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

Variations in the content of biogenic amines were studied by fluorometry in the brain of rats administered ethanol at a single dose (1.5 and 6 g/kg, intraperitoneally) and chronically at a concentration raised from 10 to 40% for 2 months, and after ethanol withdrawal. In acute ethanol poisoning the serotonin concentration grows abruptly while the content of noradrenalin and dopamine drops down. On the contrary, in chronic ethanol poisoning the content of dopamine and noradrenalin rises, while that of serotonin does not differ from the control level. Ethanol withdrawal entails a decrease in the serotonin level apart from noradrenalin and dopamine accumulation by the brain. It is suggested that interrelated variations in the content of biogenic amines in the central nervous system may underlie the mechanism of depression development in acute ethanol poisoning and convulsant activity after it is discontinued.
 ...
PMID:[Change in the biogenic amine level in the rat brain in ethanol poisoning]. 718 22

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.
 ...
PMID:Inhibition of synaptosomal calcium uptake by ethanol. 719 27

Self-intoxication by inhalation of vapors of trichloroethylene (TCE) and other solvents is widespread. In order to develop exposure protocols which typify episodes of TCE "sniffing", male Wistar-Munich rats were exposed to TCE vapor levels ranging from 9000 to 16 000 ppm. TCE in concentrations of 14 000 ppm and greater quickly produced loss of righting reflex. Recovery from the narcosis was very rapid. Central nervous system (CNS) depression was found to be cumulative in rats subjected for 5 h to alternating periods of 5 min of 15 000 ppm TCE and 15 min of fresh air. Ethanol markedly potentiated depression in these subjects. No evidence of liver or kidney damage was seen in rats subjected to the repetitive 5-h TCE inhalation regimen, nor in rats fasted for 16 h before the TCE-exposure session. Oral administration of 5 ml/kg body wt of ethanol 1 h, 16 h, or once daily for 3 days before the TCE-exposure regimen had little if any potentiating effect on hepatorenal toxicity potential. Animals that received ethanol and were fasted before TCE exposure exhibited slight elevations in SGOT and SGPT levels.
 ...
PMID:Development of an animal model of solvent abuse for use in evaluation of extreme trichloroethylene inhalation. 719 5

Two rat lines selectively bred for ethanol-induced depression of locomotor activity were studied for ethanol-induced analgesia. The effects of ethanol on startle amplitude, extent of overt movements and incidence of audible vocalizations in response to intermittent, noncontingent foot shock. All three responses were dose-dependently depressed by ethanol (0.66 to 2.0 g/kg, IP), and to greater extent in the "most affected" line (MA) than in "least affected" (LA) rats. Ethanol-induced response decrements were reinstated at higher shock intensities, indicating a sensory (i.e., analgesic) rather than a motoric or analgesic basis for these effects. Genes which influence ethanol's motoric effects might, in part, influence sensitivity to its sensory effects.
 ...
PMID:Ethanol-induced analgesia in rats selectively bred for ethanol sensitivity. 720 44

The neurotoxic effects of chronic ethanol exposure were investigated in rat hippocampus by electrophysiological analysis of the Schaffer collateral-commissural input to stratum radiatum of CA1. Experimental animals were fed an ethanol-containing liquid diet for 20 weeks but were withdrawn from the special diet at least eight weeks prior to acute electrophysiological recordings. Ethanol treatment had no effect on input-output relationships for either the population EPSP or the population spike (PS). During paired-pulse stimulation, the ethanol group exhibited a greater facilitation of the test pulse PS relative to the control group, although potentiation of the EPSP was unchanged. In addition, the ethanol group showed a trend toward greater facilitation of the PS during 5 and 10 Hz tetani. No differences between groups were observed in the magnitude or duration of the long-term potentiation produced by 5, 10 or 100 Hz stimulus trains. Ethanol treatment did significantly reduce the transient spike depression after low frequency stimulation. This pattern of results is similar to that found for treatments which reduce hippocampal recurrent inhibition. Thus, chronic ethanol treatment may produce a lasting disruption of intrinsic inhibitory neurotransmission in the rat hippocampus.
 ...
PMID:Augmentation of short-term plasticity in CA1 of rat hippocampus after chronic ethanol treatment. 728 70

The effects of ethanol (10, 20, 50, and 100 mM) have been studied on field potentials in the CA1 region of the in vitro hippocampal slice preparation. Ethanol produced depression of the orthodromically evoked CA1 population spike and raised the threshold for orthodromic spike production. The effects of ethanol on the size of the population spike were highly correlated with the amount of the inhibition present in the slice as measure by paired pulse stimulation in control medium. Ethanol increased recurrent inhibition in the slice but had no significant effect on the antidromic response and produced only small changes in the dendritic field potential amplitudes. Adaptation or acute tolerance to the depressing effects of ethanol was observed in many slices. It is suggested that ethanol acts by potentiating the intrinsic inhibitory system in the hippocampus.
 ...
PMID:Effect of low concentrations of ethanol on CA1 hippocampal neurons in vitro. 729 99

Ethanol has been infused into an isolated heart-lung type preparation in which the "isotonically" contracting left ventricle pumps blood and does work at a lower than normal value while afterload is maintained constant. The isotonic contraction permits observation of the influence of a drug or other agent on the coronary vasculature independent of the compressive effects of the musculature. Infusions of ethanol to concentrations of approximately 210 mg/100 ml over a 30- to 60-min period resulted in significant increases in coronary blood flow, decreases in coronary vascular resistance and depression of myocardial performance. Cardiac work increased concomitantly with the increase in coronary blood flow and cardiac output without significant alterations in tension-time index and oxygen consumption. A second group of animals received a smaller amount of ethanol over a 5-min period, accompanied by injection of 86Rb and 125I for nutritional flow measurements and of radioactive microspheres for flow distribution. Extraction increased slightly after alcohol but flow distribution was not significantly altered. Small concentrations of ethanol are concluded to have a direct vasodilating effect on the coronary vasculature.
 ...
PMID:Direct effects of ethanol on myocardial performance and coronary resistance. 735 23

Acute exposure of jejunal mucosa to ethanol has been reported to produce a depression of transmural glucose transport across this organ in vitro and in vivo. In an attempt to understand the mechanism of action of ethanol on intestinal transport, in the present study we have investigated the effect of ethanol on glucose uptake by purified brush-border membrane vesicles of hamster jejunum. Ethanol, in concentrations found in man after moderate drinking (1-5% w/v), was found to depress glucose uptake by the brush-border membrane in a dose-dependent and time-dependent manner. Mannose was used to measure nonspecific uptake, and we found that the ethanol-induced depression of glucose uptake was not related to an alteration of the nonspecific uptake of this sugar. The inhibition of glucose uptake of the ethanol-treated membranes completely disappeared after repeated washing of the membranes with ethanol-free buffer. Accordingly, the ethanol-induced depression of glucose uptake was not the result of irreversible damage to membrane proteins but was related to a direct effect of ethanol on the brush-border membrane. On the basis of these findings, it is concluded that a direct interference with glucose translocation across the brush border plays an important role in the ethanol-induced depression of transmural jejunal glucose absorption.
 ...
PMID:Ethanol-induced inhibition of glucose transport across the isolated brush-border membrane of hamster jejunum. 746 Jul 5

One of the ulcerogenic mechanisms by which ethanol induces mucosal lesions in the stomach is the depression of gastric mucosal blood flow (GMBF). The goal of this study was to determine whether lesion formation is the result of vascular ischemia alone or ischemia combined with congestion. The aims of this study were to answer this question by evaluating the relationship between GMBF, oxygen saturation (ISO2) and hemoglobin volume (IHb) in the gastric mucosa under the influences of ethanol and prostaglandin E2 (PGE2) in the ischemic and congestive states, using a laser Doppler flowmeter and tissue spectrum analyzer. Ligation of the gastric celiac artery or vein markedly decreased the GMBF and the ISO2 level. The former procedure also reduced but the latter increased the IHb level. Ethanol administration produced effects similar to venous ligation, i.e. vascular stasis with ischemia. There was a negative correlation between GMBF and severity of lesion formation after ethanol administration. However, at the lesion site all the hemodynamic parameters were significantly reduced, indicating that a necrotic condition had occurred. PGE2 preincubation (25 micrograms) elevated GMBF, ISO2 and IHb levels. It also alleviated the reduction of blood flow induced by ethanol and increased the recovery rate of GMBF and ISO2 after the release of arterial or venous ligation. It is concluded that the decrease in blood flow due to ethanol is probably caused by constriction of venules rather than arterioles inside the mucosa, and this effect could lead to vascular congestion. PGE2 probably dilates both arterioles and venules in the gastric mucosa and thereby increases the blood flow in the gastric mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Assessment of hemodynamic changes in rat stomachs by laser Doppler velocimetry and reflectance spectrophotometry. Effects of ethanol and prostaglandin E2 under ischemic and congestive conditions. 770 51

The effects of protein malnutrition on haematological and serum biochemical values were evaluated in gossypol-treated rats which were simultaneously fed with ethanol. Gossypol caused anaemia, leucopenia and thrombocytopenia in malnourished animals, suggesting a depression of bone marrow activity. Gossypol also caused a significant elevation of serum alkaline phosphatase and alanine aminotransferase activities and increases in the concentrations of Mg++ and Ca++ with reduced albumin, regardless of the nutritional status. These changes were more severe with malnutrition. Ethanol alone caused a thrombocytopenia but no other significant haematological changes. However, it appeared to cause derangement of lipid and protein metabolism as reflected in serum cholesterol and urea. The toxic effects seen in gossypol-treated rats were significantly reduced in animals simultaneously given ethanol. As the livers of gossypol-treated rats were significantly heavier than in these animals, it seems possible that ethanol consumption enhances the ability of the liver to metabolize gossypol, thereby reducing its accumulation and consequently its toxicity. However, further studies are needed to determine the mechanisms responsible.
 ...
PMID:Haematological and serum biochemical changes in the rat due to protein malnutrition and gossypol-ethanol interactions. 788 58


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>