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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.'
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PMID:Rats bred for ethanol sensitivity: impairment of swimming by ethanol and pentobarbital. 11 34

Ethanol through its primary catabolite, acetaldehyde, competitively inhibits oxidation of aldehyde dehydrogenase substrates. As a consequence biogenic amines form increased quantities of alcohols rather than the corresponding acids. During this biotransformation, condensation reactions between deaminated and intact amines may occur which can yield tetrahydropapaverolines. These compounds are closely related to precursors of opioids which is cause to link ethanol abuse to morphine addiction. There is, however, no pharmacological or clinical evidence suggesting similarities between ethanol dependence or opiod addiction. Acetaldehyde plays an additional role in alkaloidal formation in vitro. Biogenic amines may react with acetaldehyde to form isoquinoline or carboline compounds. Some of these substances have significant pharmacological activity. Furthermore, they may enter neural stores and displace the natural neurotransmitter. Thus, they can act as false neurotransmitters. Some investigators believe that chronic ethanol ingestion leads to significant formation of such aberrant compounds which may then upset autonomic nervous system balance. This disturbance may explain the abnormal sympathetic activity seen in withdrawal. While these ideas about the etiology of alcohol abuse have a definite appeal, they are naturally based on in vitro preliminary work. Much study of the quantitative pharmacology of these compounds in animals is required before judgement can be made as to the merits of the proposed hypotheses. In the meantime, pharmacological studies on the ability of ethanol to depress respiration in the mouse has revealed that unlike opioids or barbituates, respiratory depression induced by ethanol requires the presence in brain of serotonin. This neurotransmitter also mediates the respiratory effects of several other alcohols but curiously, not chloral hydrate, yet this compound is purported to alter biogenic amine metabolism much like ethanol. Thus, the response to ethanol can be pharmacologically separated from other major narcotic classes such as opioids and barbiturates by respiratory depression effects. The specific requirement for serotonin mediation exhibited by ethanol and several other alcohols opens the door for a rational therapeutic approach to the treatment of alcohol abuse. At the same time, this finding tends to lessen the probability that alcoholism is in some way connected with the formation of addictive alkaloids.
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PMID:Interaction of biogenic amines with ethanol. 23 68

The effect of small doses of ethanol (0.4 g/kg) on auditory evoked transient and sustained potentials was studied. Tones of 1-second duration were presented in trains of four stimuli (interstimulus interval = 1 second; intertrain interval = 1 minute). The electroencephalogram was recorded from derivation Cz-Al. Ethanol depressed the transient responses both at the first stimulus of the train and during repeated stimuli. The sustained potentials elicited by the first stimuli of the train were not affected by ethanol, whereas the sustained potentials elicited by repeated stimuli were larger in amplitude under the influence of ethanol than during control experiments. It is suggested that the decrease of the transient responses under the influence of ethanol is mainly due to depression of the reticular formation, whereas the increase of sustained potentials reflects ethanol-induced release of intracortical inhibition.
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PMID:Auditory evoked transient and sustained potentials in the human EEG: II. Effects of small doses of ethanol. 29 58

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.
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PMID:Electrophysiological responses to ethanol, pentobarbital, and nicotine in mice genetically selected for differential sensitivity to ethanol. 52 19

Physical dependence upon ehtanol induced in rats is in several respects similar to the tremulous and convulsive components of the ethanol withdrawal syndrome observed in man. These include short duration of the induction period, pattern of continuous ethanol consumption, rectilinear clearance of blood ethanol during prodromal detoxication phase and the onset of the ethanol dependence phase at relatively high blood ethanol concentrations. During the ethanol withdrawal period two phases are distinguished in both species: (1) Prodromal detoxication phase characterized by a spectrum of signs and responses of ethanol intoxication. (2) Ethanol dependence phase characterized by a spectrum of withdrawal signs and reactions. The successive onset and disappearance of the two sets of signs and reactions during both phases of the ethanol withdrawal period constitute a continuum of effects and responses and represent a reversal in the CNS function from the extremes of ethanol depression to the extremes of hyperexcitability.
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PMID:Comparison of ethanol withdrawal syndrome in humans and rats. 59 77

Ethanol (1 g/kg, iv) produced a peak depression of acetylcholine release from the cat sensorimotor cortices within 30 min of the ethanol administration but recovery to control levels occurred in the following 30 min. However, the concentrations of ethanol in the blood and in the solution bathing the cortex remained stable during this recovery period. This example of acute tolerance to ethanol is possibly related to the well-known acute tolerance that develops to the behavioural effects of ethanol.
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PMID:Acute tolerance to ethanol on the release of acetylcholine from the cat cerebral cortex. 68 92

In adult animals and man, both acute and chronic ethanol intake is associated with depression of myocardial performance. Accordingly, the cardiac effects of maternal ethanol infusions, in a manner comparable to common obstetric practice of inhibition of premature labor with ethano mighte for inhibition of premature labor, were evaluated in six chronically instrumented fetal sheep. Fetal and ewe arterial PO2, PCO2, and pH values remained within normal limits with infusion rates of 15 c.c. per kilogram of 10 per cent ethanol over two hours (blood ethanol = 110 mg. per cent) and 15 c.c. per kilogram over one hour (blood ethanol = 210 mg. per cent). Fetal instrument evaluation (for 14 to 30 days after operation) provided data concerning pressures and cardiac dimensions which allowed analysis of left ventricular performance. Ethanol produced a significant depression of the extent (p less than 0.01) and velocity (p less than 0.001) of left ventricular myocardial fiber shortening as well as in the mean rate of left ventricular myocardial fiber shortening as well as in the mean rate of left ventricular circumferential fiber shortening (p less than 0.01). These indices of cardiac contractility were depressed in the absence of changes in end diastolic diameter, left atrial pressure, and systemic arterial pressure. Thus, the practice of inhibition of premature labor with ethano6 might contribute to depressed myocardial performance in the neonatal period.
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PMID:Acute effects of maternal ethanol infusion on fetal cardiac performance. 99 81

1. Hypoxic and hypercapnic ventilatory drives were measured in eight healthy male subjects before and after ingestion of ethanol, in a dose of 17 mmol/kg body weight. 2. A significant decrease in hypoxic ventilatory drive was observed at 20 min after ethanol (P less than 0.05). A significant depression in hypercapnic drive was observed at 70 min after indigestion of ethanol (P less than 0.05). The mean peak blood ethanol (24mmol/1) occurred at 20 min, at which time the lowest mean hypoxic drive was recorded. 3. Ethanol in moderate doses produced a depression of both hypoxic and hypercapnic ventilatory drives in normal subjects. This suggests that ethanol may play a role in the precipitation of acute respiratory failure in certain patients in whom the ventilatory drive is already impaired, as in chronic airways obstruction.
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PMID:Effect of ethanol on the ventilatory responses to oxygen and carbon dioxide in man. 114 93

This paper reports findings relative to a simple, rapid and reproducible technique for the induction of physical dependence upon ethanol in the rat. The dependence was induced by intragastric intubation of 20% (w/v) ethanol solutions at 9-15 g/kg in 3-5 fractional doses daily for 4 days, maintaining blood ethanol concentrations above a threshold level sufficient to sustain observable sedation throughout the entire period of intubation. Two phases were distinguished during the withdrawal period: 1. Prodromal detoxication, characterized by a spectrum of signs and responses of diminishing severity, related to the decline in blood ethanol concentrations (mg/dl): death, greater than 640; coma, 780-460; loss of righting reflex, 640-400; ataxia 3-1, 570-250; sedation 340-190; neutrality, 220-130; 2. Ethanol dependence, characterized by a spectrum of withdrawal signs and reactions of progressively increasing severity as blood ehtanol concentration approached 100 mg/dl: hyperactivity, tremors, akinesia, spastic rigidity, and induced and spontaneous convulsions. A rapid sucession of two diverse clusters of signs and reactions represents a reversal of the central nervous system function from the extremes of ethanol intoxication (CNS depression) to the extremes of ethanol dependence (CNS hyperexcitability) during the withdrawal period. Both extremes may terminate in death.
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PMID:Induction of physical dependence upon ethanol and the associated behavioral changes in rats. 123 14

The influence of ethanol upon dynamics of rotatory (RN) and post-rotatory nystagmus (PRN), trunk pose-tonic reflexes and their vegetative (cardiac, respiratory) components was studied in chronic experiments on rabbits with the help of electronystagmo- and electromyography. Ethanol was administered once intra-abdominally (1 g/kg) and one time a day during 30 days. Alcohol concentration in blood was determined by gas-and-fluid chromatography. The animal which were given isotonic solution of sodium chloride in the same doses and quantities served as a control group. It was established that vestibular oculomotor reflexes are mainly facilitated in an acute period of ethanol administration, then their inhibition occurs. Besides, the changes of PRN are stronger expressed than those of RN. Labyrinth pose-tonic reflexes are more often inhibited under the influence of ethanol; their strongest depression was observed during the first hour after ethanol administration and on the 15th day of chronic alcoholization. In alcoholization the changes of vestibular-vegetative reaction occur; primary short-term weakening of vestibular influences upon cardiac rhythm and respiration with their subsequent increasing.
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PMID:[The effect of alcohol (ethanol) on the reactions of the vestibular system]. 130 40


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