Next Article in Journal
Wingless/Wnt Signaling in Intestinal Development, Homeostasis, Regeneration and Tumorigenesis: A Drosophila Perspective
Next Article in Special Issue
The Impact of Two Different Cold-Extruded Feeds and Feeding Regimens on Zebrafish Survival, Growth and Reproductive Performance
Previous Article in Journal / Special Issue
Imaging Neuronal Activity in the Optic Tectum of Late Stage Larval Zebrafish
Article Menu

Export Article

Open AccessArticle
J. Dev. Biol. 2018, 6(1), 7;

Ethanol Exposure Causes Muscle Degeneration in Zebrafish

School of Biology and Ecology, University of Maine, Orono, ME 04469, USA
Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, ME 04469, USA
Author to whom correspondence should be addressed.
Received: 12 January 2018 / Revised: 5 March 2018 / Accepted: 8 March 2018 / Published: 9 March 2018
(This article belongs to the Special Issue Zebrafish - A Model System for Developmental Biology Study)
Full-Text   |   PDF [5683 KB, uploaded 9 March 2018]   |  


Alcoholic myopathies are characterized by neuromusculoskeletal symptoms such as compromised movement and weakness. Although these symptoms have been attributed to neurological damage, EtOH may also target skeletal muscle. EtOH exposure during zebrafish primary muscle development or adulthood results in smaller muscle fibers. However, the effects of EtOH exposure on skeletal muscle during the growth period that follows primary muscle development are not well understood. We determined the effects of EtOH exposure on muscle during this phase of development. Strikingly, muscle fibers at this stage are acutely sensitive to EtOH treatment: EtOH induces muscle degeneration. The severity of EtOH-induced muscle damage varies but muscle becomes more refractory to EtOH as muscle develops. NF-kB induction in muscle indicates that EtOH triggers a pro-inflammatory response. EtOH-induced muscle damage is p53-independent. Uptake of Evans blue dye shows that EtOH treatment causes sarcolemmal instability before muscle fiber detachment. Dystrophin-null sapje mutant zebrafish also exhibit sarcolemmal instability. We tested whether Trichostatin A (TSA), which reduces muscle degeneration in sapje mutants, would affect EtOH-treated zebrafish. We found that TSA and EtOH are a lethal combination. EtOH does, however, exacerbate muscle degeneration in sapje mutants. EtOH also disrupts adhesion of muscle fibers to their extracellular matrix at the myotendinous junction: some detached muscle fibers retain beta-Dystroglycan indicating failure of muscle end attachments. Overexpression of Paxillin, which reduces muscle degeneration in zebrafish deficient for beta-Dystroglycan, is not sufficient to rescue degeneration. Taken together, our results suggest that EtOH exposure has pleiotropic deleterious effects on skeletal muscle. View Full-Text
Keywords: zebrafish; muscle; ethanol; alcohol; myopathy; fetal alcohol spectrum disorder; muscular dystrophy; Paxillin zebrafish; muscle; ethanol; alcohol; myopathy; fetal alcohol spectrum disorder; muscular dystrophy; Paxillin

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Supplementary material


Share & Cite This Article

MDPI and ACS Style

Coffey, E.C.; Pasquarella, M.E.; Goody, M.F.; Henry, C.A. Ethanol Exposure Causes Muscle Degeneration in Zebrafish. J. Dev. Biol. 2018, 6, 7.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
J. Dev. Biol. EISSN 2221-3759 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top