Proteomic Analysis Demonstrates Adolescent Vulnerability to Lasting Hippocampal Changes Following Chronic Alcohol Consumption

Background:  Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present study was to assess whether chronic intermittent alcohol intake during the adolescent period alters hippocampal protein express...

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Published inAlcoholism, clinical and experimental research Vol. 33; no. 1; pp. 86 - 94
Main Authors Hargreaves, Garth A., Quinn, Heidi, Kashem, Mohammed A., Matsumoto, Izuru, McGregor, Iain S.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.01.2009
Wiley
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Abstract Background:  Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present study was to assess whether chronic intermittent alcohol intake during the adolescent period alters hippocampal protein expression to a greater extent than during adulthood. Methods:  Adolescent [postnatal day (PND) 27] and adult (PND 55) male Wistar rats were given 8 hours daily access to beer (4.44% ethanol v/v) in addition to ad libitum food and water for 4 weeks. From a large subject pool, subgroups of adolescent and adult rats were selected that displayed equivalent alcohol intake (average of 6.1 g/kg/day ethanol). The 4 weeks of alcohol access were followed by a 2‐week alcohol‐free washout period after which the hippocampus was analyzed using 2‐DE proteomics. Results:  Beer consumption by the adult group resulted in modest hippocampal changes relative to alcohol naïve adult controls. The only changes observed were an up‐regulation of citrate synthase (a precursor to the Krebs cycle) and fatty acid binding protein (which facilitates fatty acid metabolism). In contrast, adolescent rats consuming alcohol showed more widespread hippocampal changes relative to adolescent controls. These included an increase in cytoskeletal protein T‐complex protein 1 subunit epsilon (TCP‐1) and a decrease in the expression of 10 other proteins, including glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH), triose phosphate isomerise, alpha‐enolase, and phosphoglycerate kinase 1 (all involved in glycolysis); glutamate dehydrogenase 1 (an important regulator of glutamate); methylmalonate‐semialdehyde dehydrogenase (involved in aldehyde detoxification); ubiquitin carboxyl‐terminal hydrolase isozyme L1 (a regulator of protein degradation); and synapsin 2 (involved in synaptogenesis and neurotransmitter release). Conclusions:  These results suggest the adolescent hippocampus is more vulnerable to lasting proteomic changes following repeated alcohol exposure. The proteins most affected include those related to glycolysis, glutamate metabolism, neurodegeneration, synaptic function, and cytoskeletal structure.
AbstractList Background:  Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present study was to assess whether chronic intermittent alcohol intake during the adolescent period alters hippocampal protein expression to a greater extent than during adulthood. Methods:  Adolescent [postnatal day (PND) 27] and adult (PND 55) male Wistar rats were given 8 hours daily access to beer (4.44% ethanol v/v) in addition to ad libitum food and water for 4 weeks. From a large subject pool, subgroups of adolescent and adult rats were selected that displayed equivalent alcohol intake (average of 6.1 g/kg/day ethanol). The 4 weeks of alcohol access were followed by a 2‐week alcohol‐free washout period after which the hippocampus was analyzed using 2‐DE proteomics. Results:  Beer consumption by the adult group resulted in modest hippocampal changes relative to alcohol naïve adult controls. The only changes observed were an up‐regulation of citrate synthase (a precursor to the Krebs cycle) and fatty acid binding protein (which facilitates fatty acid metabolism). In contrast, adolescent rats consuming alcohol showed more widespread hippocampal changes relative to adolescent controls. These included an increase in cytoskeletal protein T‐complex protein 1 subunit epsilon (TCP‐1) and a decrease in the expression of 10 other proteins, including glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH), triose phosphate isomerise, alpha‐enolase, and phosphoglycerate kinase 1 (all involved in glycolysis); glutamate dehydrogenase 1 (an important regulator of glutamate); methylmalonate‐semialdehyde dehydrogenase (involved in aldehyde detoxification); ubiquitin carboxyl‐terminal hydrolase isozyme L1 (a regulator of protein degradation); and synapsin 2 (involved in synaptogenesis and neurotransmitter release). Conclusions:  These results suggest the adolescent hippocampus is more vulnerable to lasting proteomic changes following repeated alcohol exposure. The proteins most affected include those related to glycolysis, glutamate metabolism, neurodegeneration, synaptic function, and cytoskeletal structure.
Background:Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present study was to assess whether chronic intermittent alcohol intake during the adolescent period alters hippocampal protein expression to a greater extent than during adulthood.Methods:Adolescent [postnatal day (PND) 27] and adult (PND 55) male Wistar rats were given 8hours daily access to beer (4.44% ethanol v/v) in addition to ad libitum food and water for 4weeks. From a large subject pool, subgroups of adolescent and adult rats were selected that displayed equivalent alcohol intake (average of 6.1g/kg/day ethanol). The 4weeks of alcohol access were followed by a 2-week alcohol-free washout period after which the hippocampus was analyzed using 2-DE proteomics.Results:Beer consumption by the adult group resulted in modest hippocampal changes relative to alcohol naive adult controls. The only changes observed were an up-regulation of citrate synthase (a precursor to the Krebs cycle) and fatty acid binding protein (which facilitates fatty acid metabolism). In contrast, adolescent rats consuming alcohol showed more widespread hippocampal changes relative to adolescent controls. These included an increase in cytoskeletal protein T-complex protein 1 subunit epsilon (TCP-1) and a decrease in the expression of 10 other proteins, including glyceraldehyde-3-phosphate dehydrogenase (GAPDH), triose phosphate isomerise, alpha-enolase, and phosphoglycerate kinase 1 (all involved in glycolysis); glutamate dehydrogenase 1 (an important regulator of glutamate); methylmalonate-semialdehyde dehydrogenase (involved in aldehyde detoxification); ubiquitin carboxyl-terminal hydrolase isozyme L1 (a regulator of protein degradation); and synapsin 2 (involved in synaptogenesis and neurotransmitter release).Conclusions:These results suggest the adolescent hippocampus is more vulnerable to lasting proteomic changes following repeated alcohol exposure. The proteins most affected include those related to glycolysis, glutamate metabolism, neurodegeneration, synaptic function, and cytoskeletal structure.
Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present study was to assess whether chronic intermittent alcohol intake during the adolescent period alters hippocampal protein expression to a greater extent than during adulthood. Adolescent [postnatal day (PND) 27] and adult (PND 55) male Wistar rats were given 8 hours daily access to beer (4.44% ethanol v/v) in addition to ad libitum food and water for 4 weeks. From a large subject pool, subgroups of adolescent and adult rats were selected that displayed equivalent alcohol intake (average of 6.1 g/kg/day ethanol). The 4 weeks of alcohol access were followed by a 2-week alcohol-free washout period after which the hippocampus was analyzed using 2-DE proteomics. Beer consumption by the adult group resulted in modest hippocampal changes relative to alcohol naïve adult controls. The only changes observed were an up-regulation of citrate synthase (a precursor to the Krebs cycle) and fatty acid binding protein (which facilitates fatty acid metabolism). In contrast, adolescent rats consuming alcohol showed more widespread hippocampal changes relative to adolescent controls. These included an increase in cytoskeletal protein T-complex protein 1 subunit epsilon (TCP-1) and a decrease in the expression of 10 other proteins, including glyceraldehyde-3-phosphate dehydrogenase (GAPDH), triose phosphate isomerise, alpha-enolase, and phosphoglycerate kinase 1 (all involved in glycolysis); glutamate dehydrogenase 1 (an important regulator of glutamate); methylmalonate-semialdehyde dehydrogenase (involved in aldehyde detoxification); ubiquitin carboxyl-terminal hydrolase isozyme L1 (a regulator of protein degradation); and synapsin 2 (involved in synaptogenesis and neurotransmitter release). These results suggest the adolescent hippocampus is more vulnerable to lasting proteomic changes following repeated alcohol exposure. The proteins most affected include those related to glycolysis, glutamate metabolism, neurodegeneration, synaptic function, and cytoskeletal structure.
Background:  Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present study was to assess whether chronic intermittent alcohol intake during the adolescent period alters hippocampal protein expression to a greater extent than during adulthood. Methods:  Adolescent [postnatal day (PND) 27] and adult (PND 55) male Wistar rats were given 8 hours daily access to beer (4.44% ethanol v/v) in addition to ad libitum food and water for 4 weeks. From a large subject pool, subgroups of adolescent and adult rats were selected that displayed equivalent alcohol intake (average of 6.1 g/kg/day ethanol). The 4 weeks of alcohol access were followed by a 2‐week alcohol‐free washout period after which the hippocampus was analyzed using 2‐DE proteomics. Results:  Beer consumption by the adult group resulted in modest hippocampal changes relative to alcohol naïve adult controls. The only changes observed were an up‐regulation of citrate synthase (a precursor to the Krebs cycle) and fatty acid binding protein (which facilitates fatty acid metabolism). In contrast, adolescent rats consuming alcohol showed more widespread hippocampal changes relative to adolescent controls. These included an increase in cytoskeletal protein T‐complex protein 1 subunit epsilon (TCP‐1) and a decrease in the expression of 10 other proteins, including glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH), triose phosphate isomerise, alpha‐enolase, and phosphoglycerate kinase 1 (all involved in glycolysis); glutamate dehydrogenase 1 (an important regulator of glutamate); methylmalonate‐semialdehyde dehydrogenase (involved in aldehyde detoxification); ubiquitin carboxyl‐terminal hydrolase isozyme L1 (a regulator of protein degradation); and synapsin 2 (involved in synaptogenesis and neurotransmitter release). Conclusions:  These results suggest the adolescent hippocampus is more vulnerable to lasting proteomic changes following repeated alcohol exposure. The proteins most affected include those related to glycolysis, glutamate metabolism, neurodegeneration, synaptic function, and cytoskeletal structure.
Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present study was to assess whether chronic intermittent alcohol intake during the adolescent period alters hippocampal protein expression to a greater extent than during adulthood.BACKGROUNDExcessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present study was to assess whether chronic intermittent alcohol intake during the adolescent period alters hippocampal protein expression to a greater extent than during adulthood.Adolescent [postnatal day (PND) 27] and adult (PND 55) male Wistar rats were given 8 hours daily access to beer (4.44% ethanol v/v) in addition to ad libitum food and water for 4 weeks. From a large subject pool, subgroups of adolescent and adult rats were selected that displayed equivalent alcohol intake (average of 6.1 g/kg/day ethanol). The 4 weeks of alcohol access were followed by a 2-week alcohol-free washout period after which the hippocampus was analyzed using 2-DE proteomics.METHODSAdolescent [postnatal day (PND) 27] and adult (PND 55) male Wistar rats were given 8 hours daily access to beer (4.44% ethanol v/v) in addition to ad libitum food and water for 4 weeks. From a large subject pool, subgroups of adolescent and adult rats were selected that displayed equivalent alcohol intake (average of 6.1 g/kg/day ethanol). The 4 weeks of alcohol access were followed by a 2-week alcohol-free washout period after which the hippocampus was analyzed using 2-DE proteomics.Beer consumption by the adult group resulted in modest hippocampal changes relative to alcohol naïve adult controls. The only changes observed were an up-regulation of citrate synthase (a precursor to the Krebs cycle) and fatty acid binding protein (which facilitates fatty acid metabolism). In contrast, adolescent rats consuming alcohol showed more widespread hippocampal changes relative to adolescent controls. These included an increase in cytoskeletal protein T-complex protein 1 subunit epsilon (TCP-1) and a decrease in the expression of 10 other proteins, including glyceraldehyde-3-phosphate dehydrogenase (GAPDH), triose phosphate isomerise, alpha-enolase, and phosphoglycerate kinase 1 (all involved in glycolysis); glutamate dehydrogenase 1 (an important regulator of glutamate); methylmalonate-semialdehyde dehydrogenase (involved in aldehyde detoxification); ubiquitin carboxyl-terminal hydrolase isozyme L1 (a regulator of protein degradation); and synapsin 2 (involved in synaptogenesis and neurotransmitter release).RESULTSBeer consumption by the adult group resulted in modest hippocampal changes relative to alcohol naïve adult controls. The only changes observed were an up-regulation of citrate synthase (a precursor to the Krebs cycle) and fatty acid binding protein (which facilitates fatty acid metabolism). In contrast, adolescent rats consuming alcohol showed more widespread hippocampal changes relative to adolescent controls. These included an increase in cytoskeletal protein T-complex protein 1 subunit epsilon (TCP-1) and a decrease in the expression of 10 other proteins, including glyceraldehyde-3-phosphate dehydrogenase (GAPDH), triose phosphate isomerise, alpha-enolase, and phosphoglycerate kinase 1 (all involved in glycolysis); glutamate dehydrogenase 1 (an important regulator of glutamate); methylmalonate-semialdehyde dehydrogenase (involved in aldehyde detoxification); ubiquitin carboxyl-terminal hydrolase isozyme L1 (a regulator of protein degradation); and synapsin 2 (involved in synaptogenesis and neurotransmitter release).These results suggest the adolescent hippocampus is more vulnerable to lasting proteomic changes following repeated alcohol exposure. The proteins most affected include those related to glycolysis, glutamate metabolism, neurodegeneration, synaptic function, and cytoskeletal structure.CONCLUSIONSThese results suggest the adolescent hippocampus is more vulnerable to lasting proteomic changes following repeated alcohol exposure. The proteins most affected include those related to glycolysis, glutamate metabolism, neurodegeneration, synaptic function, and cytoskeletal structure.
Author Hargreaves, Garth A.
Matsumoto, Izuru
McGregor, Iain S.
Kashem, Mohammed A.
Quinn, Heidi
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  surname: Quinn
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  organization: From the School of Psychology (GAH, HQ, MAK, ISM), The University of Sydney, and Department of Pathology (IM), The University of Sydney, New South Wales, Australia
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  givenname: Mohammed A.
  surname: Kashem
  fullname: Kashem, Mohammed A.
  organization: From the School of Psychology (GAH, HQ, MAK, ISM), The University of Sydney, and Department of Pathology (IM), The University of Sydney, New South Wales, Australia
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  givenname: Izuru
  surname: Matsumoto
  fullname: Matsumoto, Izuru
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  givenname: Iain S.
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  fullname: McGregor, Iain S.
  organization: From the School of Psychology (GAH, HQ, MAK, ISM), The University of Sydney, and Department of Pathology (IM), The University of Sydney, New South Wales, Australia
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Issue 1
Keywords Human
Consumption
Ethanol
Rat
Rodentia
Central nervous system
Proteome
Alcohol
Vulnerability
Encephalon
Alcoholic beverage
Vertebrata
Chronic
Mammalia
Animal
Adolescent
Proteomics
Glycolysis
Hippocampus
Proteome. Wistar Rat
Language English
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PublicationTitle Alcoholism, clinical and experimental research
PublicationTitleAlternate Alcohol Clin Exp Res
PublicationYear 2009
Publisher Blackwell Publishing Ltd
Wiley
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2006; 30
2006; 31
2004; 29
2002; 111
2004; 24
2004; 4
2007a; 1
2005; 21
2008; 5
2008; 32
2008; 33
2007; 31
2006; 137
1996; 35
2005; 29
1998; 350
2003; 12
2007; 29
2007; 855
1997; 94
1995a; 19
1976; 72
2007; 7
2000; 120
2006; 126
1993; 259
2008; 154
1990; 297
1995b; 19
2007b; 31
1996; 20
2003; 165
2001; 10
1998; 28
2006a; 40
2000; 157
1997; 21
2006; 11
2000; 24
1986; 15
2007
1999; 65
2006; 6
1999; 4
2002; 81
2007; 50
2000; 275
2004
2007; 51
1992; 31
2001; 66
2003; 71
1998; 22
2003; 77
2006; 312
2001; 392
1993; 17
2000; 37
2005; 289
2004; 14
2005; 5
2005; 7
2003; 27
2007; 86
2007; 42
2006b; 83
1998; 5
2004; 117
1987; 28
2003; 100
2006; 103
2003; 22
2005; 58
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Snippet Background:  Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim...
Background:  Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim...
Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of the present...
Background:Excessive teenage alcohol consumption is of great concern because alcohol may adversely alter the developmental trajectory of the brain. The aim of...
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StartPage 86
SubjectTerms Aging - drug effects
Aging - metabolism
Aging - pathology
Alcohol
Alcohol Drinking - metabolism
Alcohol Drinking - pathology
Alcohol Drinking - physiopathology
Alcoholism and acute alcohol poisoning
Animals
Biological and medical sciences
Brain Chemistry - drug effects
Brain Chemistry - physiology
Disease Susceptibility - chemically induced
Disease Susceptibility - metabolism
Disease Susceptibility - physiopathology
Glycolysis
Hippocampus
Hippocampus - chemistry
Hippocampus - drug effects
Hippocampus - physiopathology
Male
Medical sciences
Proteome
Proteomics - methods
Rats
Rats, Wistar
Toxicology
Wistar Rat
Title Proteomic Analysis Demonstrates Adolescent Vulnerability to Lasting Hippocampal Changes Following Chronic Alcohol Consumption
URI https://api.istex.fr/ark:/67375/WNG-P0CZZGT0-2/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1530-0277.2008.00814.x
https://www.ncbi.nlm.nih.gov/pubmed/18945221
https://www.proquest.com/docview/20286210
https://www.proquest.com/docview/66803817
Volume 33
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