Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

GDEE, an antagonist of the AA2 or quisqualic acid category of excitatory amino acid receptor, decreases behavioral activity and locomotor stimulation induced by cocaine and amphetamine when locally injected into the nucleus accumbens. The present experiment was intended to examine the effects of systemic GDEE and other excitatory amino acid antagonists on stimulant-induced locomotor activity. GDEE markedly attenuated the stimulant effect of amphetamine, and partially blocked the effects of phencyclidine (PCP). Apomorphine-induced cage climbing behavior was partially decreased by lower dosages of GDEE, but was almost completely blocked by the highest dosage tested. Amphetamine-induced stimulation of locomotor activity was not decreased by any of the other excitatory amino acid antagonists that were tested, including MK-801, 2-amino-7-phosphonoheptanoic acid (APH), or CNQX. APH decreased stereotypy only at a high dosage (250 mg/kg), which also produces ataxia. Several other compounds, including L-glutamic acid gamma ethyl ester (GMEE), L-glutamic acid, glycine, and L-glutamine did not block amphetamine-induced stimulation in molar dosages equivalent to the highest dosage of GDEE (8 mmol/kg). It is concluded that the AA2 excitatory amino acid receptor is important in the expression of activating effects of stimulant drugs.
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PMID:A possible role of AA2 excitatory amino acid receptors in the expression of stimulant drug effects. 197 5

Three piperidine alkaloid containing plants, Conium maculatum (poison-hemlock), Nicotiana glauca (tree tobacco) and Lupinus formosus (lunara lupine), induced multiple congenital contractures (MCC) and palatoschisis in goat kids when their dams were gavaged with the plant during gestation days 30-60. The skeletal abnormalities included fixed extension or flexure of the carpal, tarsal, and fetlock joints, scoliosis, lordosis, torticollis and rib cage abnormalities. Clinical signs of toxicity included those reported in sheep, cattle and pigs--ataxia, incoordination, muscular weakness, prostration and death. One quinolizidine alkaloid containing plant, Lupinus caudatus (tailcup lupine), on the other hand, which is also known to cause MCC in cows, caused only slight signs of toxicity in pregnant goats and no teratogenic effects in their offspring.
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PMID:Congenital skeletal malformations and cleft palate induced in goats by ingestion of Lupinus, Conium and Nicotiana species. 208 36

We describe a 40 year-old male with a ball-cage mitral valve prosthesis who suddenly developed bilateral ptosis, bilateral dilated and unreactive pupils, right third nerve palsy, bilateral failure of vertical gaze, somnolence and mild ataxia without major motor deficits. Computed Tomography (CT) revealed bilateral thalamic infarcts in the distribution of the rostral basilar artery. Infarction in this case occurred despite adequate anticoagulation. The recognition of the entity of rostral basilar artery occlusion is important as interruption of anticoagulation may be avoided.
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PMID:Nuclear third nerve palsy and somnolence due to stroke--a case report. 239 42

The adenosine agonists 5'-N-ethylcarboxamideadenosine (NECA), 2-chloroadenosine (2-CLA), N6-cyclohexyladenosine (CHA), N6-cyclopentyladenosine (CPA), 2-(phenylamino)adenosine (CV-1808) and R and S isomers of N6-phenylisopropyladenosine (R-PIA and S-PIA) decreased spontaneous locomotor activity in mice and, except for CPA, did so at doses that did not impair motor coordination, a profile shared by dopamine antagonists. CV-1808, the only agent with higher affinity for A2 as compared with A1 adenosine receptors, displayed the largest separation between locomotor inhibitory and ataxic potency. Like dopamine antagonists, NECA and CV-1808 also decreased hyperactivity caused by d--amphetamine at doses that did not cause ataxia whereas A1-selective adenosine agonists reduced amphetamine's effects only at ataxic doses. Unlike dopamine antagonists, adenosine agonists inhibited apomorphine-induced cage climbing only at doses that caused ataxia. Involvement of central adenosine receptors in these effects was suggested by the significant correlation obtained between potency for locomotor inhibition after IP and ICV administration. Affinity for A1 but not A2 adenosine receptors was significantly correlated with potency for inducing ataxia. These results suggest that the behavioral profile of adenosine agonists in mice is related to their affinity for A1 and A2 adenosine receptors and indicate that adenosine agonists produce certain behavioral effects that are similar to those seen with dopamine antagonists.
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PMID:Comparison of the behavioral effects of adenosine agonists and dopamine antagonists in mice. 249 59

CI-943 (8-ethyl-7,8-dihydro-1,3,5-trimethyl-1H-imidazo[1,2-c] pyrazolo[3,4-e]-pyrimidine) is a novel agent that is chemically unrelated to available antipsychotics and is not a dopamine receptor antagonist. Like available antipsychotics, CI-943 reduces spontaneous locomotion in mice and rats and inhibits compulsive cage climbing induced by apomorphine in mice at doses that do not produce ataxia. However, CI-943 enhances rather than inhibits the locomotor stimulant effects of d-amphetamine in mice and rats. Unlike dopamine antagonists, CI-943 does not affect stereotypy caused by apomorphine or amphetamine in rats. CI-943 displays an antipsychotic-like profile in conditioned avoidance tests, inhibiting one-way avoidance in rats at doses that do not impair escape and inhibiting continuous avoidance in rats and squirrel monkeys at doses that do not impair shock termination responding. Although high doses of CI-943 produce dystonic movements in haloperidol-sensitized monkeys, CI-943 differs from dopamine antagonists that produce extrapyramidal dysfunction in humans in that doses of CI-943 that are sufficient to inhibit avoidance responding in monkeys do not produce extrapyramidal dysfunction. Unlike dopamine antagonists that produce tardive dyskinesia, CI-943 administered repeatedly at high doses does not produce behavioral supersensitivity to dopamine agonists in rats. These results demonstrate that CI-943 resembles available antipsychotics in some preclinical behavioral tests commonly used to predict antipsychotic efficacy but differs from dopamine antagonists in tests predictive of dopamine receptor antagonism and antipsychotic-induced neurological dysfunction.
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PMID:CI-943, a potential antipsychotic agent. I. Preclinical behavioral effects. 257 12

Five vervet monkeys were administered increasing doses (4--12 mg/kg/day) of d-amphetamine over a period of 35 days. Three phases od behavioural change were discerned: phase 1 during which animals exhibited repetitive stereotyped action sequences with rapid head movements, occasional abnormal grooming, picking at the cage, hand-staring and snatching; phase 2 in which behaviour became progressively more restricted and animals became markedly unresponsive to auditory, visual and tactile stimuli; phase 3 was characterised by the abrupt development of gross over-responsiveness to environmental stimuli, ataxia and tremor. At post-mortem, by comparison with controls, amphetamine-treated monkeys showed marked depletions of the monoamines dopamine (DA), noradrenaline (NA) and serotonin (5-HT) in corpus striatum and cerebral cortex and reductions in the activities of tyrosine hydroxylase and dopa decarboxylase in striatum. Turnover of these monoamines, assessed by high-performance liquid chromatography determinations of their respective metabolites, was also reduced. These findings are interpreted as evidence of monoamine neurone destruction, most severely in the case of DA neurones. Though there was a non-significant reduction in 3H-spiperone binding (reaching almost 50% in nucleus accumbens), numbers of receptors for the monoamines nA and 5-HT were not significantly changed, and the activities of the enzymes choline acetyltransferase and glutamine decarboxylase were similar in experimental and control animals. The contrast of these findings with those seen in post-mortem brains in schizophrenia is discussed.
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PMID:Behavioural and biochemical effects of chronic amphetamine treatment in the vervet monkey. 613 May 56

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

The effect of 6-hydroxydopamine (6-OHDA) injected into the cerebral ventricles on behaviour of singly- and group-housed cats was investigated. 6-OHDA in doses of 0.5, 1 and 2 mg was administered every morning for 5 to 8 days. In small doses 6-OHDA in singly- and group-housed cats evoked motor phenomena such as tremor, ataxia, rigidity, weakness and sometimes clonic-tonic convulsions. Occasionally restlessness, irritability and rage were observed. Large doses of 6-OHDA in group-housed cats, after a short latent period (2-3 days) produced aggression which intensified on subsequent injections, and thereafter, on repeated administrations, no longer occurred. The aggression consisted of restlessness, irritability, anger, rage, apprehension, threat, attack, fighting, flight and crying. Of autonomic phenomena mydriasis, dyspnea and sometimes piloerection were observed. The aggression was initiated by the most restless cat, or by disturbing the animals, such as by moving the cage. When 6-OHDA no longer produced aggressive behaviour, motor changes such as tremor, ataxia, rigidity, walking on broad base, weakness with adynamia and clonic-tonic convulsions developed. These latter symptoms were produced by large doses of 6-OHDA in singly-housed cats. In these animals spontaneous signs of aggressive behaviour usually were not observed, although if handled they showed rage, snarling and hissing. When singly-housed cats were kept in the same cage with group-housed animals, the singly-housed cats usually became aggressive. It appears that hyperactivity induced aggression in 6-OHDA-treated cats.
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PMID:6-hydroxydopamine and aggression in cats. 719 85

Rats were fed on diets containing methyl mercury dicyandiamide (MMD) at concentrations of 1.5, 7.5 or 75 ppm, and observations made of their social and exploratory behaviour and of gross neurotoxicity (ataxia). Mercury concentration in the blood was monitored. MMD at 75 ppm (50 ppm Hg) for 24 days caused ataxia with a sudden onset at 21-27 days. Social behaviour was reduced at 16-17 days. In two experiments at 7.5 ppm MMD, activity was increased in observations of social behaviour after 2 to 17 days, and treated rats found water in an unfamiliar cage sooner than controls. No difference from controls was apparent from then until increased activity re-appeared after 9 mon of the diet (exp. 1) or after 7 days recovery from 31 or 45 days diet (exp. 2). Ataxia was not observed after 7.5 ppm MMD for up to 47 weeks or in 14 weeks recovery. No consistent effect was observed at 1.5 ppm MMD for 31-45 days. MMD, therefore, had a behavioural effect in rats, independent of gross neurotoxicity; its details were consistent with a hyperresponsiveness to stimuli. Tolerance occurred to this effect at a time when blood-mercury concentration was still rising, but the tolerance appeared to be subject to overload.
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PMID:Early change and adaptation in the social behaviour or rats given methyl mercury in the diet. 719 56

Pharmacological actions of eptazocine on the central nervous system were investigated by pharmacological and behavioral methods. Eptazocine produced sedation at low doses and Straub tail reaction in mice and ataxia in rats at high doses. In mice, eptazocine caused decreases in the spontaneous locomotor activities measured by the wheel cage and Animex methods, but caused an increase of the response in rats as determined by the open-field method. Eptazocine caused impairment of performance in the rotarod test and the traction test in mice, a decrease of activity of EMG, and an inhibition of flexor reflex in rats. Eptazocine decreased body temperature, potentiated pentobarbital-induced sleeping, and convulsion caused by pentylene-tetrazol in mice. Fighting behavior induced by electric shock and central stimulation effect of methamphetamine were inhibited by eptazocine in mice. Eptazocine showed an inhibiton of avoidance behavior in shuttle and skinner boxes in rats. These results suggest that eptazocine produces a non-specific inhibitory action on the central nervous system.
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PMID:[Pharmacological action of eptazocine (l-1,4-dimethyl-10-hydroxy-2,3,4,5,6,7-hexahydro-1,6-methano-1H-4-benzazonine). (III) Central action of eptazocine (author's transl)]. 733 66


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