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At least 37 records · Page 2Linked to original sources
PubMed1978

Comparison of the excitatory and anaesthetic effects of ethanol in C57BL/6 and BALB/c mice; relation to blood ethanol concentration.

Ethanol increased the exploratory locomotion of BALB/c mice over a wide dose range (1.15--3.1 g/kg orally), whereas only a 2.31 g/kg dose of ethanol increased the locomotion of C57BL/6 mice. After 1.15 g/kg of ethanol the blood concentrations in BALB/c and C57BL/6 mice were 65 +/- 11 and 68 +/- 13 mg %, respectively, and after 2.3 g/kg--the corresponding concentrations were 156 +/- 26 and 142 +/- 14 mg % (mean +/- SEM). Doses of 3.8 and 4.6 g/kg inhibited the exploratory locomotion of mice of both strains to an equal extent. The induction time and the duration of ethanol-induced anaesthesia, as well as the blood ethanol concentrations (428 +/- 40 and 446 +/- 40 mg %, respectively, at the onset of anaesthesia) were similar in mice of both strains after a 5.4 g/kg dose. However, motor excitement before anaesthesia was observed only in the BALB/c mice. It is suggested that the observed strain differences in response to ethanol are due to low responsivity of C57BL/6 mice to the excitatory action of ethanol and are not caused by differences in the rate of its metabolism. Apparently, the excitatory and anaesthetic effects of ethanol are under separate genetic control mechanisms.

Administration, Oral↗
PubMed1979

Electrophysiological responses to ethanol, pentobarbital, and nicotine in mice genetically selected for differential sensitivity to ethanol.

Cortical electroencephalographic (EEG) changes induced by ethanol (4.3 and 1.4 g/kg, ip), pentobarbital (50 and 16 mg/kg), and nicotine (1.0 g/kg) were examined in long-sleep (LS) and short-sleep (SS) mice that were genetically selected for differential sleep times induced by a hypnotic dosage of ethanol. Ethanol (4.3 g/kg) caused EEG changes that paralleled the behavioral differences, whereas no differences between selected lines were observed following the activating dose (1.4 g/kg). Data support the notion that the known difference in ethanol sleep times is due not to greater SS sensitivity to ethanol activation but rather to greater LS sensitivity to ethanol hypnosis. No differences between selected lines were observed following 50 mg/kg pentobarbital, which again parallels previous behavioral data. The SS mice were more responsive to pentobarbital activation (16 mg/kg). Nicotine more severely reduced EEG power and heart rate in LS mice; a continuous iv infusion of nicotine elicited a distinct pattern of behavioral stereotypy for each selected line, with more profound motor and reflex depression in LS mice. The lines do not differ in rate of nicotine metabolism, hence they must differ in central nervous system sensitivity to nicotine. Thus, lines of mice selectively bred for differential sensitivity to ethanol also display marked differences in electrophysiological and behavioral responses to nicotine.

Animals↗
PubMed1975

Effects of chronic ethanol treatment and thyroxine administration on ethanol metabolism and liver oxidative capacity.

Chronic administration of ethanol to rats leads to an increase in the rate of ethanol metabolism in vivo and in vitro. In vitro studies in liver slices showed that ouabain, an inhibitor of the Na++K+-activated adenosine triphosphatase, can completely block the extra ethanol metabolism in the livers of the treated animals only in the presence of ouabain. Administration of thyroxine led to an increase in the rate of ethanol metabolism when measured both in vitro and in vivo. This effect was biphasic; an activation occurred only with low doses of thyroxine but disappeared after administration of larger doses. Alcohol dehydrogenase activity in the liver of the animals treated with large doses of thyroxine was found to be significantly reduced. With the doses used (50-1000 mug/kg), thyroxine also increased the rate of oxygen consumption as measured in liver slices. However, a biphasic effect did not occur; a near maximum activation on the rate of oxygen consumption occurred with low doses of thyroxine (100 mug/kg). Oxygen consumption was also found to be increased in the liver of animals chronically treated with ethanol. A maximal effect was produced after 18 to 21 days of treatment. For both ethanol and thyroxine-treated animals, an increased rate of oxygen consumption occurred with a concomitant loss of dinitrophenol effect. Mitochondrial alpha-glycerophosphate oxidase was found to be increased in the liver of animals treated with ethanol or with thyroxine. In these two groups, this enzymatic activity appeared to be less affected by the treatment than the dinitrophenol-activated respiration.

Alcohol Oxidoreductases↗
PubMed1979

Rats bred for ethanol sensitivity: impairment of swimming by ethanol and pentobarbital.

Rats selectively bred for disparate degrees of ethanol-induced depression of spontaneous locomotor activity ('most affected' = MA; 'least affected' = LA) were trained on a swim task. Undrugged rats of the MA line swam significantly faster than rats of the LA line. Ethanol, 0.0--2.25 g/kg i.p., produced dose-dependent increases in swim time in rats of the 13 generation (F13). Averaged over trials, these increases were greater in LA than in MA rats and greater in males than in females, but there was no sex difference in peak impairment. Increases in swin time were uncorrelated with predrug performance. These findings were confirmed in younger F17 rats receiving 1.75 g EtOH/kg i.p. Although the lines differed in ethanol-induced impairment, F17 males of the two lines were not differentially impaired by pentobarbital (12.5--22.5 mg/kg, i.p.). The existence of task-dependent line differences in ethanol sensitivity emphasizes the nonunitary nature of ethanol-induced 'behavioral depression.'

Animals↗
PubMed1975

Ethanol as a reinforcer for rats: effects of concurrent access to water and alternate positions of water and ethanol.

Water and ethanol solutions were concurrently made available on a continuous reinforcement schedule to 4 food-deprived male albino rats during daily 1-hr sessions in an operant conditioning chamber equipped with 2 levers and 2 liquid dippers. The number of ethanol reinforcements substantially exceeded the number of water reinforcements for each rat at each concentration studied (8, 16, and 32% w/v). Water reinforcements were low in number and did not vary with ethanol concentration. As the ethanol concentration was increased, the number of ethanol reinforcements obtained decreased, while the quantity consumed (mg/100 g of body weight/hr) increased. The highest rate of responding occurred at the beginning of the session.

Alcohol Drinking↗
PubMed1978

Effect of adrenergic beta receptor blockade on ethanol elimination and on ethanol-induced changes in carbohydrate and lipid metabolism in man.

The effect of adrenergic beta receptor blockade on the elimination rate of ethanol was studied in seven healthy young men. The studies were performed before and after 14 days of propranolol 240 mg/day: the ethanol was given per-orally--0.8 mg/kg b.w. The blood concentration of ethanol, glucose, lactate and glycerol, and the plasma concentration of free fatty acids and triglycerides were followed in samples from the superior vena cava taken every 20 min for four hours. The splanchnic hepatic blood flow was estimated with a single i.v. injection of indocyanine green. The absorption rate, absorption fraction and elimination rate of ethanol were not changed by propranolol. The splanchnic hepatic blood flow was significantly reduced (mean 19 per cent) during beta receptor blockade. The ethanol-induced change in the concentration of glucose, lactate and free fatty acids was affected by propranolol, the time-concentration curves for glucose and lactate being significantly elevated and that for free fatty acids being significantly reduced. The time-concentration curves for glycerol and triglycerides did not differ in the two studies.

Adolescent↗
PubMedDate not supplied

Intraventricular ethanol and ethanol intake: a behavioral and radiographic study.

Ethanol (10% w/v) was infused intraventricularly at a rate of 11 mul/hr, delivered over 50 sec every 10 min for 10 days into 5 Sprague-Dawley and 5 Wistar rats. Thereafter, preference testing with ascending concentrations of alcohol solutions vs . water vs. food gave no significant differences between treated and sham-operated controls, in contradiction to previously reported increases in alcohol consumption. Ethanol's rate of elimination from the ventricle and its pattern of diffusion into the brain were determined using radioactive ethanol: elimination from the brain is rapid with a half-like of 24 to 35 sec, and the amount diffused throughtout the brain small, with a maximal concentration in any one section of 0.004% (such a concentration is at least 20 times less than would result from a moderately intoxicating parenteral dose of ethanol). The character of the elimination and the lack of effect on alcohol intake found here indicate that intraventricularly administered ethanol is a technique with no usefulness in elucidating the processes affecting alcohol addiction.

Alcohol Drinking↗
PubMed1976

Metabolism of 1-3H-ethanol by isolated liver cells. Time-course of the transfer of tritium from R,S-1-3H-ethanol to lactate and beta-hydroxybutyrate.

Parenchymal cells isolated from the liver of 24 h fasted rats were incubated with 65 mM R,S-1-3H -ethanol plus 3 mM pyruvate as substrates in the absence and presence of 1.7 mM 4-methylpyrazole. Metabolite levels and the time-course of the transfer of tritum from ethanol to lactate and beta-hydroxybutyrate was measured during the first 15 min of ethanol metabolism. The time-course of the loss of tritium from 2-3H-L-lactate and 3-3H-beta-D-hydroxybutyrate in experiments identical to the above-mentioned was estimated. A GLC method for the isolation of lactate and beta-hydroxybutyrate and the preparation of 2-3H-L-lactate and O-3H-beta-D-hydroxybutyrate is described. The incorporation rate of tritium from ethanol into lactate and beta-hydroxybutyrate decreased with time. Addition of 4-methyl-pyrazole decreased the incorporation rate roughly proportional to the decrease in ethanol and acetaldehyde metabolism. The observed incorporation rates of tritium to lactate were corrected for the detritiation rates measured in experiments with I-3H-L-lactate and 3-3H-beta-D-hydroxybutyrate as substrates. The rate of extramitochondrial acetaldehyde oxidation was calculated from the corrected initial rates of incorporation of tritium into lactate to 0-0.4 mumol min-1 (ml of cells)-1.

Acetaldehyde↗
PubMed1975

Brain and blood levels of ethanol and acetaldehyde in strains of mice with different preferences for ethanol.

The ethanol level in brain and blood and the blood level of acetaldehyde upon waking from an anesthetic dose of ethanol were found to be significantly higher in C57BL/6J mice which prefer to drink ethanol solution over water than in DBA/2J mice which avoid the drinking of an ethanol solution. The brain level of acetaldehyde did not differ significantly between the two mouse strains. Possible explanations for the difference in brain sensitivity toward ethanol are discussed.

Acetaldehyde↗
PubMed1977

Noradrenergic mediation of the positive reinforcing properties of ethanol: I. Suppression of ethanol consumption in laboratory rats following dopamine-beta-hydroxylase inhibition.

Ethanol-drinking rats were injected with the dopamine-beta-hydroxylase inhibitor FLA-57, prior to free-choice presentations of ethanol and water either for 5 alternate days (25 or 40 mg/kg i.p.) or for 5 consecutive days (45 mg/kg i.p.). In all cases, the FLA-57 treated animals markedly attenuated ethanol consumption while vehicle-injected controls showed no change from baseline. In the post-injection period ethanol intake gradually returned to baseline levels. Biochemical assays revealed that whole brain norepinephrine levels following injection of FLA-57 (15-60 mg/kg i.p.) were significantly depressed while dopamine and serotonin levels were slightly increased. It is suggested that norepinephrine may be involved in the mediation of the positive reinforcing properties of ethanol regulating its self-administration.

Alcohol Drinking↗
PubMed1977

Noradrenergic mediation of the positive reinforcing properties of ethanol: II. Extinction of ethanol-drinking behavior in laboratory rats by inhibition of dopamine-beta-hydroxylase. Implications for treatment procedures in human alcoholics.

Following stabilization of consumption of a 15% (v/v) ethanol solution in a free-choice with water, rats were presented with a forced-choice of ethanol for 10 consecutive alternate days. Prior to each forced-choice presentation experimental animals were injected with the non-toxic dopamine-beta-hydroxylase inhibitor FLA-57 (30 mg/kg i.p.) while control animals received only vehicle injections. At the termination of the injection phase when ethanol was again made available in a free-choice with water, ethanol consumption for the FLA-57 treated animals was markedly suppressed. These data are interpreted in terms of extinction resulting from the procedure whereby performance of the ethanol drinking response was perpetuated by force with the pharmacological reinforcing properties being blocked by FLA-57-induced depletions of norepinephrine. Applications of these procedures in the treatment of human alcoholics are discussed.

Alcohol Drinking↗
PubMed1976

Inhibition of hepatic uptake of alpha aminoisobutyric acid by ethanol: effects of pyrazole and metabolites of ethanol.

Ethanol inhibits the uptake of AIB by the isolated perfused rat liver. However, if the metabolism of ethanol is blocked by pyrazole, there is no reduction in accumulation of AIB by the liver. Acetaldehyde and acetate, metabolites of ethanol have no effect on AIB uptake by the liver. The inhibition of urea synthesis by ethanol is also prevented by pyrazole. Neither of the metabolites of ethanol inhibit urea synthesis in the isolated liver.

Acetaldehyde↗
PubMed1979

On the role of ascending dopamine systems in the control of voluntary ethanol intake and ethanol intoxication.

Selective lesions of the ascending dopamine pathways were made by bilateral injection of the neurotoxin 6-OHDA (8 micrograms/4 microliters). Catecholamine fluorescence histochemistry revealed a marked degeneration of the ascending mesostriatal and mesolimbic dopamine systems, while the hypothalamic dopamine and noradrenaline nerve terminals were unaffected. After recovery of feeding and drinking behaviors the voluntary ethanol intake was not different from that of the controls. The time of ethanol-induced narcosis and the extent of ethanol-induced hypothermia were not affected. In contrast, in a tilting-plane test conducted two months after the operation, ethanol impaired the performance of the 6-OHDA-treated rats significantly less than that of the controls. This finding suggests a role for the ascending dopamine neurons to the forebrain in the intoxicating effect of ethanol.

Alcohol Drinking↗
PubMed1978

Interaction between d-amphetamine and ethanol with respect to locomotion, stereotypies, ethanol sleeping time, and the kinetics of drug elimination.

The interaction between d-amphetamine and ethanol with respect to locomotor activity, stereotyped behavior, and sleeping time was investigated in rats. Ethanol 0.8 g/kg i.p. enhanced and prolonged locomotor activity produced by d-amphetamine 1 mg/kg s.c. The increased motility after 5 mg/kg d-amphetamine was not influenced by alcohol 0.8 g/kg i.p. or 3.2 g/kg orally, but slightly protracted. Stereotyped head and paw movements, as well as stereotyped licking, were distinctly strengthened and protracted by 3.2 g/kg ethanol orally. The modified d-amphetamine motility and stereotypies can be explained by alcohol-induced proloneation of the life of d-amphetomine. The effect is produced by alcohol's inhibition d-amphetamine p-hydroxylation in rat liver. After 3.2 g/kg ethanol i.p., the sleeping time of male rats amounted to 153 min. Simultaneous administration of 5 mg/kg d-amphetamine s.c. reduced the sleeping time to 84 min. This is obviously based on a central antagonism.

Animals↗
PubMedDate not supplied

The adaptive increase in ethanol metabolism due to pretreatment with ethanol: a rapid phenomenon.

Simple models were developed to study changes in oxygen uptake in perfused rat liver and increases in ethanol metabolism in vivo. Results obtained 2.5 hours following a large dose of ethanol were quantitatively similar to those seen after 24 hours or 5 weeks. The rapidity of the increase indicated that SIAM represents an activation rather than an adaptation. Pathways responsible for the swift increase in alcohol metabolism (SIAM) in the perfused rat liver were investigated through the use of ouabain and were found to be related to diminished glycolysis and another unidentified pathway. Investigation of pathways responsible for the increase in ethanol metabolism in vivo following ethanol treatment implicated the alcohol dehydrogenase pathway as that mainly responsible for the adaptive increase, although a catalase-H2O2-dependent component was also involved. The rate of NADH reoxidation generally appeared to be the rate-limiting step. In addition, the genetic aspect of SIAM was indicated through selective breeding resulting in F1 generations of non-SIAM and SIAM rats.

Alcohol Drinking↗
PubMed1975

Effect of pyrazole on ethanol metabolism in ethanol-tolerant rats.

Adult male rats were pair-fed liquid diets, providing 37% of calories as ethanol or sucrose, for 1 month. Alcohol dehydrogenase (ADH) activity in the cytosol fractions of liver homogenates from the two groups did not differ with respect to total activity per 100 g body weight, Km for ethanol, or Ki for pyrazole. Other rats, fed in the same way, were fasted for 18-24 H, then given an intraperitoneal injection of pyrazole followed 1 h later by an injection of ethanol, 3g/kg. Blood alcohol curves showed an unexplained slower rise to maximum level in the chronic alcohol group. Both groups showed a period of several hours in which the blood alcohol stayed at the respective maximum concentrations, which were higher in the control group. After 7-8h the alcohol concentration began to fall in both groups, significantly more rapidly in the chronic alcohol-fed animals. A kinetic analysis shows that the results are adequately explained by the known effects of pyrazole on the ADH-mitochondrial system. The results are interpreted as evidence against the function of any microsomal ethanol oxidizing system in vivo.

Alcohol Oxidoreductases↗
PubMed1977

Effects of ethanol on urinary arginine vasopressin excretion in two rat strains selected for their different ethanol preferences.

The effects of ethanol on urinary excretion of arginine vasopressin (AVP), sodium, and potassium were investigated in two rat strains specially selected for their different alcohol preferences. The alcohol preferring (AA) strain excreted more AVP and the water preferring (ANA) strain more urine and sodium during six hours after ethanol intubation (2.4 g/kg b.w.; 20% v/v). The data is insufficient to establish a causal relationship between differences in water and electrolyte metabolism and voluntary ethanol consumption.

Animals↗