Neurotoxicology and teratology
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Neurotoxicol Teratol · Mar 2017
ReviewReview of preclinical studies on pediatric general anesthesia-induced developmental neurotoxicity.
Thousands of infants and children undergo complicated surgical procedures that require prolonged periods of anesthesia and/or sedation each year. A growing body of preclinical research suggests pediatric anesthetics are harmful to the developing brain; yet, the extent to which these effects generalize to the clinical setting remains unclear. ⋯ The purpose of this paper is to provide a review of the preclinical literature examining the effects of general anesthesia on brain and behavioral development. This paper will detail the effects of different anesthetic agents on various indices of neurotoxicity and functional outcomes as well as provide a review of potential protective compounds and suggestions for areas of future research.
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Neurotoxicol Teratol · Mar 2017
ReviewAnesthetic neurotoxicity: Apoptosis and autophagic cell death mediated by calcium dysregulation.
A number of findings suggested that general anesthetics induced neural cell death by apoptosis in various animal models. Although clinical evidence regarding the correlation between anesthetic exposures at young age and subsequent cognitive impairments remains unclear, repeated or consistent exposures to general anesthetics may be a potential harmful risk in developing human brains. The mechanisms underlying the anesthetic neurotoxicity have received extensive attention recently. We will attempt a brief review to summarize current understanding on the role of both apoptosis and autophagic cell death mediated by calcium dysregulation in anesthetic neurotoxicity.
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Neurotoxicol Teratol · Nov 2015
Visual evoked potential latencies of three-year-old children prenatally exposed to buprenorphine or methadone compared with non-opioid exposed children: The results of a longitudinal study.
This study compared the latency of pattern reversal visual evoked potentials (VEP) of 36-month old children exposed to opioid pharmacotherapy in utero to that of a group of non-exposed children. Pregnant women were enrolled as part of an open-label non-randomised flexible dosing longitudinal study. Participants were 21 children whose mothers were treated with buprenorphine- (n=11) or methadone-pharmacotherapy (n=10) during pregnancy, and 15 children not exposed to opioids in pregnancy. ⋯ Nor were there any significant differences in VEP latencies between children prenatally exposed to methadone and children prenatally exposed to buprenorphine. Head circumference (HC) was significantly associated with P100 latencies for both check sizes. Data from this controlled, non-randomised study suggest that neither buprenorphine nor methadone appear to have any long-term effects on visual maturity assessed at 36months of age.
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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.
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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.