Acute ethanol administration induces changes in TRH and proenkephalin expression in hypothalamic and limbic regions of rat brain

2000 ◽  
Vol 37 (5-6) ◽  
pp. 483-496 ◽  
Author(s):  
P de Gortari ◽  
M Méndez ◽  
I Rodrı́guez-Keller ◽  
L Pérez-Martı́nez ◽  
P Joseph-Bravo
Keyword(s):  
Rat Brain ◽  
Ethanol Administration ◽  
Acute Ethanol ◽  
Limbic Regions

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 Ethanol-Induced Changes in Edema and Metabolite Concentrations in Rat Brain

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Huimin Liu ◽  
Wenbin Zheng ◽  
Gen Yan ◽  
Baoguo Liu ◽  
Lingmei Kong ◽  
...  
Keyword(s):  
Rat Brain ◽  
Frontal Lobes ◽  
Brain Regions ◽  
Ethanol Administration ◽  
Resonance Spectroscopy ◽  
Cytotoxic Edema ◽  
Acute Ethanol ◽  
Adc Values ◽  
Cerebral Metabolites

The aim of this study is to describe the acute effects of EtOH on brain edema and cerebral metabolites, using diffusion weight imaging (DWI) and proton magnetic resonance spectroscopy (1H-MRS) at a 7.0T MR and to define changes in apparent diffusion coefficient (ADC) values and the concentration of metabolites in the rat brain after acute EtOH intoxication. ADC values in each ROI decreased significantly at 1 h and 3 h after ethanol administration. ADC values in frontal lobe were decreased significantly compared with other regions at 3 h. For EtOH/Cr+PCr and cerebral metabolites (Cho, Tau, and Glu) differing over time, no significant differences for Ins, NAA, and Cr were observed in frontal lobes. Regression analysis revealed a significant association between TSEtOH/Cr+PCrand TSCho, TSTau, TSGlu, and TSADC. The changes of ADC values in different brain regions reflect the process of the cytotoxic edema in vivo. The characterization of frontal lobes metabolites changes and the correlations between TSEtOH/Cr+PCrand TSCho, TSTau, and TSGluprovide a better understanding for the biological mechanisms in neurotoxic effects of EtOH on the brain. In addition, the correlations between TSEtOH/Cr+PCrand TSADCwill help us to understand development of the ethanol-induced brain cytotoxic edema.

Effects of acute ethanol administration on methionine–enkephalin expression and release in regions of the rat brain

Neuropeptides ◽  
2010 ◽  
Vol 44 (5) ◽  
pp. 413-420 ◽  
Author(s):  
M. Méndez ◽  
I.G. Barbosa-Luna ◽  
J.M. Pérez-Luna ◽  
A. Cupo ◽  
J. Oikawa
Keyword(s):  
Rat Brain ◽  
Ethanol Administration ◽  
Methionine Enkephalin ◽  
Acute Ethanol

Glucose transporters and glucose utilization in rat brain after acute ethanol administration

2000 ◽  
Vol 15 (3) ◽  
pp. 211-222 ◽  
Author(s):  
Raj K. Handa ◽  
Mary R. DeJoseph ◽  
Leela D. Singh ◽  
Richard A. Hawkins ◽  
Sant P. Singh
Keyword(s):  
Rat Brain ◽  
Glucose Utilization ◽  
Glucose Transporters ◽  
Ethanol Administration ◽  
Acute Ethanol

Effect of acute ethanol administration on histone acetylation in mouse brain

2010 ◽  
Vol 68 ◽  
pp. e422-e423
Author(s):  
Keisuke Mizuo ◽  
Yoko Nishitani ◽  
Ryuichi Katada ◽  
Shunichiro Okazaki ◽  
Kenji Tateda ◽  
...  
Keyword(s):  
Histone Acetylation ◽  
Mouse Brain ◽  
Ethanol Administration ◽  
Acute Ethanol

scholarly journals Biphasic effect of acute ethanol administration on rat liver tyrosine-2-oxoglutarate aminotransferase activity

1980 ◽  
Vol 186 (3) ◽  
pp. 755-761 ◽  
Author(s):  
A A B Badawy ◽  
B M Snape ◽  
M Evans
Keyword(s):  
Enzyme Activity ◽  
Rat Liver ◽  
Actinomycin D ◽  
Tyrosine Aminotransferase ◽  
Ethanol Metabolism ◽  
Ethanol Administration ◽  
Aminotransferase Activity ◽  
Biphasic Effect ◽  
Initial Decrease ◽  
Acute Ethanol

1. Acute ethanol administration causes a biphasic change in rat liver tyrosine aminotransferase activity. 2. The initial decrease is significant with a 200 mg/kg dose of ethanol, is prevented by adrenoceptor-blocking agnets and by reserpine, but not by inhibitors of ethanol metabolism, and exhibits many of the characteristics of the inhibition caused by noradrenaline. 3. The subsequent enhancement of the enzyme activity by ethanol is not associated with stabilization of the enzyme, but is sensitive to actinomycin D and cycloheximide. 4. It is suggested that the initial decrease in aminotransferase activity is caused by the release of catecholamines, whereas the subsequent enhancement may be related to the release of glucocorticoids.

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