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?
| Authors | |
|---|---|
| Year of publication | 2017 |
| Type | Article in Periodical |
| Magazine / Source | Medical Hypotheses |
| MU Faculty or unit | |
| Citation | |
| Doi | http://dx.doi.org/10.1016/j.mehy.2016.11.015 |
| Keywords | ALCOHOL EXPOSURE; BRAIN; RAT; RECEPTORS; TRANSMISSION; CONSUMPTION; INSIGHTS; CELLS |
| Description | 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. |
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