Neurotoxicology and teratology
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This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal.
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Neurotoxicol Teratol · Sep 2019
Weekly ethanol exposure alters dopaminergic parameters in zebrafish brain.
Binge drinking is defined as the infrequent consumption of excessive doses of alcohol in a short period of time. Zebrafish is a reliable model to investigate ethanol consumption impact on the CNS, including reward signaling like dopaminergic neurotransmission system. The aim of this study was to evaluate zebrafish brain dopaminergic parameters after intermittent weekly ethanol exposure (WEE), which mimics binge drinking. ⋯ The MAO activity was decreased for WEE-2 and WEE-9 groups. The WEE-2 and WEE-9 groups presented an increase in brain dopamine levels, while noradrenaline levels were not affected. Therefore, dopaminergic parameters are still altered two and nine days after the last ethanol exposure in this binge experimental model, resulting in a modulatory event in this neurotransmission pathway.
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Neurotoxicol Teratol · Nov 2018
Prenatal tobacco and marijuana co-use: Impact on newborn neurobehavior.
Tobacco and marijuana are some of the most common prenatal substance exposures worldwide. The social acceptability and political landscape of marijuana and its potency have changed dramatically in the last two decades leading to increased use by pregnant women. Despite evidence for increasing marijuana use and high rates of co-use of tobacco (TOB) and marijuana (MJ) during pregnancy, the impact of prenatal exposure to each substance is typically studied in isolation. ⋯ Although results are preliminary, they highlight additional risk from dual exposure to MJ + TOB vs. TOB exposure alone, particularly for daughters. Results also highlight the critical importance of investigating prenatal exposures in concert and the need for intervention efforts to address MJ co-use in pregnant TOB users.
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Neurotoxicol Teratol · May 2017
Carbon monoxide incompletely prevents isoflurane-induced defects in murine neurodevelopment.
Commonly used anesthetics have been shown to disrupt neurodevelopment in preclinical models. It has been proposed that such anesthesia-induced neurotoxicity is mediated by apoptotic neurodegeneration in the immature brain. Low dose carbon monoxide (CO) exerts cytoprotective properties and we have previously demonstrated that CO inhibits isoflurane-induced apoptosis in the developing murine brain. Here we utilized anti-apoptotic concentrations of CO to delineate the role of apoptotic neurodegeneration in anesthesia-induced neurotoxicity by assessing the effect of CO on isoflurane-induced defects in neurodevelopment. ⋯ Anti-apoptotic concentrations of CO incompletely prevented isoflurane-induced defects in neurodevelopment, lacked concentration-dependent effects, and only provided protection in certain domains suggesting that anesthesia-related neurotoxicity is not solely mediated by activation of the mitochondrial apoptosis pathway.