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

An extract with cholinergic activities was isolated from instant regular and decaffeinated coffees and purified. Intravenous injection of this cholinomimetic extract of coffee produced an abrupt depression in blood pressure and heart rate, changes that were distinct from those of known components of coffee, including caffeine, trigonelline, catechin, and chlorogenic acid. Pretreatment of the animals with naloxone, propranolol, isobutylmethylxanthine, hexamethonium bromide, and hemicholinium-3 chloride or bilateral vagotomy did not affect the cardiodepressive effects of the extract, whereas atropine completely abolished them. Direct injection of the cholinomimetic extract of coffee (20-100 micrograms) into the periaqueductal gray area of the midbrain did not produce any cardiovascular effect. However, the extract of coffee did cause relaxation of isolated rat and rabbit aortic ring preparations that were contracted under norepinephrine. The cholinomimetic extract did not inhibit purified acetylcholinesterase. This pharmacologic profile indicates that the cholinomimetic extract of coffee acts as a direct muscarinic agonist.
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PMID:Cholinomimetic compound distinct from caffeine contained in coffee. II: Muscarinic actions. 140 78

In previous work, we studied, under conditions of ad libitum food consumption, the effect of amount and type of dietary fat on plasma esterase-1 (ES-1) and butyryl cholinesterase activity in rats. This was done by the isoenergetic replacement of dietary fat by carbohydrates or by another fat source. The observed change in enzyme activity could theoretically be determined by either the dietary omission or the addition or by the combination. In the present work, we studied under restricted feeding conditions the effect of supplemental energy in various forms to determine the effect of the supplement alone. Supplemental coconut fat, but not isoenergetic amounts of either glucose or casein, raised plasma ES-1 activity. None of these supplements influenced butyryl cholinesterase activity. In a second experiment, we demonstrated that the ES-1 enhancing effect of supplemental coconut fat also occurred with fish oil, whereas the stimulatory effects of olive oil and corn oil were less pronounced. Supplemental fish oil, but not the three other fats, significantly reduced the depression in butyryl cholinesterase activity. Plasma cholesterol concentration was negatively associated with butyryl cholinesterase activity, but was not related to ES-1 activity. The two esterases were not correlated with plasma triglyceride concentration. We conclude that both the amount and type of fat in the diet of rats have specific influences on plasma ES-1 activity and that butyryl cholinesterase activity is affected by the type of fat.
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PMID:Plasma esterase-1 (ES-1) activity in rats is influenced by the amount and type of dietary fat, and butyryl cholinesterase activity by the type of dietary fat. 143 52

Wistar rat pups (female) were exposed to methylparathion (MPTH) by gastric intubation in single doses, or in a chronic regimen of different durations. A single dose of 1 mg MPTH/kg body weight in 15-day-old pups caused a significant decrease of acetylcholinesterase (AChE) activity in cerebellum (CE), motor cortex (MC) and brain stem (BS). The effect began to appear in about 20 min after administration, the peak effect was attained in 120 min and later on this waned off completely by 24 h. The effect was similar in young (15 days) and in adult (70 days) rats. A single dose of 0.2 mg MPTH/kg in 15 day old pups caused a reduction of AChE activity only in the BS, while a 0.1 mg MPTH/kg single dose given to 15-day-old pups caused no effect even in seven regions of the brain examined. Effect of low dose chronic administration of MPTH on AChE activity was also studied in CE, MC, BS, hippocampus (HI), striatum-accumbens (SA), spinal cord (SC) and also in the hypothalamus (HY). Administration of 0.1 mg MPTH/kg from second day to 15 days of age caused significant reduction of AChE activity in only 2 of the 7 brain regions studied. Administration of double the dose (0.2 mg MPTH/kg) and for a longer duration (2nd day to 150 days of age), caused a depression in all the brain regions studied. In all these regions, the levels of NA, DA and 5HT did practically not change. The results suggest that chronic consumption of MPTH leads to a moderate decrease of AChE activity in several brain regions.
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PMID:Effect of chronic consumption of methylparathion on rat brain regional acetylcholinesterase activity and on levels of biogenic amines. 145 21

Biochemical responses of animals to environmental chemicals (biochemical biomarkers) can give measures of exposure, and sometimes also toxic effect. They are particularly valuable where they can be used to measure the toxic effects of chemicals in the field, employing non-destructive sampling methods. Measurements of exposure are useful in the case of non-persistent chemicals (e.g. organophosphorus, carbamate, or pyrethroid insecticides) which are difficult or impossible to detect by chemical analysis. They can also be useful to provide an integrated measure of the level of exposure to a group of related chemicals. Biochemical biomarkers are likely to provide a measure of toxic effect, where they are based upon a molecular mechanism which underlies toxicity. A widely-used biochemical biomarker is cholinesterase depression, which may involve destructive sampling (brain acetylcholinesterase) or non-destructive sampling (serum butyrylcholinesterase). For genotoxic chemicals, techniques which measure DNA damage (e.g. detection of DNA adducts) provide a powerful tool in measuring environmental effects. The detection of biochemical changes caused by anticoagulant rodenticides (e.g. abnormal levels of clotting proteins in blood) provides another example of this approach. In general, the development of simple, sensitive, and specific assays that are 'user-friendly' would open the way for much wider use of biochemical biomarkers in environmental monitoring.
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PMID:Biochemical responses as indicators of toxic effects of chemicals in ecosystems. 147 Dec 5

The cholinesterase (ChE) activities were measured in-season and out-season in a total of 204 greenhouse workers and 360 non-exposed controls. No seasonal ChE variation were observed in the controls, whereas an in-season depression was seen in the workers, indicating an uptake of anti-cholinesterase agents during cultivation of greenhouse flowers in the intervals between sprayings (p = 0.0001). The anti-ChE agents applied seem to persist in the greenhouses and cause continued subtoxic uptake for weeks since last application. Wearing of protective gloves did not prevent the uptake. Thus, chronic percutaneous and oral uptake occurs as a result of cultivation of greenhouse flowers.
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PMID:Anti-cholinesterase agents uptake during cultivation of greenhouse flowers. 153 94

The relationship between plasma-cholinesterase (ChE) measures and the uptake of anti-cholinesterase agents among 125 greenhouse sprayers in connection with normal working conditions were studied. An in-season ChE depression was observed indicating absorption of organophosphate (OP) or carbamate insecticides (p = 0.0001). The in-season enzyme depression among sprayers, exclusively exposed to carbamates (p = 0.06), probably reflects chronic percutaneous or oral uptake in the intervals between spraying by cultivating pretreated flowers. The frequency of applications (p = 0.03) and the wearing of protective clothings (p = 0.02) seems to be working habits, which significantly influenced the ChE activities, whereas gloves or face mask did not (p greater than 0.05). Especially, the wearing of whole-body protective clothing (p = 0.008) are of particular value in preventing percutaneous absorption.
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PMID:Indoor application of anti-cholinesterase agents and the influence of personal protection on uptake. 153 95

The subacute effects of pyridostigmine bromide were investigated on the contractile properties of rat extensor digitorum longus (EDL) and diaphragm muscles. The cholinesterase inhibitor was delivered via subcutaneously implanted osmotic minipumps (Alzet) at 9 micrograms h-1 (low dose) or 60 micrograms h-1 (high dose). Animals receiving high-dose pyridostigmine pumps exhibited marked alterations in muscle properties within the first day of exposure that persisted for the remaining 13 days. With 0.1 Hz stimulation, EDL twitch tensions of treated animals were elevated relative to control. Repetitive stimulation at frequencies greater than 1 Hz led a use-dependent depression in the amplitude of successive twitches during the train. Recovery from pyridostigmine was essentially complete by 1 day of withdrawal. Rats implanted with low-dose pyridostigmine pumps showed little or no alteration of in vivo twitch tensions during the entire 14 days of treatment. Diaphragm and EDL muscles excised from pyridostigmine-treated rats and tested in vitro showed no significant alterations in twitch and tetanic tensions and displayed the same sensitivity as muscles of control animals to subsequent pyridostigmine exposures. In the presence of atropine, subacutely administered pyridostigmine protected rats from two LD50 doses of the irreversible cholinesterase inhibitor, soman. In the absence of atropine, the LD50 of soman was not altered by subacute pyridostigmine treatment.
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PMID:Effects of subacute pyridostigmine administration on mammalian skeletal muscle function. 156 49

Physostigmine was originally isolated from the Calabar Bean, which was used for ordeal by poison in West Africa. The main alkaloid was isolated in 1864. It acts through inhibition of acetylcholinesterase, and has been of major importance in elucidating the kinetics and configuration of the enzyme. Physostigmine has been important for our understanding of neurohumoral chemical transmission, and in mapping the cholinergic nerves. It was the first antagonist to curare, and has been widely used for various therapeutic purposes. Today it has been largely replaced by more efficient and safe drugs. It is still used as an antidote to poisoning from various psychopharmacological drugs, and to treat postoperative somnolence and respiratory depression. It is considered a potent antidote to organophosphorous poisoning and is used experimentally to treat Alzheimer's disease.
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PMID:[Development of physostigmine from a poisonous plant to an antidote. One of the most important drugs in the development of modern medicine?]. 157 14

Nine fairways of a golf course located in Bellingham, Washington were treated with diazinon AG500 at a target application rate of 2.2 kg active ingredient (AI) per ha. The chemical application with a "boomless" sprayer resulted in a variable distribution of diazinon residues on the turf (associated with a deep thatch layer) that ranged from 1.0 to 6.2 kg AI/ha. The diazinon-treated turf was irrigated with 1.3 cm of water immediately following application. The post-irrigation diazinon residue levels ranged from 100 to 333 ppm (mean = 209; SD = 88; n = 8). These residue levels were higher than expected based on results of turf studies in other regions of the United States. Eighty-five American wigeon (Anas americana) died after grazing on one treated fairway on the day of application following irrigation. The brains of all 85 wigeon were analyzed for acetylcholinesterase (AChE) activity. Wigeon that died on the study area (n = 85) showed 44% to 87% depression of AChE (mean = 76%; SD = 7.1%) when compared to control wigeon (n = 3; AChE Activity = 1.86) AChE levels. Upper GI tract contents of 15 of the 85 dead wigeon contained 0.96 to 18.1 ppm diazinon. Extensive carcass searches revealed no other avian mortality attributable to diazinon toxicity on the treated study area. Although initial post-irrigation diazinon residues in grass samples were higher than expected, diazinon levels in grass samples on day seven post-application had declined to an average of 29 ppm. American wigeon appear to be vulnerable to exposure to diazinon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:American wigeon mortality associated with turf application of diazinon AG500. 160 78

Slices of human neocortex prelabelled with [3H]choline were superfused and stimulated electrically (3 Hz, 2 ms, 24 mA) in order to investigate the autoreceptor-mediated modulation of acetylcholine (ACh) release. The concentration-response curve of the muscarinic agonist oxotremorine (pKd = 6.76 +/- 0.06), which was equipotent to ACh, was shifted to the right in a parallel manner by atropine (pA2 = 8.56 +/- 0.11), as evaluated by non-linear regression analysis. Calculation of the biophase concentration of ACh showed that no ACh could be assumed to be present under these conditions, whereas following inhibition of the acetylcholinesterase by physostigmine (0.1 microM) a biophase concentration of 10(-6.89 +/- 0.11) M was estimated. The depression of ACh release due to physostigmine and tacrine, another anticholinesterase, was antagonized by atropine. When the autoinhibition was operative atropine and the M2 subtype specific muscarinic antagonists, AF-DX 116 and methoctramine, significantly increased the release of ACh whereas the 'facilitatory' effects of the M1 and M3-specific drugs, pirenzepine and hexahydrosiladifenidol, were not significant. Although different disinhibitory effects of the subtype-specific antagonists were found, they did, however, not show a pattern which would allow a clear characterisation of the subtype of muscarinic receptor associated with the autoreceptor. The release of ACh from neocortex tissue of the (non-demented) neurosurgical patients decreased with their age. This finding is consistent with the hypothesis that the normal aging process resembles a delayed and attenuated disease process of senile dementia of Alzheimer's type.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The autoinhibitory feedback control of acetylcholine release in human neocortex tissue. 161 39


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