Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The responses of men and women alcoholics to the Defense Mechanism Inventory showed that the women scored significantly higher in "turning against self" and the men in "turning against others." Although such differences may underlie reported sex differences in the incidence of depression and sociopathic personality disorder, they have also been found in studies of nonalcoholics and psychiatric outpatients.
J Stud Alcohol 1975 Mar
PMID:Defense mechanisms in men and women alcoholics. 23 86

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

The widespread use of ethyl alcohol suggests its potential importance in clinical medicine. There is no proven therapeutic effect in cardiac patients and its role as an etiologic factor in heart disease has been disputed over the years and attributed to coexistent malnutrition. The latter factor, however, has been dissociated from ethanol use in many patients with the cardiomyopathic form of heart failure. Major support for the role of ethanol as a toxic agent when used in large amounts for a prolonged period has been obtained in various species of animals, including the subhuman primate. Abnormalities include depression of ventricular function, and metabolic and morphologic changes that parallel the changes in humans with preclinical malfunction of the heart. While the mechanism of progression to heart failure or arrhythmias is not known, several factors may be associated. These include, particularly in males, the cumulative effects of ethanol alone or after intensified drinking episodes, simultaneous exposure to trace metals in excess, and occasional specific nutritional deficiency or superimposed infection. The low prevalence of clinical nutritional deficiency in patients with alcoholic cardiomyopathy and the infrequency of heart disease in patients with cirrhosis or neuropathy supports the view that the cardiac abnormality is commonly not dependent on malnutrition. Clinical data indicate that the cessation of alcohol intake may reverse the disease or interrupt its progression in many patients. However, the pathogenic process may continue unabated in some patients who become abstinent.
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PMID:The role of ethanol in cardiac disease. 32 69

Mice were placed on an immunization schedule known to result in the production of antibodies directed against a variety of barbiturates (antibody binding capacity = 2.71 pmole 3H-phenobarbital bound/ml undiluted serum). The pharmacologic response to barbiturate in these actively immunized mice and suitably treated controls was investigates using rotarod apparatus for monitoring CNS depression. It was found that the response to pentobarbital in actively immunized mice was decreased, as reflected by an increase in the time the mice remained on the rotarod and a shift of the dose--response curve to the right. The decreased pharmacologic response to pentobarbital was not the result of changes in levels of the hepatic drug metabolism components. Furthermore, the alteration of pharmacologic response in actively immunized mice was selective for barbiturate and did not modify the ataxia produced by administration of another depressant agent, ethanol.
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PMID:Pharmacologic response to pentobarbital in actively immunized mice. 40 75

The effects of various doses of ethanol (ETOH) on spontaneous locomotor activity (SLMA) in mice were measured using photocell activity chambers. Of the 4 i.p. doses injected, the 2 lowest doses (0.5 and 1.0 g/kg) stimulated SLMA, the next higher dose (2.0 g/kg) produced a biphasic effect of depression followed by stimulation, and the highest dose (4.0 g/kg) depressed SLMA. The mechanism of the biphasic effect of the 2.0 g/kg dose was studied in tests with central catecholamine antagonists at various doses 30 min before ETOH. Doses of 5, 10, and 20 mg/kg of propranolol, a beta-receptor blocker, significantly antagonized the depressant effect of ETOH but had no influence on the stimulant effect. High doses (10 and 20 mg/kg) of phentolamine, an alpha-receptor blocker, significantly antagonized the stimulant phase of ETOH action but had no significant effect on the depressant phase. All doses (0.062-0.250 mg/kg) of spiroperidol, a dopaminergic blocking drug, significantly enhanced the SLMA depression produced by ETOH. These results indicate that the SLMA-depressant effect of ETOH may be mediated by central "beta-type" receptors, that the SLMA-stimulant effect of ETOH may be mediated by central "alpha-type" receptors, and that at least part of ETOH's action may be due to dopaminergic mechanisms.
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PMID:Alteration of ethanol-induced changes in locomotor activity by adrenergic blockers in mice. 40 5

Preoperative folate levels were initially normal in 30 patients with gastrointestinal tract disease but fell within 48 h by 60-95% in 20 patients who received intravenous nutrition for 6-12 d with aminoacid-sorbitol-ethanol (ASE). This depression persisted in patients not given folate supplements. Folate levels in 10 control patients not given ASE showed only minimal decline. Haematological changes were reduced to a minimum in 10 patients given 0.5 mg i.v. folic acid daily whilst eight unsupplemented patients showed evidence of megaloblastic haemopoiesis. Three of these eight patients developed thrombocytopenia and/or leukopenia which was fatal in one patient.
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PMID:Acute folate deficiency associated with intravenous nutrition with aminoacid-sorbitol-ethanol: prophylaxis with intravenous folic acid. 41 77

The role of cholinergic neurons in the motor depressant effects of ethanol was examined. Choline chloride pretreatment (30-90 mg/kg i.p.) potentiated the hypomotility produced by 2 g/kg of ethanol. Physostigmine pretreatment (0.2 mg/kg i.p.) also enhanced the motor depression produced by ethanol. Conversely, in animals pretreated with scopolamine (0.25 and 0.5 mg/kg) the depressant effect of ethanol was less. The potentiation produced by choline was not associated with changes in levels of ethanol in blood. It is concluded that cholinergic neurons are involved in the motor activity changes produced by ethanol. Such a mechanism may operate in conjunction with the dopaminergic neuronal system.
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PMID:Cholinergic mediation of motor effects of ethanol in rats. 43 43

Studies of depression associated with oral contraceptive use present conflicting results. Individual susceptibility may affect psychiatric symptoms more than biochemical composition of the pill. In the authors' study 40 women without previous histories of depression were assigned to 4 regimens: 1) mestranol 80 mcg, norethisterone 1.0 mg; 2) pill 1 and pyridoxine; 3) mestranol 5 mcg, norethisterone 1.0 mg; and 4) pill 3 and pyridoxine. Alcohol and other chemicals were avoided. The 40 subjects completed self-reporting ratings on depression and a libido rating. 24 hour urine samples were collected on day 14 and 21 of the menstrual cycle. A brief psychiatric interview was conducted monthly. Adrenaline, noradrenaline, and 5 HIAA were measured throughout the year long study. 10 women completed 3 cycles. 20 of 10 complained of lethargy, loss of libido, irritability, and moodiness. The study concludes that biochemical and pharmacological effects affect a minority of women. A psychologic and negative placebogenic effect is possible. Depending on the composition of the contraceptive, a differential effect may occur. Sequential pills caused less depression than combination types.
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PMID:Oral contraceptives and depression. 44 Dec 35

The effect of taurine, of some of its precursors and major metabolic products on spontaneous locomotor activity were studied in mice. The effect of taurine and some analogues on certain ethanol-mediated responses were observed. Administration of taurine, 50 mg/kg, IP, did not significantly alter motility in experimental animals compared to controls. Behavioral depression was evident subsequent to injection of cysteine hydrochloride or taurocholic acid (50 mg/kg). Administration of taurocholic acid, 50 mg/kg, IP, 30 min prior to a narcotic dose of ethanol, 5 g/kg, IP, reduced the time required for the onset of ethanol-narcosis. Pretreatment with cysteic acid, 50 mg/kg, IP, prolonged ethanol-produced narcosis. Treatment with cysteic acid 30 min prior to ethanol, 2.5 g/kg, IP, was found to decrease whole blood ethanol concentration as compared to the respective controls without a concomitant changes in brain ethanol levels. Administration of taurocholic acid, 100 mg/kg, IP, decreased the intake of an ethanol solution in rats preferring 5% ethanol solution over water as the drinking fluid of choice. None of the compounds tested altered endogenous specific activity of mouse liver alcohol dehydrogenase when given once daily (50 mg/kg, IP) for 10 consecutive days. The results suggest that both taurocholic acid and cysteic acid exert additive action to some ethanol-elicited responses studied.
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PMID:Taurine, analogues and ethanol elicited responses. 48 15


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