Interactions of alcohol and nitric-oxide synthase in the brain

Davis, Randall L.; Syapin, Peter J.

doi:10.1016/j.brainresrev.2005.01.008

Cited by 36 publications

(17 citation statements)

References 73 publications

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“…One of the several possible mechanisms for alcohol-induced neurotoxicity may be attributable to alcohol's modulation of hypothalamic-pituitary responsiveness by nitric oxide-generating systems (49). For example, alcohol may regulate nitric oxide synthase, a rate-limiting enzyme for nitric oxide to increase local nitric oxide levels, thus producing neurotoxicity (50,51). Although a few articles support these hypotheses, a consensus mechanism for alcohol's neurotoxicity has yet to be demonstrated.…”

Section: Discussionmentioning

confidence: 99%

Long-lasting reduction in hippocampal neurogenesis by alcohol consumption in adolescent nonhuman primates

Taffe

Kotzebue

Crean

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

144

129

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Binge alcohol consumption in adolescents is increasing, and studies in animal models show that adolescence is a period of high vulnerability to brain insults. The purpose of the present study was to determine the deleterious effects of binge alcohol on hippocampal neurogenesis in adolescent nonhuman primates. Heavy binge alcohol consumption over 11 mo dramatically and persistently decreased hippocampal proliferation and neurogenesis. Combinatorial analysis revealed distinct, actively dividing hippocampal neural progenitor cell types in the subgranular zone of the dentate gyrus that were in transition from stem-like radial glia-like cells (type 1) to immature transiently amplifying neuroblasts (type 2a, type 2b, and type 3), suggesting the evolutionary conservation of milestones of neuronal development in macaque monkeys. Alcohol significantly decreased the number of actively dividing type 1, 2a, and 2b cell types without significantly altering the early neuronal type 3 cells, suggesting that alcohol interferes with the division and migration of hippocampal preneuronal progenitors. Furthermore, the lasting alcohol-induced reduction in hippocampal neurogenesis paralleled an increase in neural degeneration mediated by nonapoptotic pathways. Altogether, these results demonstrate that the hippocampal neurogenic niche during adolescence is highly vulnerable to alcohol and that alcohol decreases neuronal turnover in adolescent nonhuman primate hippocampus by altering the ongoing process of neuronal development. This lasting effect, observed 2 mo after alcohol discontinuation, may underlie the deficits in hippocampus-associated cognitive tasks that are observed in alcoholics.self-administration | binge drinking | hippocampal stem cells | neuronal development | cell death

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Section: Discussionmentioning

confidence: 99%

Long-lasting reduction in hippocampal neurogenesis by alcohol consumption in adolescent nonhuman primates

Taffe

Kotzebue

Crean

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

144

129

View full text Add to dashboard Cite

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“…It has a broad range of pharmacological and toxicological actions, some of which overlap with those thought to be modulated or mediated by NO. For instance, EtOH alters NOS expression and activity in the brain [36,37]. Therefore, this review will be focused on the effects of EtOH on production of NO, NOS activities, and interactions of NO with alcohol metabolism enzymes as well as EtOH.…”

Section: Introductionmentioning

confidence: 99%

Ethanol Metabolism and Effects: Nitric Oxide and its Interaction

Deng

Deitrich²

2007

CCP

110

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Ethanol (EtOH) in alcoholic beverages is consumed by a large number of individuals and its elimination is primarily by oxidation. The role of nitric oxide (NO) in EtOH's effects is important since NO is one of the most prominent biological factors in mammals. NO is constantly formed endogenously from L-arginine. Dose and length of EtOH exposure, and cell type are the main factors affecting EtOH effects on NO production. Either acute or chronic EtOH ingestion affects inducible NO synthase (iNOS) activity. However it seems that EtOH suppresses induced-NO production by inhibition of iNOS in different cells. On the other hand, it is clear that acute low doses of EtOH increase both the release of NO and endothelial NOS (eNOS) expression, and augment endothelium-mediated vasodilatation, whereas higher doses impair endothelial functions. EtOH selectively affects neuronal NOS (nNOS) activity in different brain cells, which may relate to various behavioral interactions. Therefore, there is an excellent chance for EtOH and NO to react with each other. Effects of EtOH on NO production and NOS activity may be important to EtOH modification of cell or organ function. Nitrosated compounds (alkyl nitrites) are often found as the interaction products, which might be one of the minor pathways of EtOH metabolism. NO also inhibits EtOH metabolizing enzymes. Furthermore, NO is involved in EtOH induced liver damage and has a role in fetal development during EtOH exposure in pregnancy. The mechanisms underlying these effects are only partially understood. Hence, the current discussion of the interaction of EtOH and NO is presented.

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“…Several publications have emphasized a potential role of nitric oxide (NO) in alcohol-seeking behavior (Naassila et al, 2000) and even in ethanol-induced sedation and ethanol withdrawal (Adams et al, 1994). Alcohol exposure has diverse effects on the expression and activity of all isoforms of nitric oxide synthase (NOS) involved in NO synthesis in the brain (Naasila et al, 2003;Davis and Syapin, 2005). Modulation of NOS has been suggested to be involved in alcohol-induced behavioral modifications.…”

Section: Introductionmentioning

confidence: 99%

“…Modulation of NOS has been suggested to be involved in alcohol-induced behavioral modifications. Furthermore, alcohol-induced changes in NOS may be implicated in ethanol-mediated neurodegeneration and neurotoxicity (Davis and Syapin, 2005). To predict a role of NO in any particular alcoholmediated action, however, it must be emphasized that the interactions of NO with different brain areas at different times depend mostly on its concentration and on the redox potential of the surrounding milieu (Thippeswamy et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Chronic Alcohol Consumption Affects Gastrointestinal Motility and Reduces the Proportion of Neuronal NOS‐Immunoreactive Myenteric Neurons in the Murine Jejunum

Bagyánszki

Krecsmarik

Winter

et al. 2010

The Anatomical Record

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Alcohol consumption interferes with gastrointestinal transit causing symptoms in alcoholic patients. Nitric oxide (NO), synthesized by neuronal nitric oxide synthase (nNOS) plays an important role in the control of gastrointestinal motility. Our aim was to investigate whether chronic alcohol intake in a murine model induces gastrointestinal motility disturbances and affects the nitrergic myenteric neurons in the stomach and jejunum. Gastric emptying, small intestinal transit and geometric centre were measured in vivo after intragastric gavage of Evans blue. Nitrergic relaxations to electrical field stimulation (EFS) and exogenous NO were recorded in jejunal muscle strips in vitro. The proportion of nNOS-immunopositive myenteric neurons was assessed using PGP9.5 and nNOS immunostaining. After chronic alcohol consumption, gastric emptying and small intestinal transit were delayed compared with control mice, and the nitrergic nervemediated relaxations to EFS in the jejunum were decreased, whereas relaxations to exogenous NO did not differ. The proportion of nNOS-immunoreactive neurons did not change in the stomach, whereas in the jejunum the percentage decreased from 33% to 27% (P < 0.001) after chronic alcohol intake. The total number of myenteric neurons remained unchanged. These results suggest that chronic alcohol consumption disturbs gastric and small intestinal motility in vivo and in vitro and is associated with a decrease in the proportion of nNOS-immunoreactive myenteric neurons in the murine jejunum. Anat Rec, 293:1536Rec, 293: -1542Rec, 293: , 2010.

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Interactions of alcohol and nitric-oxide synthase in the brain

Cited by 36 publications

References 73 publications

Long-lasting reduction in hippocampal neurogenesis by alcohol consumption in adolescent nonhuman primates

Long-lasting reduction in hippocampal neurogenesis by alcohol consumption in adolescent nonhuman primates

Ethanol Metabolism and Effects: Nitric Oxide and its Interaction

Chronic Alcohol Consumption Affects Gastrointestinal Motility and Reduces the Proportion of Neuronal NOS‐Immunoreactive Myenteric Neurons in the Murine Jejunum

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