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Book ; Thesis: In-vivo-Analyse morphologischer, mikrovaskulärer und zellulärer Veränderungen der Leber während chronischer Tetrachlorkohlenstoff-Exposition

Siegmund, Sören Volker

2001

Author's details	vorgelegt von Sören Volker Siegmund
Language	German
Size	IV, 139 Bl., Ill., graph. Darst.
Edition	[Mikrofiche-Ausg.]
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Saarbrücken, Univ., Diss., 2001
HBZ-ID	HT013328520
Database	Catalogue ZB MED Medicine, Health

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Article: Endocannabinoids and liver disease. II. Endocannabinoids in the pathogenesis and treatment of liver fibrosis.

Siegmund, Sören V / Schwabe, Robert F

American journal of physiology. Gastrointestinal and liver physiology

2008 Volume 294, Issue 2, Page(s) G357–62

Abstract: Hepatic fibrosis is the response of the liver to chronic injury and is associated with portal hypertension, progression to hepatic cirrhosis, liver failure, and high incidence of hepatocellular carcinoma. On a molecular level, a large number of signaling ...

Abstract	Hepatic fibrosis is the response of the liver to chronic injury and is associated with portal hypertension, progression to hepatic cirrhosis, liver failure, and high incidence of hepatocellular carcinoma. On a molecular level, a large number of signaling pathways have been shown to contribute to the activation of fibrogenic cell types and the subsequent accumulation of extracellular matrix in the liver. Recent evidence suggests that the endocannabinoid system is an important part of this complex signaling network. In the injured liver, the endocannabinoid system is upregulated both at the level of endocannabinoids and at the endocannabinoid receptors CB1 and CB2. The hepatic endocannabinoid system mediates both pro- and antifibrogenic effects by activating distinct signaling pathways that differentially affect proliferation and death of fibrogenic cell types. Here we will summarize current findings on the role of the hepatic endocannabinoid system in liver fibrosis and discuss emerging options for its therapeutic exploitation.
MeSH term(s)	Animals ; Cannabinoid Receptor Modulators/physiology ; Cell Death/physiology ; Cell Proliferation ; Endocannabinoids ; Humans ; Hypertension, Portal/pathology ; Hypertension, Portal/physiopathology ; Inflammation/pathology ; Inflammation/physiopathology ; Liver/cytology ; Liver/enzymology ; Liver Cirrhosis/drug therapy ; Liver Cirrhosis/enzymology ; Liver Cirrhosis/pathology ; Liver Cirrhosis/physiopathology ; Receptors, Cannabinoid/physiology
Chemical Substances	Cannabinoid Receptor Modulators ; Endocannabinoids ; Receptors, Cannabinoid
Language	English
Publishing date	2008-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00456.2007
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Article: Animal models and their results in gastrointestinal alcohol research.

Siegmund, Soren V / Haas, Stephan / Singer, Manfred V

Digestive diseases (Basel, Switzerland)

2005 Volume 23, Issue 3-4, Page(s) 181–194

Abstract: Alcohol-induced diseases of the gastrointestinal tract play an important role in clinical gastroenterology. However, the precise pathophysiological mechanisms are still largely unknown. Alcohol research depends essentially on animal models due to the ... ...

Abstract	Alcohol-induced diseases of the gastrointestinal tract play an important role in clinical gastroenterology. However, the precise pathophysiological mechanisms are still largely unknown. Alcohol research depends essentially on animal models due to the fact that controlled experimental studies of ethanol-induced diseases in humans are unethical. Animal models have already been successfully applied to disclose and analyze molecular mechanisms in alcohol-induced diseases, partially by using knockout technology. Because of a lack of transferability of some animal models to the human condition, results have to be interpreted cautiously. For some alcohol-related diseases like chronic alcoholic pancreatitis, the ideal animal model does not yet exist. Here we provide an overview of the most commonly used animal models in gastrointestinal alcohol research. We will also briefly discuss the findings based on animal models as well as the current concepts of pathophysiological mechanisms involved in acute and chronic alcoholic damage of the esophagus, stomach, small and large intestine, pancreas and liver.
MeSH term(s)	Alcohol-Related Disorders/diagnosis ; Animals ; Disease Models, Animal ; Ethanol/pharmacology ; Forecasting ; Gastritis/epidemiology ; Gastritis/etiology ; Gastrointestinal Diseases/etiology ; Gastrointestinal Diseases/pathology ; Intestinal Diseases/etiology ; Intestinal Diseases/pathology ; Liver Cirrhosis, Alcoholic/diagnosis ; Liver Cirrhosis, Alcoholic/pathology ; Pancreatitis, Alcoholic/etiology ; Pancreatitis, Alcoholic/pathology ; Research/standards ; Research/trends ; Risk Factors ; Sensitivity and Specificity
Chemical Substances	Ethanol (3K9958V90M)
Language	English
Publishing date	2005
Publishing country	Switzerland
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632798-9
ISSN	1421-9875 ; 0257-2753
ISSN (online)	1421-9875
ISSN	0257-2753
DOI	10.1159/000090165
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Article: Molecular mechanisms of alcohol-induced hepatic fibrosis.

Siegmund, Soren V / Dooley, Steven / Brenner, David A

Digestive diseases (Basel, Switzerland)

2005 Volume 23, Issue 3-4, Page(s) 264–274

Abstract: Alcohol abuse is a major cause of liver fibrosis and cirrhosis in developed countries. Before alcoholic liver fibrosis becomes evident, the liver undergoes several stages of alcoholic liver disease including steatosis and steatohepatitis. Although the ... ...

Abstract	Alcohol abuse is a major cause of liver fibrosis and cirrhosis in developed countries. Before alcoholic liver fibrosis becomes evident, the liver undergoes several stages of alcoholic liver disease including steatosis and steatohepatitis. Although the main mechanisms of fibrogenesis are independent of the etiology of liver injury, alcoholic liver fibrosis is distinctively characterized by a pronounced inflammatory response due to elevated gut-derived endotoxin plasma levels, an augmented generation of oxidative stress with pericentral hepatic hypoxia and the formation of cell-toxic and profibrogenic ethanol metabolites (e.g. acetaldehyde or lipid oxidation products). These factors, based on a complex network of cytokine actions, together result in increased hepatocellular damage and activation of hepatic stellate cells, the key cell type of liver fibrogenesis. Although to date removal of the causative agent, i.e. alcohol, still represents the most effective intervention to prevent the manifestation of alcoholic liver disease, sophisticated molecular approaches are underway, aiming to specifically blunt profibrogenic signaling pathways in liver cells or specifically induce cell death in activated hepatic stellate cells to decrease the scarring of the liver.
MeSH term(s)	Cytochrome P-450 CYP2E1/genetics ; Ethanol/adverse effects ; Ethanol/metabolism ; Female ; Gene Expression Regulation ; Hepatocytes/cytology ; Hepatocytes/metabolism ; Humans ; Liver Cirrhosis, Alcoholic/genetics ; Liver Cirrhosis, Alcoholic/pathology ; Male ; Molecular Biology ; Oxidative Stress ; Polymerase Chain Reaction ; Polymorphism, Genetic ; RNA, Messenger/analysis ; Sensitivity and Specificity ; Signal Transduction ; Transforming Growth Factor alpha/metabolism
Chemical Substances	RNA, Messenger ; Transforming Growth Factor alpha ; Ethanol (3K9958V90M) ; Cytochrome P-450 CYP2E1 (EC 1.14.13.-)
Language	English
Publishing date	2005
Publishing country	Switzerland
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632798-9
ISSN	1421-9875 ; 0257-2753
ISSN (online)	1421-9875
ISSN	0257-2753
DOI	10.1159/000090174
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Article: Molecular pathogenesis of alcohol-induced hepatic fibrosis.

Siegmund, Sören V / Brenner, David A

Alcoholism, clinical and experimental research

2005 Volume 29, Issue 11 Suppl, Page(s) 102S–109S

Abstract: Alcohol abuse is a main cause of liver fibrosis and cirrhosis in the western world. Although the major mechanisms of fibrogenesis are independent of the origin of liver injury, alcoholic liver fibrosis features distinctive characteristics, including the ... ...

Abstract	Alcohol abuse is a main cause of liver fibrosis and cirrhosis in the western world. Although the major mechanisms of fibrogenesis are independent of the origin of liver injury, alcoholic liver fibrosis features distinctive characteristics, including the pronounced inflammatory response of immune cells due to elevated gut-derived endotoxin plasma levels, increased formation of reactive oxygen species (ROS), ethanol-induced pericentral hepatic hypoxia or formation of cell-toxic and pro-fibrogenic ethanol metabolites (e.g., acetaldehyde or lipid oxidation products). These factors are together responsible for increased hepatocellular cell death and activation of hepatic stellate cells (HSCs), the key cell type of liver fibrogenesis. To date, removing the causative agent is the most effective intervention to prevent the manifestation of liver cirrhosis. A novel experimental approach in fibrosis therapy is the selective induction of cell death in HSCs. Substances such as gliotoxin, anandamide or antibody against tissue inhibitor of metalloproteinase (TIMP)-1 can selectively induce cell death in activated HSCs. These new results in basic science are encouraging for the search of new antifibrotic treatment.
MeSH term(s)	Animals ; Apoptosis ; Arachidonic Acids/therapeutic use ; Endocannabinoids ; Extracellular Matrix/pathology ; Gliotoxin ; Humans ; Liver/pathology ; Liver/physiopathology ; Liver Cirrhosis, Alcoholic/drug therapy ; Liver Cirrhosis, Alcoholic/pathology ; Liver Cirrhosis, Alcoholic/physiopathology ; Oxidative Stress/physiology ; Polyunsaturated Alkamides ; Tissue Inhibitor of Metalloproteinase-1/therapeutic use
Chemical Substances	Arachidonic Acids ; Endocannabinoids ; Polyunsaturated Alkamides ; Tissue Inhibitor of Metalloproteinase-1 ; Gliotoxin (67-99-2) ; anandamide (UR5G69TJKH)
Language	English
Publishing date	2005-11-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1097/01.alc.0000189275.97419.58
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Article: Fatty acid amide hydrolase but not monoacyl glycerol lipase controls cell death induced by the endocannabinoid 2-arachidonoyl glycerol in hepatic cell populations

Siegmund, Sören V / Wojtalla, Alexandra / Schlosser, Monika / Zimmer, Andreas / Singer, Manfred V

Biochemical and biophysical research communications. 2013 July 19, v. 437, no. 1

2013

Abstract: The endogenous cannabinoids anandamide (N-arachidonoylethanolamide, AEA) and 2-arachidonoyl glycerol (2-AG) are upregulated during liver fibrogenesis and selectively induce cell death in hepatic stellate cells (HSCs), the major fibrogenic cells in the ... ...

Abstract	The endogenous cannabinoids anandamide (N-arachidonoylethanolamide, AEA) and 2-arachidonoyl glycerol (2-AG) are upregulated during liver fibrogenesis and selectively induce cell death in hepatic stellate cells (HSCs), the major fibrogenic cells in the liver, but not in hepatocytes. In contrast to HSCs, hepatocytes highly express the AEA-degrading enzyme fatty acid amide hydrolase (FAAH) that protects them from AEA-induced injury. However, the role of the major 2-AG-degrading enzyme monoacylglycerol lipase (MGL) in 2-AG-induced hepatic cell death has not been investigated. In contrast to FAAH, MGL protein expression did not significantly differ in primary mouse hepatocytes and HSCs. Hepatocytes pretreated with selective MGL inhibitors were not sensitized towards 2-AG-mediated death, indicating a minor role for MGL in the cellular resistance against 2-AG. Moreover, while adenoviral MGL overexpression failed to render HSCs resistant towards 2-AG, FAAH overexpression prevented 2-AG-induced death in HSCs. Accordingly, 2-AG caused cell death in hepatocytes pretreated with the FAAH inhibitor URB597, FAAH⁻/⁻ hepatocytes, or hepatocytes depleted of the antioxidant glutathione (GSH). Moreover, 2-AG increased reactive oxygen species production in hepatocytes after FAAH inhibition, indicating that hepatocytes are more resistant to 2-AG treatment due to high GSH levels and FAAH expression. However, 2-AG was not significantly elevated in FAAH⁻/⁻ mouse livers in contrast to AEA. Thus, FAAH exerts important protective actions against 2-AG-induced cellular damage, even though it is not the major 2-AG degradation enzyme in vivo. In conclusion, FAAH-mediated resistance of hepatocytes against endocannabinoid-induced cell death may provide a new physiological concept allowing the specific targeting of HSCs in liver fibrosis.
Keywords	acylglycerol lipase ; antioxidants ; cannabinoids ; cell death ; death ; fatty acids ; glutathione ; glycerol ; hepatocytes ; liver ; liver cirrhosis ; mice ; protein synthesis ; reactive oxygen species
Language	English
Dates of publication	2013-0719
Size	p. 48-54.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2013.06.033
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Article ; Online: Fatty acid amide hydrolase but not monoacyl glycerol lipase controls cell death induced by the endocannabinoid 2-arachidonoyl glycerol in hepatic cell populations.

Siegmund, Sören V / Wojtalla, Alexandra / Schlosser, Monika / Zimmer, Andreas / Singer, Manfred V

Biochemical and biophysical research communications

2013 Volume 437, Issue 1, Page(s) 48–54

Abstract	The endogenous cannabinoids anandamide (N-arachidonoylethanolamide, AEA) and 2-arachidonoyl glycerol (2-AG) are upregulated during liver fibrogenesis and selectively induce cell death in hepatic stellate cells (HSCs), the major fibrogenic cells in the liver, but not in hepatocytes. In contrast to HSCs, hepatocytes highly express the AEA-degrading enzyme fatty acid amide hydrolase (FAAH) that protects them from AEA-induced injury. However, the role of the major 2-AG-degrading enzyme monoacylglycerol lipase (MGL) in 2-AG-induced hepatic cell death has not been investigated. In contrast to FAAH, MGL protein expression did not significantly differ in primary mouse hepatocytes and HSCs. Hepatocytes pretreated with selective MGL inhibitors were not sensitized towards 2-AG-mediated death, indicating a minor role for MGL in the cellular resistance against 2-AG. Moreover, while adenoviral MGL overexpression failed to render HSCs resistant towards 2-AG, FAAH overexpression prevented 2-AG-induced death in HSCs. Accordingly, 2-AG caused cell death in hepatocytes pretreated with the FAAH inhibitor URB597, FAAH(-/-) hepatocytes, or hepatocytes depleted of the antioxidant glutathione (GSH). Moreover, 2-AG increased reactive oxygen species production in hepatocytes after FAAH inhibition, indicating that hepatocytes are more resistant to 2-AG treatment due to high GSH levels and FAAH expression. However, 2-AG was not significantly elevated in FAAH(-/-) mouse livers in contrast to AEA. Thus, FAAH exerts important protective actions against 2-AG-induced cellular damage, even though it is not the major 2-AG degradation enzyme in vivo. In conclusion, FAAH-mediated resistance of hepatocytes against endocannabinoid-induced cell death may provide a new physiological concept allowing the specific targeting of HSCs in liver fibrosis.
MeSH term(s)	Amidohydrolases/genetics ; Amidohydrolases/metabolism ; Animals ; Arachidonic Acids/pharmacology ; Cell Death/drug effects ; Cells, Cultured ; Cytoprotection/drug effects ; Endocannabinoids/pharmacology ; Glycerides/pharmacology ; Hepatic Stellate Cells/cytology ; Hepatic Stellate Cells/drug effects ; Hepatic Stellate Cells/enzymology ; Hepatocytes/cytology ; Hepatocytes/drug effects ; Hepatocytes/enzymology ; Male ; Mice ; Mice, Inbred C57BL ; Monoacylglycerol Lipases/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Arachidonic Acids ; Endocannabinoids ; Glycerides ; Reactive Oxygen Species ; glyceryl 2-arachidonate (8D239QDW64) ; ABHD6 protein, mouse (EC 3.1.1.23) ; Abhd12 protein, mouse (EC 3.1.1.23) ; Monoacylglycerol Lipases (EC 3.1.1.23) ; Amidohydrolases (EC 3.5.-) ; fatty-acid amide hydrolase (EC 3.5.1.-)
Language	English
Publishing date	2013-07-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2013.06.033
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Article ; Online: Serum Amyloid A Induces Inflammation, Proliferation and Cell Death in Activated Hepatic Stellate Cells.

Siegmund, Sören V / Schlosser, Monika / Schildberg, Frank A / Seki, Ekihiro / De Minicis, Samuele / Uchinami, Hiroshi / Kuntzen, Christian / Knolle, Percy A / Strassburg, Christian P / Schwabe, Robert F

PloS one

2016 Volume 11, Issue 3, Page(s) e0150893

Abstract: ... Annexin V staining. Serum amyloid A induced HSC proliferation, which depended on JNK, Erk and Akt activity ...

Abstract	Serum amyloid A (SAA) is an evolutionary highly conserved acute phase protein that is predominantly secreted by hepatocytes. However, its role in liver injury and fibrogenesis has not been elucidated so far. In this study, we determined the effects of SAA on hepatic stellate cells (HSCs), the main fibrogenic cell type of the liver. Serum amyloid A potently activated IκB kinase, c-Jun N-terminal kinase (JNK), Erk and Akt and enhanced NF-κB-dependent luciferase activity in primary human and rat HSCs. Serum amyloid A induced the transcription of MCP-1, RANTES and MMP9 in an NF-κB- and JNK-dependent manner. Blockade of NF-κB revealed cytotoxic effects of SAA in primary HSCs with signs of apoptosis such as caspase 3 and PARP cleavage and Annexin V staining. Serum amyloid A induced HSC proliferation, which depended on JNK, Erk and Akt activity. In primary hepatocytes, SAA also activated MAP kinases, but did not induce relevant cell death after NF-κB inhibition. In two models of hepatic fibrogenesis, CCl4 treatment and bile duct ligation, hepatic mRNA levels of SAA1 and SAA3 were strongly increased. In conclusion, SAA may modulate fibrogenic responses in the liver in a positive and negative fashion by inducing inflammation, proliferation and cell death in HSCs.
MeSH term(s)	Animals ; Carbon Tetrachloride ; Cell Death/drug effects ; Cell Proliferation/drug effects ; Chemokine CCL2/genetics ; Chemokine CCL2/metabolism ; Chemokine CCL5/genetics ; Chemokine CCL5/metabolism ; Cholestasis/genetics ; Cholestasis/metabolism ; Cholestasis/pathology ; Disease Models, Animal ; Gene Expression Regulation ; Hepatic Stellate Cells/drug effects ; Hepatic Stellate Cells/metabolism ; Hepatic Stellate Cells/pathology ; Humans ; I-kappa B Kinase/genetics ; I-kappa B Kinase/metabolism ; Inflammation ; Ligation ; Liver Cirrhosis/chemically induced ; Liver Cirrhosis/genetics ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; MAP Kinase Kinase 4/genetics ; MAP Kinase Kinase 4/metabolism ; Male ; Matrix Metalloproteinase 9/genetics ; Matrix Metalloproteinase 9/metabolism ; Mice, Inbred BALB C ; Mitogen-Activated Protein Kinase 1/genetics ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/genetics ; Mitogen-Activated Protein Kinase 3/metabolism ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Primary Cell Culture ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Sprague-Dawley ; Serum Amyloid A Protein/pharmacology ; Signal Transduction
Chemical Substances	CCL2 protein, human ; CCL5 protein, human ; Chemokine CCL2 ; Chemokine CCL5 ; NF-kappa B ; SAA1 protein, human ; Serum Amyloid A Protein ; Carbon Tetrachloride (CL2T97X0V0) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; I-kappa B Kinase (EC 2.7.11.10) ; MAPK1 protein, human (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; MAP Kinase Kinase 4 (EC 2.7.12.2) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0150893
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Article: Systemic mediators induce fibrogenic effects in normal liver after partial bile duct ligation.

Osawa, Yosuke / Seki, Ekihiro / Adachi, Masayuki / Taura, Kojiro / Kodama, Yuzo / Siegmund, Soren V / Schwabe, Robert F / Brenner, David A

Liver international : official journal of the International Association for the Study of the Liver

2006 Volume 26, Issue 9, Page(s) 1138–1147

Abstract: Background/aims: Collagen production by activated hepatic stellate cells (HSCs) is a key event in liver fibrosis, and a number of factors have been characterized that trigger HSC activation and collagen production. However, it remains unclear if these ... ...

Abstract	Background/aims: Collagen production by activated hepatic stellate cells (HSCs) is a key event in liver fibrosis, and a number of factors have been characterized that trigger HSC activation and collagen production. However, it remains unclear if these factors act locally at the site of injury or also affect HSCs distant to the site of injury. Methods: A model of partial bile duct ligation (PBDL) in which fibrogenesis can be compared between the injured ligated lobe and the non-ligated lobe. Results: After PBDL, HSCs showed an increased expression of procollagen type I alpha1 mRNA and collagen-reporter gene activity not only in the ligated lobe, but also in the non-ligated lobe, albeit at a lower level. In contrast, an increase in the number of desmin- and alpha-smooth muscle actin positive HSCs, and accumulation of inflammatory cells were observed only in the ligated lobe. Although transforming growth factor-beta (TGF-beta) mRNA was increased only in the ligated lobe, Smad2/3 were activated in the ligated and the non-ligated lobe. These data suggest that the systemic increase in profibrogenic mediators including TGF-beta induces collagen transcription in the uninjured liver. Conclusion: Systemic profibrogenic mediators from the injury site affect the residual non-injured liver.
MeSH term(s)	Actins/metabolism ; Animals ; Bile Ducts ; Collagen/genetics ; Collagen Type I/genetics ; Collagen Type I/metabolism ; Desmin/metabolism ; Genes, Reporter ; Inflammation/etiology ; Ligation ; Liver/cytology ; Liver/metabolism ; Liver/physiology ; Liver Cirrhosis/etiology ; Mice ; Mice, Transgenic ; Muscle, Smooth/metabolism ; Phosphorylation ; RNA, Messenger/metabolism ; Smad2 Protein/metabolism ; Smad3 Protein/metabolism ; Tissue Distribution ; Transforming Growth Factor beta/genetics ; Up-Regulation
Chemical Substances	Actins ; Collagen Type I ; Desmin ; RNA, Messenger ; Smad2 Protein ; Smad3 Protein ; Transforming Growth Factor beta ; Collagen (9007-34-5)
Language	English
Publishing date	2006-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2102783-3
ISSN	1478-3231 ; 1478-3223
ISSN (online)	1478-3231
ISSN	1478-3223
DOI	10.1111/j.1478-3231.2006.01346.x
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Article: Influence of age at drinking onset on long-term ethanol self-administration with deprivation and stress phases.

Siegmund, Sören / Vengeliene, Valentina / Singer, Manfred V / Spanagel, Rainer

Alcoholism, clinical and experimental research

2005 Volume 29, Issue 7, Page(s) 1139–1145

Abstract: Background: Onset of alcohol use during adolescence has potentially long-lasting consequences, e.g., prospective alcohol dependence. To obtain new insight into the effects of early chronic ethanol consumption, we compared the drinking behavior of two ... ...

Abstract	Background: Onset of alcohol use during adolescence has potentially long-lasting consequences, e.g., prospective alcohol dependence. To obtain new insight into the effects of early chronic ethanol consumption, we compared the drinking behavior of two adult male Wistar rat groups: one that initiated alcohol consumption during adolescence (adolescent group) and the other that initiated their drinking during adulthood (adult group) in a model of long-term alcohol self-administration. We investigated the magnitude of the effects of deprivation and stress on alcohol intake and the influence of these events on the alcohol drinking behavior across time. Methods: Heterogeneous Wistar rats aged 31 days (adolescents) and 71 days (adults) were given ad libitum access to water, as well as 5% and 20% ethanol solutions during an observation period of 30 wk. A deprivation phase of 14 days was instituted after eight wk of access to alcohol. After 16 and 26 wk of alcohol access, all animals were subjected for three consecutive days to forced swimming and electric foot shocks, respectively. Results: At the onset of drinking, adolescent animals consumed less alcohol and showed lower preference than adults. The deprivation phase was followed by increased intake of highly concentrated ethanol solution without appreciable differences between age groups. Repeated swim stress produced a slight increase in ethanol consumption in both animal groups; however, alcohol intake was not significantly different between groups, whereas the foot shock stress-induced increase in alcohol intake was significantly higher in the animal group that initiated alcohol consumption during adolescence. After swim stress, the drinking behavior of the adolescent group resembled that of the adult group. In particular, the adolescent group increased their preference for 20% ethanol solution for the remainder of the experiment. Conclusions: Age of voluntary alcohol drinking onset does not appear to be a strong predictor for prospective alcohol intake and relapse-like drinking behavior under the present experimental conditions. However, male Wistar rats that initiated alcohol consumption during adolescence seem to be more susceptible to acute stressor-specific effects in terms of alcohol consumption.
MeSH term(s)	Age Factors ; Alcohol Drinking/psychology ; Alcoholism/psychology ; Animals ; Arousal ; Ethanol/toxicity ; Fear ; Male ; Rats ; Rats, Wistar ; Stress, Psychological/complications ; Substance Withdrawal Syndrome/psychology
Chemical Substances	Ethanol (3K9958V90M)
Language	English
Publishing date	2005-06-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1097/01.alc.0000171928.40418.46
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