scholarly journals Regulation of brain anandamide by acute administration of ethanol

2007 ◽  
Vol 404 (1) ◽  
pp. 97-104 ◽  
Author(s):  
Belen Ferrer ◽  
Francisco Javier Bermúdez-Silva ◽  
Ainhoa Bilbao ◽  
Lily Alvarez-Jaimes ◽  
Irene Sanchez-Vera ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Nucleus Accumbens ◽  
Time Course ◽  
Intraperitoneal Administration ◽  
Ethanol Exposure ◽  
In Vivo Studies ◽  
Ethanol Administration ◽  
Acute Administration ◽  
Peripheral Tissues ◽  
Acute Ethanol

The endogenous cannabinoid acylethanolamide AEA (arachidonoylethanolamide; also known as anandamide) participates in the neuroadaptations associated with chronic ethanol exposure. However, no studies have described the acute actions of ethanol on AEA production and degradation. In the present study, we investigated the time course of the effects of the intraperitoneal administration of ethanol (4 g/kg of body mass) on the endogenous levels of AEA in central and peripheral tissues. Acute ethanol administration decreased AEA in the cerebellum, the hippocampus and the nucleus accumbens of the ventral striatum, as well as in plasma and adipose tissue. Parallel decreases of a second acylethanolamide, PEA (palmitoylethanolamide), were observed in the brain. Effects were observed 45–90 min after ethanol administration. In vivo studies revealed that AEA decreases were associated with a remarkable inhibition of the release of both anandamide and glutamate in the nucleus accumbens. There were no changes in the expression and enzymatic activity of the main enzyme that degrades AEA, the fatty acid amidohydrolase. Acute ethanol administration did not change either the activity of N-acyltransferase, the enzyme that catalyses the synthesis of the AEA precursor, or the expression of NAPE-PLD (N-acylphosphatidylethanolamine-hydrolysing phospholipase D), the enzyme that releases AEA from membrane phospholipid precursors. These results suggest that receptor-mediated release of acylethanolamide is inhibited by the acute administration of ethanol, and that this effect is not derived from increased fatty acid ethanolamide degradation.

scholarly journals The role of free serum tryptophan in the biphasic effect of acute ethanol administration on the concentrations of rat brain tryptophan, 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid

1976 ◽  
Vol 160 (2) ◽  
pp. 315-324 ◽  
Author(s):  
A A Badawy ◽  
M Evans
Keyword(s):  
Rat Brain ◽  
Tryptophan Metabolism ◽  
Ethanol Administration ◽  
Acute Administration ◽  
Free Tryptophan ◽  
Biphasic Effect ◽  
Acute Ethanol ◽  
Comparison Of The Results ◽  
Ylacetic Acid

1. Acute administration of ethanol exerts a biphasic effect on the concentrations of rat brain tryptophan, 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid. Both effects are associated with corresponding changes in the availability of circulating free tryptophan. 2. The initial increases in the above concentrations are prevented by ergotamine, are unaltered by allopurinol and are potentiated by theophylline, whereas the later decreases are prevented by both ergotamine and allopurinol. 3. It is suggested that the initial enhancement by ethanol of brain tryptophan metabolism is caused by catecholamine-mediated lipolysis followed by displacement of protein-bound serum tryptophan, whereas the activation of liver tryptophaan pyrrolase, which is produced by the same mechanism, leads to the later decreases in the brain concentrations of tryptophan and its metabolites. 4. The initial effects of ethanol can be reproduced by an equicaloric dose of sucrose, and a comparison of the two treatments alone could therefore be misleading. 5. The effects of ethanol on liver and brain tryptophan metabolism have also been examined in mice, and a comparison of the results with those previously reported suggests that the ethanol effects are strain-dependent.

scholarly journals Acute effect of EtOH on Mg2+homeostasis in liver cells: evidence for the activation of an Na+/Mg2+exchanger

1998 ◽  
Vol 275 (5) ◽  
pp. G1106-G1116 ◽  
Author(s):  
Patrick A. Tessman ◽  
Andrea Romani
Keyword(s):  
Choline Chloride ◽  
Acute Effect ◽  
Isolated Hepatocytes ◽  
Cellular Level ◽  
Ethanol Administration ◽  
Acute Administration ◽  
Extracellular Medium ◽  
Ethanol Addition ◽  
Dose Dependent Fashion ◽  
Acute Ethanol

The acute administration of ethanol mobilizes a considerable amount of Mg2+ from perfused rat livers and isolated hepatocytes in a dose-dependent fashion in the absence of release of cellular K+ or lactate dehydrogenase (LDH) in the extracellular medium. Mg2+extrusion becomes detectable within 2 min and reaches the maximum within 8 min after ethanol addition, declining toward the basal value thereafter irrespective of the persistence of alcohol in the perfusion system and the dose of ethanol administered. The effect is the result of a specific impairment of Mg2+transport and/or regulatory mechanisms. In fact, Mg2+ extrusion does not occur under conditions in which 1) ethanol is replaced by an equivalent dose of DMSO, 2) amiloride or imipramine are used as inhibitors of the Na+/Mg2+exchanger, 3) extracellular Na+ is replaced by an equimolar concentration of choline chloride, and 4) 4-methylpyrazole is used to specifically inhibit alcohol dehydrogenase and cytochrome P-4502E1. Finally, the observation that the cellular level of ATP is markedly reduced after acute ethanol administration would suggest that Mg2+ extrusion results from a decreased buffering capacity of cytosolic Mg-ATP complex.

scholarly journals Effects of acute ethanol administration on rat liver 5-aminolaevulinate synthase activity

1989 ◽  
Vol 262 (2) ◽  
pp. 491-496 ◽  
Author(s):  
A A B Badawy ◽  
C J Morgan ◽  
N R Davis
Keyword(s):  
Alcohol Dehydrogenase ◽  
Rat Liver ◽  
Intraperitoneal Administration ◽  
Reciprocal Relationship ◽  
Ethanol Administration ◽  
Simultaneous Increase ◽  
Acute Ethanol ◽  
Tryptophan Pyrrolase ◽  
Dose Dependent Decrease ◽  
Dose Dependent

1. Liver 5-aminolaevulinate (ALA) synthase activity of 24 h-starved rats is maximally increased at 4 h after intraperitoneal administration of a 1.6 g/kg body wt. dose of ethanol. Larger doses cause a dose-dependent decrease in the extent of this stimulation, exhibiting a reciprocal relationship with an elevation of hepatic haem concentration, as suggested by the simultaneous increase in the haem saturation of tryptophan pyrrolase. 2. ALA synthase induction by ethanol is abolished if the above increase in pyrrolase saturation with haem is enhanced by theophylline, but is potentiated when the increase in the haem saturation is inhibited by anti-lipolytic agents. 3. ALA synthase induction by ethanol is also inhibited by inhibitors of alcohol dehydrogenase and aldehyde dehydrogenase. Acetaldehyde and acetate are, however, not responsible; they both decrease ALA synthase activity and increase the haem saturation of tryptophan pyrrolase. These latter effects of acetaldehyde are not mediated by acetate. 4. ALA synthase activity is also stimulated by succinate, which, however, also increases the haem saturation of tryptophan pyrrolase. 5. Ethanol does not influence the rate of ALA synthase degradation. 6. It is suggested that ethanol increases rat liver ALA synthase activity as a result of its own metabolism by the alcohol dehydrogenase-dependent pathway by a mechanism not involving decreased degradation of the former enzyme or the participation of the metabolites acetaldehyde and acetate.

The Effect of Acute Ethanol Administration on Parathion Toxicity and In Vitro Parathion Degradation in the Rat

1971 ◽  
Vol 49 (5) ◽  
pp. 481-483 ◽  
Author(s):  
D. C. Villeneuve ◽  
W. E. J. Phillips
Keyword(s):  
Enzyme Induction ◽  
Intraperitoneal Administration ◽  
Oral Route ◽  
Ethanol Administration ◽  
Acute Ethanol ◽  
Liver Homogenates

Both the oral and intraperitoneal administration of acute doses of ethanol resulted in decreased toxicity of parathion in the rat. The rate of in vitro parathion degradation by liver homogenates from rats administered ethanol by the oral route was lower than in the control rats. These results indicate that the altered toxicity is not due to enzyme induction.

Role of endotoxin in the hypermetabolic state after acute ethanol exposure

1998 ◽  
Vol 275 (6) ◽  
pp. G1252-G1258 ◽  
Author(s):  
Chantal A. Rivera ◽  
Blair U. Bradford ◽  
Vitor Seabra ◽  
Ronald G. Thurman
Keyword(s):  
Oxygen Uptake ◽  
Kupffer Cells ◽  
Ethanol Exposure ◽  
Ethanol Administration ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Hypermetabolic State ◽  
Acute Ethanol ◽  
Eicosanoid Release

This study investigated the role of endotoxin in the hypermetabolic state or swift increase in alcohol metabolism (SIAM) due to acute ethanol exposure. Female Sprague-Dawley rats (100–120 g) were given ethanol (5 g/kg) by gavage. Endotoxin measured in plasma from portal blood was not detectable in saline-treated controls; however, 90 min after ethanol, endotoxin was increased to 85 ± 14 pg/ml, and endotoxin clearance was diminished by ∼50%. Oxygen uptake in perfused livers was increased 48% by ethanol, and production of PGE2 by isolated Kupffer cells was increased similarly. These effects were blunted by elimination of gram-negative bacteria and endotoxin with antibiotics before ethanol administration. To reproduce ethanol-induced endotoxemia, endotoxin was infused via the mesenteric vein at a rate of 2 ng ⋅ kg−1 ⋅ h−1. Endotoxin mimicked the effect of ethanol on oxygen uptake. The specific Kupffer cell toxicant GdCl3completely prevented increases in oxygen uptake due to endotoxin. These findings demonstrate that endotoxin plays a pivotal role in SIAM, most likely by stimulating eicosanoid release from Kupffer cells.

Ethanol, growth hormone and testosterone in peripubertal rats

1997 ◽  
Vol 152 (3) ◽  
pp. 477-487 ◽  
Author(s):  
J J Tentler ◽  
N LaPaglia ◽  
J Steiner ◽  
D Williams ◽  
M Castelli ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Serum Testosterone ◽  
The United States ◽  
Ethanol Exposure ◽  
Ethanol Administration ◽  
Testicular Function ◽  
Mrna Levels ◽  
Stage Of Development ◽  
Acute Ethanol ◽  
Serum Gh

The deleterious effects of ethanol on the hypothalamic pituitary growth hormone axis in adult male humans and animals have been well documented. It is also well established that ethanol has toxic effects on testicular function in adult humans and animals. Much less is known, however, about the effects of ethanol on the growth hormone (GH) axis and testicular function in adolescence. Recent studies have established that adolescent problem drinking is a widespread and growing threat to the health of young people in the United States. In the present study, therefore, we investigated if acute ethanol exposure in peripubertal male Sprague–Dawley rats altered normal pituitary and testicular function. Serum levels of GH and testosterone were measured at 1·5, 3, 6, and 24 h after a single i.p. injection of either saline or 3 g/kg body weight ethanol. Histologic analysis as well as serum testosterone levels allowed us to assign animals to either early puberty (35-day-old animals), mid-puberty (41-day-old animals), or young adult (51- and 66-day-old animals) status. Ethanol produced significant decrements in serum testosterone in the 51-and 66-day-old animals, with a trend toward suppression in the 41-day-old group. Furthermore acute ethanol administration significantly decreased serum GH (P< 0·0001 by 3 way ANOVA) demonstrating a significant effect of ethanol on serum GH in all age groups and at all time points studied when compared with saline injected controls (P<0·01 by Tukey's studentized range test). Despite this significant fall in peripheral GH levels, there was no decrease in either GH mRNA or growth hormone-releasing factor (GRF) mRNA levels nor in hypothalamic concentration of GRF peptide. We conclude that, as in adult animals, acute exposure to ethanol causes a prolonged and severe decrement in serum GH which is possibly mediated at the level of secretion. In addition, there is attenuation in testosterone secretion. These data are all the more important since GH and testosterone play critical roles in organ maturation during this stage of development. Journal of Endocrinology (1997) 152, 477–487

scholarly journals Acute ethanol effects on neural encoding of reward size and delay in the nucleus accumbens

2016 ◽  
Vol 116 (3) ◽  
pp. 1175-1188 ◽  
Author(s):  
Andrea L. Gutman ◽  
Sharif A. Taha
Keyword(s):  
Nucleus Accumbens ◽  
Lever Press ◽  
Central Element ◽  
Ethanol Administration ◽  
Operant Response ◽  
Neural Firing ◽  
Neural Encoding ◽  
Acute Ethanol ◽  
Lever Pressing

Acute ethanol administration can cause impulsivity, resulting in increased preference for immediately available rewards over delayed but more valuable alternatives. The manner in which reward size and delay are represented in neural firing is not fully understood, and very little is known about ethanol effects on this encoding. To address this issue, we used in vivo electrophysiology to characterize neural firing in the core of the nucleus accumbens (NAcc) in rats responding for rewards that varied in size or delay after vehicle or ethanol administration. The NAcc is a central element in the circuit that governs decision-making and importantly, promotes choice of delayed rewards. We found that NAcc firing in response to reward-predictive cues encoded anticipated reward value after vehicle administration, but ethanol administration disrupted this encoding, resulting in a loss of discrimination between immediate and delayed rewards in cue-evoked neural responses. In addition, NAcc firing occurring at the time of the operant response (lever pressing) was inversely correlated with behavioral response latency, such that increased firing rates were associated with decreased latencies to lever press. Ethanol administration selectively attenuated this lever press-evoked firing when delayed but not immediate rewards were expected. These effects on neural firing were accompanied by increased behavioral latencies to respond for delayed rewards. Our results suggest that ethanol effects on NAcc cue- and lever press-evoked encoding may contribute to ethanol-induced impulsivity.

scholarly journals Acute ethanol exposure induces behavioural differences in two zebrafish (Danio rerio) strains: A time course analysis

2014 ◽  
Vol 259 ◽  
pp. 174-185 ◽  
Author(s):  
Emanuela Pannia ◽  
Steven Tran ◽  
Mindy Rampersad ◽  
Robert Gerlai
Keyword(s):  
Danio Rerio ◽  
Time Course ◽  
Ethanol Exposure ◽  
Acute Ethanol
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