Impacts of early exposure to ethanol on adenosine functioning in zebrafish

Abstract

AbstractExposure to ethanol at the beginning of development can impact the formation of the Nervous System. The set of symptoms resulting from ethanol consumption during pregnancy is called FASD (Fetal Alcohol Spectrum Disorders) and ranges from cognitive alterations to the most severe form called FAS (Fetal Alcohol Syndrome). The effect caused by ethanol on the formation of brain architecture directly affects the adenosine neuromodulation system. In this work, a single exposure regimen of 24 to 26 hpf to 1% ethanol transdermally was used as a model to assess adenosine signaling in the context of seizure susceptibility in zebrafish larvae and adults. To test sensitivity, a 2.5 mM subconvulsant dose of pentylenetetrazole (PTZ) was used, which was not able to increase seizure events in larvae or adults exposed to ethanol during embryonic phase. However, the duration of stage I was increased and the latency to reach stage II was decreased in larvae, showing a possible proconvulsant profile in these ethanol-treated animals. Also, the exposure of larvae to CPA (75 μM) was able to reverse the effect of embryonic ethanol treatment on the latency to reach stage II of seizure. Adenosine and ecto-5’-nucleotidase receptor mRNA expression did not show significant difference in both developmental stages. These results demonstrated that even a short and specific exposure to ethanol can promote, even if mild, effects on neuronal modulation, increasing susceptibility to seizures.