Could ethanol-induced alterations in the expression of glutamate transporters in testes contribute to the effect of paternal drinking on the risk of abnormalities in the offspring?

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• 作者：Mohammed Abul Kashem^a ; ^{abul.kashem@sydney.edu.au} ; Aven Lee^b ; ^{aven.lee@uq.edu.au} ; David V. Pow^b ; ^c ; ^{d.pow@uq.edu.au} ; Omar &Scaron ; erý ; ^d ; ^e ; ^{omarsery@sci.muni.cz} ; Vladimir J. Balcar^a ; ^{vibar@anatomy.usyd.edu.au}
• 关键词：ADHD ; attention deficit hyperactivity disorder ; CpG ; cytosine and guanine separated by phosphate (the target of DNA methyltransferases) ; DAT ; dopamine transporter ; EAAT ; excitatory amino acid transporter ; FASD ; Foetal Alcohol Spectrum Disorder ; GABA ; γ-aminobutyric acid ; GLAST ; glutamate and aspartate transporter ; GLT ; glutamate transporter ; SLC ; solute carrier family of membrane transporter proteins
• 刊名：Medical Hypotheses
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：98
• 期：Complete
• 页码：57-59
• 全文大小：228 K
• 卷排序：98

文摘

It has been known that a preconception paternal alcoholism impacts adversely on the offspring but the mechanism of the effect is uncertain. Several findings suggest that there are signalling systems in testis that are analogous to those known to be altered by alcoholism in brain. We propose that chronic alcohol affects these systems in a manner similar to that in brain. Specifically, we hypothesise that excessive alcohol may disturb glutamatergic-like signalling in testis by increasing expression of the glutamate transporter GLAST (EAAT1). We discuss ways how to test the hypothesis as well as potential significance of some of the tests as tools in the diagnostics of chronic alcoholism.