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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have developed a precise quantal method for assessing the sensitivity to ethanol in the mouse. Mice placed on a clamped stationary horizontal dowel are scored ataxic or not ataxic depending on whether they are able to remain on the dowel during a 30-s observation period. A threshold blood ethanol concentration is determined by assaying tail blood drawn immediately upon recovery from ethanol-induced ataxia. This threshold is quite reproducible within a population of Swiss-Webster mice (coefficient of variation 9%). The precision of this method allowed us to follow the onset of rapid tolerance during a series of sequential IP ethanol doses. Tolerance persisted overnight in the absence of ethanol, and was found not to increase further with additional ethanol exposure on 2 subsequent days. The observed tolerance was shown not to be due to circadian changes in ethanol sensitivity or repeated practice on the task, indicating a true tissue tolerance.
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PMID:The rapid onset of tolerance to ataxic effects of ethanol in mice. 681 99

The sensitivity of several inbred strains of mice was assessed for ethanol's effects on activity, body temperature, ataxia, balance, and the righting reflex. Genotypic correlations among the mean responses for the strains were estimated as indexes of pleiotropic influences of genes on drug responses. Three major groups of genetic influence were detected: (a) hypothermic sensitivity to ethanol, (b) activity change (increase after ethanol), and (c) high basal activity. In the first group of variables, strains that had large reductions in body temperature after being given ethanol had high baseline temperatures, pronounced ataxic response to ethanol, and a long-lasting loss of righting reflex. Home cage baseline activity was negatively correlated with body temperature variables. The second group of variables was composed largely of ethanol-induced increases and decreases in activity, which were negatively intercorrelated. Strains with larger increases in activity showed more rapid loss of balance after ethanol. The third group of variables indicated that high levels of basal activity in an open field and in the home cage were determined by the action of common genes. Strains with higher basal activity levels had reduced sensitivity to ambulatory ataxia following ethanol. Thus, there were substantial pleiotropic effects of common genes on several behavioral responses to ethanol in inbred mice. Conversely, the three major groups were not systematically correlated with one another to a major extent. This suggests the influence of three reasonably distinct sets of genes on these responses to ethanol.
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PMID:Sensitivity to ethanol in inbred mice: genotypic correlations among several behavioral responses. 684 90

Aqueous and organic extractions of ground seeds of Cassia occidentalis were obtained. Chickens were dosed with extracted material to assess the toxicity of the extracts. Organic extracts with methanol, ethanol, chloroform, ethyl acetate, and benzene were ineffective in removing the toxin from the seeds. Aqueous extractions, using 25 mM sodium bicarbonate or 250 mM sodium citrate, removed the toxin from the seeds, but left the toxin bound to particulate matter in the extract. Addition of Triton X-100 to the aqueous buffers effectively solubilized the toxin from the particulate matter. Signs of intoxication in the chickens were loss of weight, weakness, diarrhea, hypothermia, occasionally ataxia, and recumbency; then death. Gross lesions included paleness of skeletal and cardiac muscles and congestion of the liver. Microscopic lesions in muscle tissue were vacuolation, proliferation of sarcolemmal nuclei, and separation of myofibrils. Electron microscopic examination revealed disruption of mitochondrial cristae and swelling and rupture of mitochondria.
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PMID:Preliminary isolation of a myodegenerative toxic principle from Cassia occidentalis. 688 74

We investigated the time course for development of functional tolerance to the ataxic effects of ethanol in four genetically distinct mouse populations. Two inbred-strains (C57BL/6J and DBA/2J) and two lines of mice (long-sleep and short-sleep) selectively bred for differences in acute ethanol sensitivity were used. Mice were injected i.p. with ethanol in doses that produced ataxia and were tested repeatedly for their ability to balance on a wooden rod. When they regained their balance at threshold, brain ethanol levels were measured in some mice and booster injections of ethanol were administered to the remaining animals. This sequence was repeated for five injections, delivering a total of 6 g/kg of ethanol to the final group of animals. Functional tolerance developed in all four populations of mice as evidence by threshold brain ethanol levels that were significantly higher after two or three successive injections than after one injection. The magnitude of tolerance was not increased by practice on the dowel. To investigate whether alterations in membrane lipid composition accompanied this rapid development of tolerance, we used erythrocytes as a model system and measured the cholesterol and phospholipid content of their membranes. The erythrocyte membranes from ethanol-tolerant mice of each population contained more cholesterol than those from controls. The erythrocyte membrane phospholipid content of ethanol-tolerant animals changed only slightly in two populations.
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PMID:Rapidly developing functional tolerance to ethanol is accompanied by increased erythrocyte cholesterol in mice. 713 1

The physical dependence and tolerance characteristics of barbiturates and ethanol were compared. One group of cats was given anesthetic doses of pentobarbital chronically to produce severe physical dependence ("high dose" group). Two other groups of animals were given barbital or ethanol at "chronically equivalent" doses which produced gross ataxia without anesthesia ("low dose" groups). The doses required to produce the preset level of central nervous system depression progressively increased in all three groups during the chronic administration. Functional tolerance estimated by measuring the drug concentration in the blood at the peak of the drug response was demonstrated in all three groups. Drug administration was terminated after various durations and withdrawal was rated. Severity of withdrawal was assessed by monitoring spontaneous convulsions and by rating motor, autonomic and behavioral signs. These ratings were used to compute peak intensity of withdrawal. The number of convulsions, incidence of lethality during withdrawal and peak withdrawal intensity ratings were considerably higher in the ethanol groups than in the low dose barbiturate groups. Similarly, the number of convulsions, incidence of lethality during withdrawal and peak intensity ratings were consistently higher in the high dose barbiturate groups than in the low dose barbiturate groups. The results indicate that ethanol produced more severe withdrawal than barbiturate when the level of chronic intoxication was comparable in the two groups. Also, the level of central nervous system depression during administration was an important factor influencing intensity of barbiturate withdrawal.
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PMID:Comparison of ethanol and barbiturate physical dependence. 719 50

The effects in vivo of acute doses of ethanol on impulse transmission in the region of the neuromuscular junction are poorly known. These effects were studied with a new procedure, using mouse tails in a constant temperature chamber to study the delay in nerve-to-muscle impulse transmission. A saline control and five ethanol doses (0.5, 1.0, 1.4, 2.0, 4.24 g/kg) were used with 96 mice. The interval ("residual latency", RL), between (a) the peak of the compound nerve action potential and (b) the first peak of the associated compound muscle action potential, was measured. Ethanol was given IP and tail nerve stimulations were done at 4 min intervals to 16 min post-ethanol. The mean pre-ethanol RL was 0.93 +/- 0.01 (SE) msec; about 25% of this time should be synaptic delay and the remainder is nerve and muscle fiber conduction time. Individual post-ethanol relative RL (RRL) values were calculated for each moue, based on its pre-ethanol value. With doses of 1.0 g/kg and higher there was a mean increase in RRL; at 16 min this increase was 0.8 to 4.4% (all p less than 0.01). At 0.5 g/kg, and also at higher doses, there was a significantly (p less than 0.01) increased variance in RRL 8 to 16 min post-ethanol. A marked correspondence between mean RRL and ataxia is apparent. This appears to be the first in vivo demonstration of acute effects of ethanol on neuromuscular transmission. The methods and mice used may comprise a useful animal model for detecting acute effects of low doses of ethanol on synaptic function.
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PMID:Acute effects of ethanol in vivo on neuromuscular transmission. 720 48

Dosages of 95% ethanol (0, .5, or 1 ml) with variable quantities of water were administered to mixed sex chicks (263 g initial weight) on each of 7 consecutive days. The 1 ml dosage of ethanol significantly reduced body weight gains and feed consumption and increased liver weight per 100 g of body weight. Gross crop lesions (accumulation of exudates and hemorrhage) were observed for both the .5 and 1 ml dosage level of ethanol. For birds given the .5 ml ethanol dosage, dilution with water tended to reduce the severity of crop lesions but not for birds given 1 ml ethanol. All levels of ethanol produced mild ataxia within 5 to 10 min of dosage. Mild or moderate hepatocellular fatty change was present in livers from 5 to 6 birds given 1 ml ethanol. Crop exudates were composed of necrotic cells, fibrin and bacteria. Crop walls of birds given 1 ml of undiluted ethanol were ulcerated and inflamed. Areas within the crop wall were hemorrhagic, edematous, and infiltrated by heterophils and mononuclear cells.
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PMID:Toxic effects of repeated ethanol intubations to chicks. 726 48

The ability of ethanol to affect hindlimb ataxia and body weight changes induced by methyl mercury was studied in rats. Animals treated with either water or ethanol increased in body weight during the experiment and showed no impairment of hindlimb movement. Rats treated with methyl mercury also increased in body weight but developed moderate hindlimb ataxia. Animals treated with ethanol and methyl mercury initially gained but subsequently lost weight and exhibited severe hindlimb ataxia. The results provide evidence that ethanol can potentiate methyl mercury toxicity in rats and, by implication, in humans.
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PMID:Ethanol potentiation of methyl mercury toxicity: a preliminary report. 728 7

Pigeons were trained on a fixed consecutive number schedule of reinforcement, pecking eight or nine times on one key (a run) before making the single response on a second key that was reinforced if the number requirement had been met. A run of fewer than eight or more than nine responses reset the response requirement. They then were given methylmercury chronically until behavioral signs of poisoning occurred. Where possible, recovery was followed. Percentage of reinforcers earned and rate at which the birds pecked both decreased whereas variability of run length increased after enough methylmercury had been given to produce blood mercury concentrations between 13 and 27 ppm. Some birds also showed consistent shortening of run length throughout the time of maximum poisoning. Because ataxia was a common accompaniment of the changes in operant behavior, other methods of producing ataxia (hobbling one foot or dosing with ethanol) were also studied in some birds. The pattern of changes induced with these methods did not match that seen after methylmercury.
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PMID:Methylmercury-induced changes in operant discrimination by the pigeon. 740 Sep 64

Fifty-seven cases of meprobamate ingestion from 1974 through 1979 were reviewed. Serum meprobamate concentrations, clinical findings, and epidemiologic data were studied to determine the present status of the abuse of this compound. The average patient was a 37-year-old woman who ingested meprobamate and at least one other drug (usually a benzodiazepine, a barbiturate, ethanol, or an opiate) in a suicide attempt of gesture. She arrived at the hospital either alert or lethargic with equal frequency. Half of the time she was seen only in the emergency room, and half of the time she was hospitalized. She was usually treated with supportive care alone and survived the ingestion. Serum meprobamate concentrations exceeding 12 mg/dl were consistent with coma. Dysarthria, hypotension, tachycardia, and ataxia were the most common physical findings. Meprobamate addiction was present in six patients.
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PMID:The present status of meprobamate ingestion. A five-year review of cases with serum concentrations and clinical findings. 745 16


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