Pre- and postnatal exposure to moderate levels of ethanol can have long-lasting effects on hippocampal glutamate uptake in adolescent offspring
The developing brain is vulnerable to the effects of ethanol. Glutamate is the main mediator of excitatory signals in the brain and is probably involved in most aspects of normal brain function during development. The aim of this study was to investigate vulnerability to and the impact of ethanol to...
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| description | The developing brain is vulnerable to the effects of ethanol. Glutamate is the main mediator of excitatory signals in the brain and is probably involved in most aspects of normal brain function during development. The aim of this study was to investigate vulnerability to and the impact of ethanol toxicity on glutamate uptake signaling in adolescent rats after moderate pre and postnatal ethanol exposure. Pregnant female rats were divided into three groups and treated only with water (control), non-alcoholic beer (vehicle) or 10% (v/v) beer solution (moderate prenatal alcohol exposure-MPAE). Thirty days after birth, adolescent male offspring were submitted to hippocampal acute slice procedure. We assayed glutamate uptake and measured glutathione content and also quantified glial glutamate transporters (EAAT 1 and EAAT 2). The glutamate system vulnerability was tested with different acute ethanol doses in naïve rats and compared with the MPAE group. We also performed a (lipopolysaccharide-challenge (LPS-challenge) with all groups to test the glutamate uptake response after an insult. The MPAE group presented a decrease in glutamate uptake corroborating a decrease in glutathione (GSH) content. The reduction in GSH content suggests oxidative damage after acute ethanol exposure. The glial glutamate transporters were also altered after prenatal ethanol treatment, suggesting a disturbance in glutamate signaling. This study indicates that impairment of glutamate uptake can be dose-dependent and the glutamate system has a higher vulnerability to ethanol toxicity after moderate ethanol exposure In utero. The effects of pre- and postnatal ethanol exposure can have long-lasting impacts on the glutamate system in adolescence and potentially into adulthood. |
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Glutamate is the main mediator of excitatory signals in the brain and is probably involved in most aspects of normal brain function during development. The aim of this study was to investigate vulnerability to and the impact of ethanol toxicity on glutamate uptake signaling in adolescent rats after moderate pre and postnatal ethanol exposure. Pregnant female rats were divided into three groups and treated only with water (control), non-alcoholic beer (vehicle) or 10% (v/v) beer solution (moderate prenatal alcohol exposure-MPAE). Thirty days after birth, adolescent male offspring were submitted to hippocampal acute slice procedure. We assayed glutamate uptake and measured glutathione content and also quantified glial glutamate transporters (EAAT 1 and EAAT 2). The glutamate system vulnerability was tested with different acute ethanol doses in naïve rats and compared with the MPAE group. We also performed a (lipopolysaccharide-challenge (LPS-challenge) with all groups to test the glutamate uptake response after an insult. The MPAE group presented a decrease in glutamate uptake corroborating a decrease in glutathione (GSH) content. The reduction in GSH content suggests oxidative damage after acute ethanol exposure. The glial glutamate transporters were also altered after prenatal ethanol treatment, suggesting a disturbance in glutamate signaling. This study indicates that impairment of glutamate uptake can be dose-dependent and the glutamate system has a higher vulnerability to ethanol toxicity after moderate ethanol exposure In utero. The effects of pre- and postnatal ethanol exposure can have long-lasting impacts on the glutamate system in adolescence and potentially into adulthood.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0127845</identifier><identifier>PMID: 25978644</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adolescents ; Alcoholic beverages ; Alcoholism ; Animal behavior ; Animals ; Beer ; Biochemistry ; Brain ; Cell adhesion & migration ; Ethanol ; Ethanol - adverse effects ; Excitatory amino acid transporters ; Exposure ; Female ; Glutamate ; Glutamic Acid - metabolism ; Glutathione ; Glutathione - metabolism ; Health aspects ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - metabolism ; Intrauterine exposure ; Lipopolysaccharides ; Male ; Nervous system ; Neurosciences ; Offspring ; Oxidative stress ; Pregnancy ; Pregnant women ; Prenatal experience ; Prenatal Exposure Delayed Effects - chemically induced ; Prenatal Exposure Delayed Effects - metabolism ; Progeny ; Rats ; Rodents ; Science ; Signaling ; Teenagers ; Toxicity ; Water treatment</subject><ispartof>PloS one, 2015-05, Vol.10 (5), p.e0127845</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Brolese et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Brolese et al 2015 Brolese et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-aec419018ae45b84749284d57131b6642809d8b63e8803df0c22c7e5f9217cd23</citedby><cites>FETCH-LOGICAL-c758t-aec419018ae45b84749284d57131b6642809d8b63e8803df0c22c7e5f9217cd23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4433332/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4433332/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,2098,2917,23853,27911,27912,53778,53780,79355,79356</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25978644$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Homberg, Judith</contributor><creatorcontrib>Brolese, Giovana</creatorcontrib><creatorcontrib>Lunardi, Paula</creatorcontrib><creatorcontrib>de Souza, Daniela F</creatorcontrib><creatorcontrib>Lopes, Fernanda M</creatorcontrib><creatorcontrib>Leite, Marina C</creatorcontrib><creatorcontrib>Gonçalves, Carlos-Alberto</creatorcontrib><title>Pre- and postnatal exposure to moderate levels of ethanol can have long-lasting effects on hippocampal glutamate uptake in adolescent offspring</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The developing brain is vulnerable to the effects of ethanol. 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The effects of pre- and postnatal ethanol exposure can have long-lasting impacts on the glutamate system in adolescence and potentially into adulthood.</description><subject>Adolescents</subject><subject>Alcoholic beverages</subject><subject>Alcoholism</subject><subject>Animal behavior</subject><subject>Animals</subject><subject>Beer</subject><subject>Biochemistry</subject><subject>Brain</subject><subject>Cell adhesion & migration</subject><subject>Ethanol</subject><subject>Ethanol - adverse effects</subject><subject>Excitatory amino acid transporters</subject><subject>Exposure</subject><subject>Female</subject><subject>Glutamate</subject><subject>Glutamic Acid - metabolism</subject><subject>Glutathione</subject><subject>Glutathione - metabolism</subject><subject>Health aspects</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Intrauterine exposure</subject><subject>Lipopolysaccharides</subject><subject>Male</subject><subject>Nervous system</subject><subject>Neurosciences</subject><subject>Offspring</subject><subject>Oxidative stress</subject><subject>Pregnancy</subject><subject>Pregnant women</subject><subject>Prenatal experience</subject><subject>Prenatal Exposure Delayed Effects - 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Glutamate is the main mediator of excitatory signals in the brain and is probably involved in most aspects of normal brain function during development. The aim of this study was to investigate vulnerability to and the impact of ethanol toxicity on glutamate uptake signaling in adolescent rats after moderate pre and postnatal ethanol exposure. Pregnant female rats were divided into three groups and treated only with water (control), non-alcoholic beer (vehicle) or 10% (v/v) beer solution (moderate prenatal alcohol exposure-MPAE). Thirty days after birth, adolescent male offspring were submitted to hippocampal acute slice procedure. We assayed glutamate uptake and measured glutathione content and also quantified glial glutamate transporters (EAAT 1 and EAAT 2). The glutamate system vulnerability was tested with different acute ethanol doses in naïve rats and compared with the MPAE group. We also performed a (lipopolysaccharide-challenge (LPS-challenge) with all groups to test the glutamate uptake response after an insult. The MPAE group presented a decrease in glutamate uptake corroborating a decrease in glutathione (GSH) content. The reduction in GSH content suggests oxidative damage after acute ethanol exposure. The glial glutamate transporters were also altered after prenatal ethanol treatment, suggesting a disturbance in glutamate signaling. This study indicates that impairment of glutamate uptake can be dose-dependent and the glutamate system has a higher vulnerability to ethanol toxicity after moderate ethanol exposure In utero. The effects of pre- and postnatal ethanol exposure can have long-lasting impacts on the glutamate system in adolescence and potentially into adulthood.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25978644</pmid><doi>10.1371/journal.pone.0127845</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescents Alcoholic beverages Alcoholism Animal behavior Animals Beer Biochemistry Brain Cell adhesion & migration Ethanol Ethanol - adverse effects Excitatory amino acid transporters Exposure Female Glutamate Glutamic Acid - metabolism Glutathione Glutathione - metabolism Health aspects Hippocampus Hippocampus - drug effects Hippocampus - metabolism Intrauterine exposure Lipopolysaccharides Male Nervous system Neurosciences Offspring Oxidative stress Pregnancy Pregnant women Prenatal experience Prenatal Exposure Delayed Effects - chemically induced Prenatal Exposure Delayed Effects - metabolism Progeny Rats Rodents Science Signaling Teenagers Toxicity Water treatment |
| title | Pre- and postnatal exposure to moderate levels of ethanol can have long-lasting effects on hippocampal glutamate uptake in adolescent offspring |
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