Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The administration of p-chlorophenylalanine to mice prevents the rise in brain 5-hydroxytryptamine concentration associated with ethanol withdrawal but does not affect the increase in brain catecholamines which occurs at the same time. The locomotor excitement, piloerection, tremor and handling convulsions which occur during ethanol withdrawal were not affected. These results suggest that the increase in brain 5-hydroxytryptamine which occurs in ethanol withdrawal is a consequence of increased 5-hydroxytryptamine synthesis and that it is probably not involved in the above behavioural changes of ethanol withdrawal.
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PMID:Effect of p-chlorophenylalanine on brain monoamines and behaviour during ethanol withdrawal in mice. 428 35

1. The drug HA-966 (1-hydroxy-3-amino-pyrrolidone-2), which chemically resembles the cyclic form of GABA, has been studied for neuro-pharmacological properties and for effects on the catecholamine content of the corpus striatum.2. The acute effects on spontaneous behaviour of rodents included flaccid catalepsy and reversible tranquillization in doses which were 5% or less of the lethal dose. Long lasting depression of the CNS, followed by complete recovery, was produced in the cat and the dog. In the monkey HA-966 caused periodical sleeping episodes.3. The exploratory behaviour and the amphetamine-induced motor activity in mice were blocked by HA-966. The toxicity of amphetamine in aggregated mice was only moderately reduced, suggesting that HA-966 differs from neuroleptics.4. Tremors induced by chemical agents (nicotine, zinc and tremorine) were markedly inhibited by HA-966. The muscarinic effects of tremorine were not reduced by HA-966, indicating a selective central antitremor effect.5. HA-966 elevated the threshold to strychnine convulsions and abolished the ipsilateral flexor reflex, while not having motor endplate blocking properties. It is suggested that HA-966 depresses central internuncial neurones.6. In rats and rabbits HA-966 produced synchronous EEG and inhibited the sensory arousal in doses not causing sedation. In the monkey the drug caused a periodical dissociation between ;sleep-EEG' and behaviour.7. In rat brain, HA-966 selectively elevated the dopamine content in the corpus striatum, while no changes in noradrenaline and 5-hydroxytryptamine contents could be demonstrated. The effect was still present when dopa synthesis was inhibited with alpha-methyl-p-tyrosine.8. Several effects of intravenously administered HA-966 became manifest after an appreciable delay and in hepatectomized mice the effects were much reduced. It is postulated that HA-966 is converted to a pharmacologically active metabolite.9. The results are discussed in the light of current views on drug therapy in extrapyramidal conditions and a GABA-related hypothesis as to the mode of action of HA-966 is presented.
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PMID:1-Hydroxy-3-amino-pyrrolidone-2(HA-966): a new GABA-like compound, with potential use in extrapyramidal diseases. 515 20

1. The effect of obidoxime on the rise in brain acetylcholine caused by the anticholinesterase paraoxon was studied in the rat.2. In animals poisoned with a sublethal dose of paraoxon and thereafter treated with obidoxime the levels of both "free" and total brain acetylcholine were practically the same as those in rats injected with paraoxon only.3. After poisoning with doses of paraoxon which are lethal unless an oxime is also given, the total acetylcholine in the brain of obidoxime-protected rats continued to accumulate, reaching a peak 2 h after injection of paraoxon. At this time no signs of central effects such as convulsions or tremor were seen.4. Atropine, given 30 min before paraoxon, markedly reduced the rise in total brain acetylcholine seen when the anticholinesterase is given alone.5. In rats pretreated with atropine and obidoxime excessive doses of paraoxon which are lethal in the absence of the antidotes produced a rise in total brain acetylcholine which was directly proportional to the dose of paraoxon administered.
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PMID:Acetylcholine content in the brain of rats treated with paraoxon and obidoxime. 548 48

The anticonvulsive activity of cholecystokinin octapeptide sulphate ester (CCK-8-SE), non-sulphated cholecystokinin octapeptide (CCK-8-NS) and three different N- and C-terminal fragments were investigated against seizures induced by picrotoxin and electroshock in rats after intracerebroventricular administration. Doses of 0.8 and 80 pmol of CCK-8-SE and CCK-8-NS significantly enhanced the latency of seizures induced by picrotoxin and shortened the duration of the clonic phase of the seizures induced by electroshock. Only CCK-8-SE shortened the recovery time and only 0.8 pmol of CCK-8-SE could shorten the duration of the tonic phase of convulsions induced by electroshock. Doses of the octapeptides of 8000 pmol were ineffective, with the exception of CCK-8-NS in the picrotoxin test. Of the fragments tested, the C-terminal tetrapeptide, CCK-5-8, enhanced the latency of seizures induced by picrotoxin in a dose of 0.8 pmol, and had a dose-dependent biphasic effect on the duration of the clonic phase of seizures induced by electroshock. Intracerebroventricular administration of diazepam enhanced only the latency of tremor and clonic seizures induced with picrotoxin in a dose of 40 nmol. Twelve nmole of diazepam shortened the clonic phase of convulsions induced by electroshock. The peptides tested were much more active than diazepam, and their effective doses were comparable to the amounts of cholecystokinin octapeptide found in brain structures.
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PMID:Inhibition of seizures induced by picrotoxin and electroshock by cholecystokinin octapeptides and their fragments in rats after intracerebroventricular administration. 609 Sep 68

The onset pressures for the tremor, myoclonus and convulsions seen in the high pressure neurological syndrome (HPNS) are increased following cis-2,3-piperidine dicarboxylic acid 1 mmol/kg in the rat. Glutamic acid diethyl ester 1-3 mmol/kg has no effect on tremor or myoclonus, but increases the convulsion pressure when 3 mmol/kg is given immediately before compression. These and earlier data with 2-amino-7-phosphonoheptanoic acid suggest that excitation at the N-methyl-D-aspartate receptor is important in HPNS tremor, and that excitation at the quisqualate receptor contributes to HPNS convulsions.
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PMID:Effect of excitatory amino acid antagonists on the high pressure neurological syndrome in rats. 609 58

The symptoms include, by ascending order of severity: nightmares and insomnia, nausea and vomiting, muscular weakness or tremor, postural hypotension, hyperthermia, muscle twitching, convulsions, confusional state or psychosis. Prominent features are the late onset of these symptoms, several days after treatment has been discontinued, and the sometimes difficult diagnosis, since patients are usually unaware of their dependence on these drugs. Reinstituting benzodiazepine treatment, then withdrawing it progressively are the best curative measures. Prevention is easy if treatment is gradually rather than abruptly withdrawn in all patients who receive the compound in high dosage for more than one month.
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PMID:[Benzodiazepine physical dependence. 6 cases (author's transl)]. 610 22

The benzodiazepines are the most effective, safest, and most widely used antianxiety drugs. As a class of drugs, there are few major differences between the various benzodiazepine derivatives. The main distinguishing features are different plasma half-lives and the presence or absence of pharmacologically active metabolites. Plasma half-lives vary considerably, from 2 to 3 hours to more than 100 hours. All benzodiazepines are equally effective in the short term management of anxiety and insomnia, and their classification into 'anxiolytics' and 'hypnotics' is not justified. There are numerous other indications for benzodiazepine use, such as muscle spasm in osteoarthritic conditions, and acute alcohol withdrawal, but the benzodiazepines have no antidepressive or analgesic effects. While there is no good evidence for their long term efficacy in the treatment of anxiety and insomnia, the benzodiazepines are more effective and safer than their main predecessors, the barbiturates. Some of the benzodiazepines, particularly those with long plasma half-lives which are commonly used as hypnotics, have a prolonged duration of action and cause marked 'hang-over' effects. Alcohol enhances the effects of these drugs, and thus can also increase their side effects. Adversely effects such as oversedation, tremor, ataxia and confusion are much more common in elderly patients. Ever since the benzodiazepines were first marketed 20 years ago their use has increased rapidly, and it is now estimated that between 12 and 16% of the adult population in developed countries use tranquillisers at some time each year. However, their overall use has probably diminished somewhat in the last few years. Although their indications are very common, it is possible that some of this extensive usage may be the result of dependence. Until recently, published reports of such dependence were comparatively few. However, withdrawal symptoms have now been demonstrated in a substantial proportion of patients on long term, normal dose benzodiazepine treatment. The abstinence syndrome usually lasts for 8 to 10 days, and is characterised by insomnia, anxiety, loss of appetite and bodyweight, tremor, perspiration, and a host of perceptual disturbances. More serious developments such as epileptic fits and psychosis are probably infrequent during withdrawal from therapeutic doses. The overall incidence of benzodiazepine dependence remains unknown.
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PMID:Rational use of anxiolytic/sedative drugs. 613 9

Dogs, surgically implanted with a gastric fistula, were chronically dosed with diazepam or lorazepam. Diazepam (60 mg/kg/day) or lorazepam (100 mg/kg/day) was administered intragastrically in four divided daily doses. Beginning no less than 2 weeks after the attainment of stabilization doses, dogs underwent withdrawal experiments, repeated at 2-week intervals. At a time of withdrawal determined by a Latin square crossover design, dogs were observed for 8 hr for signs of abstinence. Both diazepam and lorazepam caused a withdrawal abstinence syndrome to appear upon abrupt discontinuation of the drug. The two abstinence syndromes had many signs in common, including tremor, hot foot walking, rigidity and decreased food intake, but the lorazepam withdrawal abstinence syndrome was much less intense and had a shorter latency to onset than the diazepam abstinence syndrome, which also included clonic and tonic-clonic convulsions and was lethal in two dogs. Furthermore, the diazepam withdrawal abstinence syndrome was biphasic, the first phase apparent by 24 hr and a second phase beginning at 48 hr, whereas the lorazepam syndrome was not. Diazepam suppressed the major signs of diazepam abstinence in a dose-related manner, but failed to completely suppress all signs of abstinence. CGS-8216, a pyrazoloquinoline benzodiazepine antagonist, precipitated abstinence in the diazepam-dependent dog, but did not precipitate tonic-clonic seizures. No abstinence syndrome was precipitated in the lorazepam-dependent dog. These results would suggest that whereas diazepam and lorazepam both cause physical dependence the two syndromes are not the same and, furthermore, that physical dependence on, and withdrawal from, diazepam involves at least two separate mechanisms with different selectivity for benzodiazepine agonists and antagonists.
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PMID:Physical dependence on diazepam and lorazepam in the dog. 613 1

The elevated atmospheric pressure at which the main features of the high pressure neurological syndrome (HPNS), i.e. tremor, myoclonus and convulsions, successively appear, have been studied in fed and fasted rats with and without pretreatment with 2-amino-7-phosphonoheptanoic acid (180 mg/kg). The onset pressure for tremor is lower in fasted rats. 2-Amino-7-phosphonoheptanoic acid raises the onset pressure for all three phases of HPNS in fed rats, but only for tremor and convulsions in fasted rats. The results are interpreted in terms of changes in aspartergic and related excitatory neurotransmission.
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PMID:The high pressure neurological syndrome and 2-amino-7-phosphonoheptanoic acid: differences between fed and fasted rats. 614 24

Fumitremorgin A (FTA), a neurotropic mycotoxin induced dose-dependent abnormal behaviors, including tremor, clonic convulsion, kangaroo posture and tonic extensor convulsion in the mouse. FTA-induced tonic extensor convulsion was markedly suppressed by anticonvulsant, e.g. phenobarbital, phenytoin. Phenobarbital, trimethadione, valproic acid and mephenesin decreased the occurrence of abnormal behaviors induced by FTA. Although pentylenetetrazol-induced tonic extensor convulsion was not affected by antipsychotic drugs (dopaminergic drugs) except chlorpromazine, FTA-induced abnormal behaviors were inhibited by antipsychotic drugs, e.g. chlorpromazine, haloperidol. Chlordiazepoxide, diazepam and muscimol inhibited FTA-induced abnormal behaviors. These findings suggest that both dopaminergic and gamma-aminobutyric acid (GABA)-ergic systems are involved in FTA-induced abnormal behaviors. FTA-induced abnormal behaviors may be useful as a common experimental model for the primary evaluation of anticonvulsants, antipsychotic drugs and anxiolytic drugs.
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PMID:Abnormal behavioral effects elicited by a neurotropic mycotoxin, fumitremorgin A in mice. 615 72


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