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)

Ethanol, in vitro, decreases muscle fiber twitch tension by a mechanism unrelated to the electrical events of the motor end-plate or muscle surface membranes, an effect which may be attributable to a primary ethanol effect on the calcium release process of the sarcoplasmic reticulum. In this study, ethanol was found to progressively decrease a form of calcium release from isolated sarcoplasmic reticulum vesicles seen after calcium loading in high-phosphate media (spontaneous calcium release). Elevated extravesicular free calcium concentrations are known to inhibit spontaneous calcium release, and the ability of sarcoplasmic reticulum to achieve and maintain submicromolar extravesicular free calcium concentrations in the presence of ethanol was therefore determined. Ethanol had no effect on the low extravesicular free calcium concentrations achieved by isolated sarcoplasmic reticulum, and had no effect on residual ATPase activity remaining after cessation of calcium pumping. This latter result suggests that efflux of vesicular calcium and persistent calcium reaccumulation do not occur in the presence of ethanol. These results suggest that ethanol-induced depression of spontaneous calcium release is not attributable to ethanol effects on sarcoplasmic reticulum membrane calcium leakage or on sarcoplasmic reticulum calcium pumping. Ethanol inhibition of spontaneous calcium release from isolated sarcopasmic reticulum may reflect an effect of ethanol on the calcium release process in intact muscle fibers responsible for ethanol-induced decreases in muscle fiber twitch tension.
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PMID:Ethanol inhibition of spontaneous calcium release from isolated sarcoplasmic reticulum. 253 74

Ethanol (ETH) and general anesthetics have been reported to facilitate the chloride channel opening, possibly, or at least partly, through an interaction with the GABA-benzodiazepine (BZ) receptor-gated chloride ionophore "supramolecular complex". Recently Ro 15-4513, a novel BZ ligand, has been indicated as a potent and selective antagonist of various ETH-induced behavioral and biochemical effects. However, since its precise characterization is still a matter of debate, we have tested and compared the effect of Ro 15-4513, as well as its antagonism against ETH, in two objective electrophysiological parameters, i.e., the electroencephalograph (EEG) pattern in freely moving rats and single unit activity of reticulata neurons. Ro 15-4513 produced an EEG state of alertness and antagonized the behavioral impairment and the EEG deterioration by ETH. However, while its protective action was consistent against moderate doses (2 g/kg) of ETH, it was much less evident versus higher doses (4 and 8 g/kg). On reticulata cells, Ro 15-4513 potently stimulated their spontaneous firing and reversed the depression by both ETH and Na-pentobarbital. Moreover, the beta-carboline DMCM also had similar effects. The "pure" BZ antagonist Ro 15-1788 was completely inefective against ETH, yet fully cancelled the reversing actions of Ro 15-4513 and DMCM upon ETH or Na-pentobarbital effects. It is concluded that Ro 15-4513 behaves as a BZ inverse agonist, so that its opposition to ETH and Na-pentobarbital is probably the result of its "negative" coupling with the BZ recognition site that triggers the closing of chloride channels. It suggests that BZ inverse agonists might constitute, in the near future, a new class of analeptic drugs.
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PMID:Antagonism of ethanol effects by Ro 15-4513: an electrophysiological analysis. 253 42

The effects of U50488H, a kappa agonist, and WIN 44441-3, a kappa antagonist, and their modification of the effects of ethanol, on the behavior of rats in a modified open field apparatus, was examined. Crossover activity was increased by U50488H. Headpoke activity was decreased by WIN 44441-3 and increased by U50488H. Rearing activity was increased by WIN 44441-3 but was not affected by U50488H. The effect of both drugs was dose related, with the largest doses having no effect. Ethanol (0.5 g/kg) stimulated crossover activity while it depressed rearing, headpoke and corner activities; except for crossover activity the 2.0 g/kg dose of ethanol depressed these activities. Pretreatment with WIN 44441-3 (0.5 mg/kg) potentiated the stimulant effect of ethanol on crossover activity and partially reversed the depressant effect of ethanol on rearing and headpoke activities. U50488H potentiated the ethanol-induced depression of headpoke and reversed the depression of corner activity. Pretreatment with U50488H had no effect on ethanol's action on crossover and rearing behaviors. Our results indicate that kappa opiate receptors may mediate some behaviors exhibited by rats in a modified open field apparatus. Activation of these receptors increases locomotor and headpoke activity but had no effect on rearing activity. Furthermore, the 0.5 g/kg dose of ethanol has differential effects on different measures of open field behavior, while the 2.0 g/kg dose was largely depressant. Our data suggest that some of these effects of ethanol may be mediated via kappa opioid receptors.
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PMID:Effects of ethanol in an open field apparatus: modification by U50488H and WIN 44441-3. 254 20

Ethanol and ethanol-water extracts of endophyte-infected tall fescue seed were effective for extracting toxin(s) responsible for feed intake and average daily weight gain (ADG) depression in Sprague Dawley rats. Although the ethanol extract of endophyte-infected seed depressed serum prolactin (Prl) concentrations, the data were less reflective of overall toxicity than feed intake and weight gain. Inclusion of commercially available ergonovine maleate, ergocryptine and ergotamine tartrate had no effect on rat feed intake, ADG or serum Prl at the levels tested. Dietary addition of a recombination of hexane, ethanol and ethanol-water extracts caused a toxicity response (depressed feed intake, ADG, and serum Prl) equivalent to that of the whole seed. The toxic factor(s) were extracted primarily in more polar solvents such as ethanol and ethanol-water. Rat assays can be used successfully in lieu of cattle assays as a routine evaluation of toxic components in endophyte-infected tall fescue. However, species differences dictate that eventually all suspected toxins be evaluated in the bovine.
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PMID:Physiological responses in rats fed extracts of endophyte-free and endophyte-infected tall fescue seed relative to some known ergot alkaloids. 259 31

Brain mitochondria isolated from rats following 10 weeks of chronic exposure to ethanol were not deficient in respiratory function or in rates of calcium uptake under control conditions. Ethanol (80 mM) in the incubation medium caused significant depression in the respiratory and ATP-dependent rates of calcium uptake in control mitochondria, but did not affect mitochondria from ethanol-tolerant rats. Chronic exposure to ethanol causes mitochondria to take calcium up at a normal rate when challenged acutely by ethanol.
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PMID:Development of tolerance in brain mitochondria for calcium uptake following chronic ethanol ingestion. 260 3

A study was carried out on the effects of midazolam 15 mg in conjunction with ethanol 0.5 g/kg on objective and subjective sleep parameters and psychomotor performance in normal subjects. Midazolam significantly decreased total wake time. Total sleep time (TST) increase was related to larger amounts of stage 2 NREM sleep. Ethanol showed similar effects on sleep, although TST increase was associated with nonsignificant increments of NREM sleep and REM sleep. Ethanol slightly potentiated midazolam effects on sleep. Accordingly, total wake time, REM sleep time and number of wakes showed further depression than with midazolam alone. Subjective evaluations showed relatively good correlation with sleep laboratory findings. In addition, the different treatments did not impair subject's psychomotor performance the morning after their administration.
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PMID:Combined effects of midazolam and ethanol on sleep and on psychomotor performance in normal subjects. 261 61

This study was prompted by previous findings that prenatal ethanol exposure may interfere with the differentiation of the sexual behavior in rats. Ethanol (6 g/kg) administered daily from day 15 postconception, resulted in elevated testosterone (T) levels on Day 18 in male and female fetuses. No alterations of sexual behavior in the ethanol-treated male offspring were seen under these conditions. However, in ethanol-treated female offspring the onset of regular estrous cycling was significantly delayed. Acute treatment with doses of ethanol, 2, 4 or 6 g/kg, was ineffective in influencing plasma T levels of the fetuses. Acute treatment with 3 g/kg ethanol did not prevent the rise of T levels normally occurring immediately after birth. In adulthood, but not at prepubertal age (Day 30), treatment of male rats with 2 g/kg ethanol caused a depression of plasma T levels. Possible mechanisms affected by ethanol exposure and influencing on the fetal development were discussed.
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PMID:Effects of chronic and acute ethanol treatment during prenatal and early postnatal ages on testosterone levels and sexual behaviors in rats. 261 6

Acute exposure of an animal to ethanol has a biphasic effect on activity; at low doses incurring stimulation of locomotor activity whilst at higher doses eliciting a depression in activity level. The present study reports the effect of short-term (10 days) exposure to ethanol on running wheel activity in female Wistar rats. Ethanol treatment (3 g/100 ml in drinking water) increased significantly the rate of accumulation of total distance run but not the daily rate of running when compared to control animals. This increase was attributable to an increased rate of running stimulated by daily feeding and handling by the experimenter.
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PMID:Chronic ingestion of ethanol increases stimulation-induced voluntary activity in the rat. 270 27

The effects of spontaneous respiration and mechanical ventilation were examined by investigating the interaction between elevated intracranial pressure and alcohol intoxication. Ethanol (200 ml 48%) was infused in 11 young pigs with elevated cerebral pressure during mechanical ventilation (group 1), 7 young pigs with elevated cerebral pressure during spontaneous respiration (group 2), and 4 young pigs without elevated cerebral pressure during spontaneous respiration (group 3). While the behavior of intracranial pressure during mechanical ventilation in the animals from group 1 was inhomogeneous with a tendency to rise (29-34 mmHg), cerebral pressure (28-55 mmHg) increased drastically in the animals from group 2. This increase was associated with a sharp rise of Pa,CO2 (37.6-73.3 mmHg) and a decrease of Pa,O2 (74 mmHg to 13 mmHg). None of the animals in group 2 survived. Pa,CO2 also rose in alcoholized animals without elevated cerebral pressure (group 3) (41.9-63.9 mmHg); intracranial pressure, however, remained within the normal range. All animals in group 3 survived. Our findings indicate that elevated intracranial pressure and alcohol intoxication have a cumulative or potentiating effect on depression of the respiratory center. Respiratory depression can be prevented by mechanical ventilation and, therefore, a further rise of intracranial pressure generally avoided.
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PMID:The respiratory aspect of the treatment of brain injury associated with acute alcohol intoxication--results of an animal experiment. 303 60

Ethanol, a highly lipid-soluble compound, appears to exert its effects through interactions with the cell membrane. Cell membrane alterations indirectly affect the functioning of membrane-associated proteins, which function as channels, carriers, enzymes and receptors. For example, studies suggest that ethanol exerts an effect upon the gamma-aminobutyric acid (GABA)-benzodiazepine-chloride ionophore receptor complex, thereby accounting for the biochemical and clinical similarities between ethanol, benzodiazepines and barbiturates. The patient with acute ethanol poisoning may present with symptoms ranging from slurred speech, ataxia and incoordination to coma, potentially resulting in respiratory depression and death. At blood alcohol concentrations of greater than 250 mg% (250 mg% = 250 mg/dl = 2.5 g/L = 0.250%), the patient is usually at risk of coma. Children and alcohol-naive adults may experience severe toxicity at blood alcohol concentrations less than 100 mg%, whereas alcoholics may demonstrate significant impairment only at concentrations greater than 300 mg%. Upon presentation of a patient suspected of acute ethanol poisoning, cardiovascular and respiratory stabilisation should be assured. Thiamine (vitamin B1) and then dextrose should be administered, and the blood alcohol concentration measured. Subsequent to stabilisation, alternative aetiologies for the signs and symptoms observed should be considered. There are presently no agents available for clinical use that will reverse the acute effects of ethanol. Treatment consists of supportive care and close observation until the blood alcohol concentration decreases to a non-toxic level. In the non-dependent adult, ethanol is metabolised at the rate of approximately 15 mg%/hour. Haemodialysis may be considered in cases of a severely ill child or comatose adult. Follow-up may include referral for counselling for alcohol abuse, suicide attempts, or parental neglect (in children). The ethanol withdrawal syndrome may be observed in the ethanol-dependent patient within 8 hours of the last drink, with blood alcohol concentrations in excess of 200 mg%. Symptoms consist of tremor, nausea and vomiting, increased blood pressure and heart rate, paroxysmal sweats, depression, and anxiety. Alterations in the GABA-benzodiazepine-chloride receptor complex, noradrenergic overactivity, and hypothalamic-pituitary-adrenal axis stimulation are suggested explanations for withdrawal symptomatology.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute ethanol poisoning and the ethanol withdrawal syndrome. 304 Dec 44


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