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

Ethanol-induced sedation in Sprague-Dawley rats was antagonized by intracisternally administered thyrotropin releasing hormone (TRH) at a dose as low as 1 microgram. Furthermore, when a dose of 25 micrograms or greater of TRH was combined with ethanol doses above 2 g/kg, the locomotor activity was significantly greater than observed for TRH alone. A dose-related increase in activity was observed when varying doses of ethanol were administered with a constant dose of TRH (100 micrograms). This increase in locomotion induced by the TRH-ethanol combination could not be attributed to a change in TRH concentration, ethanol distribution or to a pituitary action of TRH. Inasmuch as tert-butanol in combination with TRH produced the same effects as ethanol, the hyperactivity does not appear to be associated with acetaldehyde formation. TRH acid and His-Pro-diketopiperazine, metabolites of TRH, did not produce hyperactivity when administered with ethanol, whereas MK-771, a TRH analog, produced a significant increase in locomotion in ethanol-treated rats greater than that for MK-771 alone. Three lines of evidence suggested that the hyperactivity induced by the TRH-ethanol combination could not be attributed to an influence of ethanol on the stimulant effects of TRH. First, pentobarbital- and chlordiazepoxide-induced depression of locomotion was antagonized by TRH (100 micrograms) but, unlike ethanol, locomotor stimulation greater than that for TRH was not observed. Second, behavioral observations did not reveal ethanol altering any effects of TRH that would compete with locomotion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ethanol-induced locomotor stimulation in rats after thyrotropin-releasing hormone. 642 48

The development of the human fovea has been traced from 22 weeks gestation to 45 months postpartum using aldehyde-fixed, plastic embedded, serially-sectioned normal retinas. Five anatomical indicators of foveal maturity were used in this study: the shape of the foveal curvatures; the presence of the transient layer of Chievitz; the width of rod-free zone in the central retina; the width and length of the individual foveal cones; and the number and thickness of layers of nuclei within the fovea. The future fovea is identifiable at 22 weeks by the presence of a thick layer of ganglion cells and a photoreceptor layer containing only cones. By 1 week after birth, there is a shallow foveal depression, but the thick cones still lack outer segments and are only 1 cell deep in the fovea. The inner nuclear layer contains a thick transient layer of Chievitz. As judged by these anatomical criteria and compared to normal adult foveas similarly processed, the human fovea reaches maturity between 15 and 45 months of age.
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PMID:The morphological development of the human fovea. 646 23

Three out of 4 adoption and 2 out of 3 twin studies imply a genetic contribution to alcoholism in males. A recent study of moderate drinking in male twins suggests that familial factors account for some two-thirds of the variance in alcohol consumption, and that the genetic component slightly outweighs the effects of the within family culture. There has been little support for the notion of a genetic entity which expresses itself as alcoholism in males and depressive illness in females, but among normal male twins anxiety and depression are genetically correlated with alcohol consumption. Increased liability to form acetaldehyde and the potentially additive tetrahydroisoquinolines could be one factor predisposing to alcoholism but human studies have been less convincing than their animal counterparts.
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PMID:Current genetic and biological approaches to alcoholism. 667 10

The effects of ethanol and acetaldehyde on basal tension of canine small and large coronary arteries were examined in vitro. Ethanol in a concentration as little as 8.5 mM can induce threshold contractions of coronary arteries. High concentrations of ethanol produce concentration-dependent coronary vasospasms equivalent to those induced by supra-maximal concentrations of KCl. Acetaldehyde (10(-5) to 10(-2)M) resulted in concentration-dependent relaxation of basal tone. Use of a variety of pharmacological antagonists (i.e., phentolamine, methysergide, diphenhydramine, metiamide, propranolol and indomethacin) did not attenuate or prevent the spasmogenic actions of ethanol. These findings could help to explain why alcohol can induce cardiac depression, arrhythmias, cardiomyopathy and the higher than normal incidence of sudden death observed in 'binge' drinkers.
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PMID:Ethanol produces coronary vasospasm: evidence for a direct action of ethanol on vascular muscle. 683 Nov 12

Data are reviewed that suggest that the peripheral vasodilation and hypotension that often result from ingestion (or administration) of ethanol may, in large part, be a consequence of its direct actions on vascular smooth muscle cells, at both the macro- and microcirculatory levels. At lest two mechanisms appear to contribute to this vasodilator effect: 1) inhibition of the normal rhythm or vasomotion (spontaneous mechanical activity) of vascular smooth muscle; and 2) depression of the contractile responses to endogenous neurohumoral substances that play a role in maintaining vascular tone and regulation of blood flow. The information acquired so far suggests that these dilator actions are related causally to interference with movement and/or translocation of Ca2+ across the vascular membranes. Although acetaldehyde and acetate can evoke some actions on isolated blood vessels that somewhat resemble the actions of ethanol, in situ studies on the splanchnic microcirculation reveal that neither acetaldehyde nor acetate can mimic the dilator actions of ethanol on the microvessels. Evidence is also reviewed that indicates that certain concentrations of ethanol, acting on certain peripheral blood vessels (e.g., cerebral and coronary arteries), can induce direct contractile responses (dose-dependent) and potentiate certain hormones, the effects of which are dependent on free, ionized Ca2+ ions. Lastly, data are reviewed in experimental animals, maintained on liquid diets of ethanol, which may provide insights into why a high incidence of hypertensive vascular disease has been noted in alcoholics.
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PMID:Microvascular and vascular smooth muscle actions of ethanol, acetaldehyde, and acetate. 704 29

In vitro addition of ethanol or pentobarbital to synaptosomes isolated from rat or mouse brain inhibited the depolarization-dependent uptake of calcium without affecting uptake under nondepolarizing conditions. Ethanol inhibited the uptake in a concentration-dependent manner over the range of 45 to 720 mM. Analysis of the effects of ethanol and pentobarbital on calcium uptake at different temperatures indicated that the drugs did not change the activation energy of the process but shifted the Arrhenius curves toward higher temperatures. Synaptosomes isolated from mice chronically ingesting ethanol were found to be tolerant to the inhibitory effects of ethanol and pentobarbital but not tolerant to the inhibitory effects of acetaldehyde. Synaptosomes from ethanol tolerant-dependent mice accumulated less calcium in the absence of ethanol than did synaptosomes from control mice. This depression of uptake was reversed by in vitro exposure of the synaptosomes to a low concentration of ethanol, suggesting that it represents a biochemical response to withdrawal of alcohol. A single acute injection of ethanol 1 hr before sacrifice did not alter the calcium uptake activity or the drug sensitivity of the synaptosomes. These results suggest that the known inhibitory effects of ethanol and pentobarbital on the stimulated release of neurotransmitters and the development of tolerance of these effects may be mediated by the inhibition of the depolarization-dependent influx of calcium by these drugs.
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PMID:Inhibition of synaptosomal calcium uptake by ethanol. 719 27

(1) Ca2+-binding lipoprotein was purified from dog heart plasma membrane and the effect of several general anesthetics, ethanol, and acetaldehyde on the Ca2+ binding was studied. (2) These drugs, which are known to cause myocardial depression increased the Ca2+ binding at clinically useful concentrations. (3) These results raise the possibility that these drugs, by increasing the Ca2+ binding to the plasma membrane, limit the availability of superficially located Ca2+ for excitation-contraction coupling and result in depression of myocardial contractile force.
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PMID:The increase in calcium binding of cardiac plasma membrane lipoprotein caused by general anesthetics and alcohol. 741 79

Carbohydrate-deficient transferrin (CDT) is now considered to be the most sensitive and specific biological marker of alcohol abuse. However, the mechanism by which chronic alcohol consumption causes an elevation of CDT levels in serum is still not understood. Therefore, we fed eight pairs of male rats a nutritionally adequate liquid diet containing either alcohol (36% of energy) or isocaloric dextrose (control) for 4 weeks, after which blood and liver samples were obtained. Serum CDT content in alcohol-treated rats increased by 45% (P < .05) in ethanol-fed animals compared with their corresponding controls. In contrast, in rats fed ethanol, the activities of sialyltransferase (ST), galactosyltransferase (GT), and N-acetylglucosamine transferase (N-AGT), which are glycosyltransferases involved in transferrin carbohydrate side chain synthesis, were diminished by 24% and 40% (P < .05), 23% and 51% (P < .05, .001), and 20% and 26% (P < .05) in total liver homogenates and Golgi fraction (GF) 1, respectively, when expressed as units/100 g body weight. These enzymes were also significantly less active in hepatic GFs 2 and 3. The depression of the transferase activities in ethanol-fed rats appeared to be due, at least in part, to enzyme inactivation by acetaldehyde, whereas ethanol itself was without effect. Similar results were obtained in humans: five alcohol abusers were found to exhibit a 23% decrease in hepatic sialyltransferase and a 41% increase in sialidase activities, respectively, when compared with three nondrinking subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum carbohydrate-deficient transferrin: mechanism of increase after chronic alcohol intake. 759 Jun 64

The effect of ethanol exposure upon several parameters relating to oxidative stress has been examined in brain and liver. A single administration of either acetaldehyde or ethanol was able to enhance rates of generation of reactive oxygen species in liver but this effect was not apparent in the cerebral cortex. Glutamine synthetase is especially sensitive to inactivation by free radicals and evidence for cumulative oxidative damage to this enzyme was found in liver and to a lesser extent in cerebral cortex. This enzyme was depressed in liver after both a single injection of acetaldehyde or ethanol, or after more extended dosing. The liver was also more susceptible than cerebral cortex, to pro-oxidant effects as judged by depression of glutathione after acute dosing with either solvent. Enzyme inhibition representing temporally summated oxidative events may be a more sensitive procedure than direct measurement of rates of formation of active oxygen species and may find especially utility in the detection of prolonged low level pro-oxidant activity.
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PMID:Effect of ethanol treatment on indices of cumulative oxidative stress. 780 84

Several biochemical parameters that reflect the presence of excess levels of reactive oxygen species were modulated in the brains of rats exposed acutely or subchronically to ethanol. These parameters included depression of cytosolic glutathione (GSH) concentration and of glutamine synthetase levels. However, using these indices, there was a significant difference in susceptibility to ethanol in different brain regions. After dietary exposure to ethanol for 12 days, these indices were selectively depressed in the striatum but not in the cerebral cortex or cerebellum. Eighteen hours after a single acute dose of ethanol (4.5 g/kg body wt), the striatum was also the only one of these areas in which proteolytic activity was elevated by ethanol treatment. Two injections of acetaldehyde (300 mg/kg), given 18 and 2 hr prior to tissue preparation, caused a specific reduction of glutamine synthetase in the striatum and a decrease of GSH levels in both striatum and cerebellum. Taken together, the results suggest a distinctive vulnerability of the striatum to ethanol-promoted oxidative events. Rather than ethanol exerting effects directly, the metabolite acetaldehyde may be the primary agent responsible for these changes.
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PMID:Regional selectivity in ethanol-induced pro-oxidant events within the brain. 784 Jul 85


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