Premium
The Effect of Chronic Ethanol Exposure and Thiamine Deficiency on Myelin‐related Genes in the Cortex and the Cerebellum
Author(s) -
Chatterton Bradley J.,
Nunes Polliana T.,
Savage Lisa M.
Publication year - 2020
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.14484
Subject(s) - myelin , thiamine , cerebellum , wernicke encephalopathy , cortex (anatomy) , medicine , endocrinology , biology , neuroscience , chemistry , central nervous system
Background Long‐term alcohol consumption has been linked to structural and functional brain abnormalities. Furthermore, with persistent exposure to ethanol (EtOH), nutrient deficiencies often develop. Thiamine deficiency is a key contributor to alcohol‐related brain damage and is suspected to contribute to white matter pathology. The expression of genes encoding myelin proteins in several cortical brain regions is altered with EtOH exposure. However, there is limited research regarding the impact of thiamine deficiency on myelin dysfunction. Methods A rat model was used to assess the impact of moderate chronic EtOH exposure (CET; 20% EtOH in drinking water for 1 or 6 months), pyrithiamine‐induced thiamine deficiency treatment (PTD), both conditions combined (CET‐PTD), or CET with thiamine injections (CET + T) on myelin‐related gene expression (Olig1, Olig2, MBP, MAG, and MOG) in the frontal and parietal cortices and the cerebellum. Results The CET‐PTD treatments caused the greatest suppression in myelin‐related genes in the cortex. Specifically, the parietal cortex was the region that was most susceptible to PTD‐CET‐induced alterations in myelin‐related genes. In addition, PTD treatment, with and without CET, caused minor fluctuations in the expression of several myelin‐related genes in the frontal cortex. In contrast, CET alone and PTD alone suppressed several myelin‐related genes in the cerebellum. Regardless of the region, there was significant recovery of myelin‐related genes with extended abstinence and/or thiamine restoration. Conclusion Moderate chronic EtOH alone had a minor effect on the suppression of myelin‐related genes in the cortex; however, when combined with thiamine deficiency, the reduction was amplified. There was a suppression of myelin‐related genes following long‐term EtOH and thiamine deficiency in the cerebellum. However, the suppression in the myelin‐related genes mostly occurred 24 h after EtOH removal or following thiamine restoration; within 3 weeks of abstinence or thiamine recovery, gene expression rebounded.