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Long-lasting microbial dysbiosis and altered enteric neurotransmitters in adult rats following adolescent binge ethanol exposure.

Vetreno Ryan P RP Massey Veronica V Crews Fulton T FT

Addiction biology 20191227 1

Human alcoholism and ethanol exposure of adult mice cause acute microbial dysbiosis. Adolescent binge drinking is common, but the effect of adolescent ethanol exposure on the adult microbiome and enteric neurotransmitters has not been studied. In the current study, male Wistar rats received adolescent intermittent ethanol (AIE) treatment, and fecal samples were collected on postnatal day (P)54 and P95 for bacterial 16S rRNA amplicon sequencing. Cecal tissue was collected on P95 for analysis of i ...[more]

PMID: 31880056

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Project description:Heavy alcohol consumption followed by periods of abstinence (i.e., binge drinking) during adolescence is a concern for both acute and chronic health issues. Persistent brain damage after adolescent intermittent ethanol exposure in rodents, a model of binge drinking, includes reduced hippocampal neurogenesis and a loss of neurons in the basal forebrain that express the cholinergic phenotype. The circuit formed between those regions, the septohippocampal pathway, is critical for learning and memory. Furthermore, this circuit is also altered during the aging process. Thus, we examined whether pathology in septohippocampal circuit and impairments in spatial behaviors are amplified during aging following adolescent intermittent ethanol exposure. Female and male rats were exposed to intermittent intragastric gavage of water (control) or 20% ethanol (dose of 5 g/kg) for a 2 days on/off cycle from postnatal days 25-55. Either 2 (young adult) or 12-14 (middle-age) months post exposure, rats were tested on two spatial tasks: spontaneous alternation and novel object in place. Acetylcholine efflux was assessed in the hippocampus during both tasks. There was no adolescent ethanol-induced deficit on spontaneous alternation, but middle-aged male rats displayed lower alternation rates. Male rats exposed to ethanol during adolescence had blunted behavioral evoked acetylcholine during spontaneous alternation testing. All ethanol-exposed rats displayed suppression of the cholinergic neuronal phenotype. On the novel object in place task, regardless of sex, ethanol-exposed rats performed significantly worse than control-treated rats, and middle aged-rats, regardless of sex or ethanol exposure, were significantly impaired relative to young adult rats. These results indicate that male rats display earlier age-related cognitive impairment on a working memory task. Furthermore, male rats exposed to ethanol during adolescence have blunted behavior-evoked hippocampal acetylcholine efflux. In addition, middle-aged and ethanol-exposed rats, regardless of sex, are impaired at determining discrete spatial relationship between objects. This type of pattern separation impairment was associated with a loss of neurogenesis. Thus, binge-type adolescent ethanol exposure does affect the septohippocampal circuit, and can accelerate age-related cognitive impairment on select spatial tasks.

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Long-lasting microbial dysbiosis and altered enteric neurotransmitters in adult rats following adolescent binge ethanol exposure.

Publications

Long-lasting microbial dysbiosis and altered enteric neurotransmitters in adult rats following adolescent binge ethanol exposure.

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