Effect of acute ethanol or acetaldehyde adminstration on the uptake, release, metabolism and turnover rate of norepinephrine in rat brain

Thadani, Pushpa V.; Truitt, Edward B.

doi:10.1016/0006-2952(77)90059-4

Cited by 43 publications

(14 citation statements)

References 16 publications

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“…Table 1 and Fig. 1 (11,12) or an increase in a release of NE (13). Simultaneous assay of DBH activity, however, revealed that its activity tended to decrease in this region.…”

Section: Discussionmentioning

confidence: 86%

Effects of ethanol on catecholamine levels and related enzyme activities in different brain regions of rats.

Yamanaka

Egashira

1982

Jpn.J.Pharmacol

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Abstract-The effects of ethanol on the contents of norepinephrine (NE) and dopamine (DA) and the activities of related enzymes in the various regions of rat brains with different doses and mode of administration of ethanol were investigated. In acute ethanol intoxication, steady-state levels of NE were not altered. Continuous ethanol intoxication, however, significantly reduced NE contents and tended to decrease the activity of dopamine-Q-hydroxylase in the hippocampus. The decrease in NE con tents became more significant during ethanol withdrawal, especially in the medulla oblongata and the striatum. DA contents were increased in the brain-stem region in all ethanol-treated rats. The increase in DA contents correlated with the increase in tyrosine hydroxylase activity. The present data suggest that the dopaminergic system may contribute to the develop ment of physical dependence on ethanol.

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“…Table 1 and Fig. 1 (11,12) or an increase in a release of NE (13). Simultaneous assay of DBH activity, however, revealed that its activity tended to decrease in this region.…”

Section: Discussionmentioning

confidence: 86%

Effects of ethanol on catecholamine levels and related enzyme activities in different brain regions of rats.

Yamanaka

Egashira

1982

Jpn.J.Pharmacol

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“…14, 23]. It has been suggested that the turnover rate o f norepinephrine is reduced following acute administration of ethanol in both peripheral and central ner vous systems as evidenced by high postinjec tion levels of labeled norepinephrine and low levels of its metabolites in these areas [24,26], Several reports indicate that the rate of metabolism o f catecholamines changes dur ing the first 90-180 min following acute ad ministration o f ethanol [11,26,31], To ex amine whether responsiveness to P-adrenergic stimulation also changes temporally fol lowing treatment with ethanol, isoproterenol was administered at both 10 and 90 min fol lowing administration o f ethanol and ther moregulatory responses recorded. Injection o f isoproterenol at 10 min after treatment with ethanol significantly attenuated the re duction in Tco accompanying administration of ethanol ( fig.…”

Section: Discussionmentioning

confidence: 99%

β-Adrenergic Responsiveness in the Rat following Acute Administration of Ethanol

Spiers¹,

Fregly²,

Barney³

1986

Pharmacology

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Ethanol has been shown to induce a hypothermia in rats maintained in air at 26 °C. The objective of the present study was to assess the metabolic responsiveness of ethanol-treated rats to administration of isoproterenol, a β-adrenoceptor agonist, and to assess whether ethanol per se, or the hypothermia accompanying its administration, contribute to changes in β-adrenergic responsiveness. In the present study, administration of ethanol (3 g/ kg, i.p.) reduced both colonic temperature (T_co) and rate of oxygen consumption (metabolic rate) of rats maintained at 26 °C to levels below those of saline-treated controls within 20 min after treatment. Maximal decreases in both parameters occurred within approximately 40 min. Administration of isoproterenol (50 μg/kg, s.c.) 10 min after treatment with either ethanol or saline was accompanied by an increase in the metabolic rates of both groups, although the magnitude of the increase in the ethanol-treated group was less than that of controls. Maximal increases in tail skin temperatures (T_sk) following treatment with isoproterenol were similar in both groups but an increase in T_sk occurred earlier in the ethanol-treated group. T_co increased after treatment with isoproterenol in the saline-treated group but decreased in the ethanol-treated group. When isoproterenol was administered 90 min after treatment with ethanol, increases in metabolic rate, T_sk, and T_co were similar in both groups, although the increase in T_sk of ethanol-treated animals was delayed until T_co reached pretreatment level. Exposure to 30 °C minimized ethanol-induced hypothermia. At this temperature the metabolic responses to administration of isoproterenol at 90 min after treatment with ethanol did not differ significantly between the two groups. These results suggest that the metabolic responsiveness to administration of a β-adrenoceptor agonist is not altered by prior treatment with ethanol but is affected by the hypothermia accompanying its administration.

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“…Acetaldehyde, a toxic by-product of ethanol metabolization, has been described as a causative agent of the alterations to the CNS during its consumption (Hunt, 1996;Bergamaschi et al, 1988;Zimatkin & Deitrich, 1997;Thadani & Truitt, 1977;Heap et al, 1995). Its consequences can be divided into two categories: the first is the direct binding to proteins (Jennett et al, 1987;McKinnon et al, 1987;Nakamura et al, 2003;Zimatkin et al, 1992), nucleic acids (Wang et al, 2000) and phospholipids (Trudell et al, 1990(Trudell et al, , 1991Kenney, 1982Kenney, , 1984, and the second is the indirect action of ethanol oxidation, which produces inhibition of the endogenous production of acetaldehyde.…”

Section: Introductionmentioning

confidence: 99%

Ethanol Intake and Toxicity: In Search of New Treatments

et al. 2017

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SANDOVAL, C.; VÁSQUEZ, B.; MANDARIM-DE-LACERDA, C. & DEL SOL, M.Ethanol intake and toxicity: In search of new treatments. Int. J. Morphol., 35(3):942-949, 2017. SUMMARY:Prolonged alcohol consumption has consequences on the liver, producing necrotic precipitates and fibrosis, on the pancreas, causing the pancreatic acini to atrophy and destroying insulin-producing cells, and on the central nervous system (CNS), causing the gray and white matter in the frontal lobes of the brain and cerebellum to atrophy. Generally, alcohol is metabolized via oxidative pathways, where the enzymes alcohol dehydrogenase and aldehyde dehydrogenase participate during its metabolization in the liver and CNS, or via nonoxidative pathways during its metabolization in the pancreas. Ethanol metabolism can produce oxidative stress and tissue damage mediated by free radicals, causing morphological and functional alterations in the liver. In the pancreas, it can cause progressive and irreversible damage affecting the endocrine and exocrine functions, a result of the activation of the stellate cells, which are activated directly by alcohol, causing pancreatic fibrosis. In the CNS ethanol can bind directly to proteins, nucleic acids and phospholipids to develop its pathogenesis. The effects produced by alcohol can be counteracted by supplementation with antioxidants, which reduce the inflammation and areas of focal necrosis in the liver, inhibit the activation of pancreatic stellate cells, and reduce oxidative stress in the CNS. Additionally, in order to reduce the negative effects associated with alcohol consumption, recent studies have suggested the administration of antioxidants as a treatment strategy.

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Effect of acute ethanol or acetaldehyde adminstration on the uptake, release, metabolism and turnover rate of norepinephrine in rat brain

Cited by 43 publications

References 16 publications

Effects of ethanol on catecholamine levels and related enzyme activities in different brain regions of rats.

Effects of ethanol on catecholamine levels and related enzyme activities in different brain regions of rats.

β-Adrenergic Responsiveness in the Rat following Acute Administration of Ethanol

Ethanol Intake and Toxicity: In Search of New Treatments

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Effect of acute ethanol or acetaldehyde adminstration on the uptake, release, metabolism and turnover rate of norepinephrine in rat brain

Cited by 43 publications

References 16 publications

Effects of ethanol on catecholamine levels and related enzyme activities in different brain regions of rats.

Effects of ethanol on catecholamine levels and related enzyme activities in different brain regions of rats.

&beta;-Adrenergic Responsiveness in the Rat following Acute Administration of Ethanol

Ethanol Intake and Toxicity: In Search of New Treatments

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β-Adrenergic Responsiveness in the Rat following Acute Administration of Ethanol