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 in | Alcoholism, clinical and experimental research Vol. 33; no. 1; pp. 86 - 94 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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. |
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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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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 |
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Medina KL, McQueeny T, Nagel BJ, Hanson KL, Schweinsburg AD, Tapert SF (2008) Prefrontal cortex volu 2002; 59 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 e_1_2_7_5_1 e_1_2_7_3_1 e_1_2_7_9_1 e_1_2_7_7_1 e_1_2_7_19_1 e_1_2_7_60_1 e_1_2_7_83_1 e_1_2_7_17_1 e_1_2_7_62_1 e_1_2_7_81_1 e_1_2_7_15_1 e_1_2_7_41_1 e_1_2_7_64_1 e_1_2_7_13_1 e_1_2_7_43_1 e_1_2_7_66_1 e_1_2_7_11_1 e_1_2_7_45_1 e_1_2_7_68_1 e_1_2_7_47_1 e_1_2_7_26_1 e_1_2_7_49_1 e_1_2_7_28_1 e_1_2_7_73_1 e_1_2_7_50_1 e_1_2_7_71_1 e_1_2_7_25_1 e_1_2_7_31_1 e_1_2_7_52_1 e_1_2_7_77_1 e_1_2_7_23_1 e_1_2_7_33_1 e_1_2_7_54_1 e_1_2_7_75_1 e_1_2_7_21_1 e_1_2_7_35_1 e_1_2_7_56_1 e_1_2_7_37_1 e_1_2_7_58_1 e_1_2_7_39_1 e_1_2_7_6_1 e_1_2_7_4_1 e_1_2_7_80_1 e_1_2_7_8_1 e_1_2_7_18_1 e_1_2_7_16_1 e_1_2_7_40_1 e_1_2_7_61_1 e_1_2_7_82_1 e_1_2_7_2_1 e_1_2_7_14_1 e_1_2_7_42_1 e_1_2_7_63_1 e_1_2_7_12_1 e_1_2_7_44_1 e_1_2_7_65_1 e_1_2_7_10_1 e_1_2_7_46_1 e_1_2_7_67_1 e_1_2_7_48_1 e_1_2_7_69_1 e_1_2_7_27_1 e_1_2_7_29_1 Johnston LD (e_1_2_7_36_1) 2007 e_1_2_7_72_1 e_1_2_7_51_1 e_1_2_7_70_1 e_1_2_7_30_1 e_1_2_7_53_1 e_1_2_7_76_1 e_1_2_7_24_1 e_1_2_7_32_1 e_1_2_7_55_1 e_1_2_7_74_1 White V (e_1_2_7_79_1) 2004 e_1_2_7_22_1 e_1_2_7_34_1 e_1_2_7_57_1 e_1_2_7_20_1 e_1_2_7_59_1 e_1_2_7_78_1 e_1_2_7_38_1 |
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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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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 |
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