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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pharmacological effects of N-[4-(2-bromoethylmethylamino)-2-butynyl]-2-pyrrolidone (BR 401) were compared in the mouse with those of N-[4-(2-chloroethylmethylamino)-2-butynl]-2-pyrrolidone (BM 123) and oxotremorine. BR 401 was more toxic than oxotremorine and BM 123 when administered i.v. (LD50, 0.7 mumol kg-1), but less toxic than oxotremorine when given i.p. (LD50, 39 mumol kg-1). Atropine and methylatropine (10 mumol kg-1 i.p.) increased the LD50 value of BR 401, given i.v., 75- to 100-fold. Upon i.v. administration, BR 401 was 2- to 3-fold more potent than oxotremorine and 10 to 20 times more potent than BM 123 in producing central (tremor and analgesia) and peripheral (salivation) muscarinic effects. However, after i.p. administration BR 401 was 3-fold less potent than oxotremorine in eliciting tremor and analgesia. The aziridinium ion (BR 401A), formed by cyclization of BR 401, produced salivation but no tremor. These observations suggest that BR 401 when given i.v. penetrates effectively into the central nervous system where it cyclizes rapidly to the pharmacologically active aziridinium ion. In contrast, after i.p. administration a large proportion of BR 401 will cyclize before it can reach the central nervous system. BM 123, because of its slower cyclization, enters the central nervous system effectively also by the i.p. route. Thus, central potency of 2-haloethylamines such as BR 401 and BM 123 is critically dependent not only on the rate of cyclization, but also on the route of administration. The duration of tremor induced by BR 401 and BM 123 was considerably shorter than that induced by oxotremorine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Muscarinic actions of an N-methyl-N-2-bromoethylamino analog of oxotremorine (BR 401) in the mouse. 380 1

The tremors induced by harmine, LON-954 (N-carbamoyl-2-(2,6-dichlorophenyl)acetamidine hydrochloride) and 5-hydroxytryptophan (5-HTP) were studied in control rats and in rats withdrawn for 16-48 hrs from 6 to 9 days' ethanol administration. The frequencies and the intensities of the tremors were determined electronically. In control rats the frequency spectra of the tremors induced by harmine (20 mg/kg) and LON-954 (10 mg/kg) showed a narrow peak frequency at about 10 Hz. Atropine (1.2 mg/kg) altered neither the frequency nor the intensity of these tremors. 5-HTP (50 mg/kg) when given 3.5 hrs after iproniazid (100 mg/kg) induced tremor with peak frequencies at 6-7 Hz and 12 Hz. In ethanol-withdrawn rats treated with harmine or LON-954 the frequency analysis of tremor revealed a narrow peak frequency at about 12 Hz, which was neither the characteristic frequency of ethanol withdrawal tremor (6 Hz) nor that of harmine or LON-954 (10 Hz). The intensity of both harmine- and LON-954-induced tremor was significantly increased in ethanol-withdrawn rats. The ethanol-withdrawn rats were markedly sensitized to the effect of iproniazid+ 5-HTP, shown by deaths. The peak frequencies of this tremor were the same as those in control rats. The results suggest that harmine-induced tremor involves a dopaminergic-5-HT'ergic imbalance and the tremor induced by LON-954 a dopaminergic-cholinergic imbalance in the brain. The tremor in ethanol-withdrawn rats seems to be mediated by alterations in the activity of the cerebral 5-HT'ergic system.
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PMID:Harmine-, LON-954- and 5-hydroxytryptophan-induced tremors in rats withdrawn from ethanol. 387 87

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

1. An investigation of central cholinoceptors in the mouse has been made by injecting cholinomimetic drugs into the cerebral ventricles and seeing how their effects were modified by prior administration of atropine-like substances and other drugs.2. Carbachol or oxotremorine injected in small doses intracerebroventricularly into conscious mice caused hypothermia, gross tremor and a variety of parasympathomimetic effects including lachrymation and salivation. Acetylcholine injected in this way was active only in much larger doses.3. Methacholine and pilocarpine also caused a variety of parasympathomimetic effects after intracerebroventricular injection but virtually no hypothermia or tremor.4. Nicotine injected intracerebroventricularly caused mild hypothermia, fine tremor but no parasympathomimetic effects.5. Atropine-like drugs, tricyclic antidepressants and amphetamine antagonized the hypothermia induced by intracerebroventricular carbachol or oxotremorine.6. The sites of action of the atropine-like drugs are in the brain; those of the tricyclic antidepressants and amphetamine are in the periphery probably on heat generating beta-adrenoceptor mechanisms.7. It is concluded that the atropine sensitive cholinoceptors in the brain vary in their sensitivities to cholinomimetic drugs, other than acetylcholine, and may exist in isoreceptor forms.8. Peripheral atropine sensitive cholinoceptors may also exist in isoreceptor forms.
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PMID:Investigation of central cholinergic mechanisms in the conscious mouse. 558 Jun 97

1. Injection of oxotremorine in the rat results in tremor and an increase in brain acetylcholine. The effects of atropine and dyflos have been investigated on both these actions.2. Atropine decreased brain acetylcholine concentration and inhibited oxotremorine-tremor. It did this in doses which did not prevent the oxotremorine-induced increase in whole brain acetylcholine.3. Dyflos increased brain acetylcholine concentration, but it was without effect on oxotremorine tremor. Some mutual antagonism was observed between the actions of oxotremorine and dyflos on rat brain acetylcholine concentration.4. These results do not support a causal relationship between the increase in whole brain acetylcholine and the tremor produced by oxotremorine.
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PMID:The effects of atropine and dyflos on tremor and increase in whole brain acetylcholine produced by injection of oxotremorine in the rat. 580 41

In an attempt to elucidate the mechanism of wet dog shakes (WDS) produced by carbachol administered into the rat lateral brain ventricle, the effects of blockade of muscarinic and nicotinic receptors on shaking response and the effects of carbachol on central catecholaminergic, serotonergic (5-HT) and GABAergic functions were studied in rats. The muscarinic receptor antagonists, atropine and scopolamine attenuated WDS produced by carbachol, whilst a peripherally active muscarinic receptor antagonist, scopolamine methyl nitrate, failed to influence WDS. The nicotine antagonist, mecamylamine, did not affect WDS caused by carbachol either. Carbachol dose dependently decreased brain concentration of noradrenaline (NA) but failed to affect the concentration of dopamine (DA). While the brain concentration of 5-HT was unchanged, the concentration of 5-hydroxyindoleacetic acid (5-HIAA) was increased in a dose-related manner. The catecholamine turnover times were unaffected whereas 5-HT turnover time was significantly prolonged. Atropine, but not mecamylamine, prevented the decrease in brain NA induced by carbachol. Consequently, the carbachol-induced enhancement in the level of 5-HIAA was completely blocked by atropine and only slightly influenced by mecamylamine. Neither brain GABA concentration nor glutamic acid decarboxylase activity were affected by carbachol. Behavioral and biochemical data suggest that WDS produced by carbachol may be mediated through the stimulation of central muscarinic receptors. The anatomical localization and exact mechanism of carbachol-induced WDS remain to be elucidated.
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PMID:Studies on the mechanism of wet dog shakes produced by carbachol in rats. 620 Aug 91

Bronchodilating drugs can be divided into three main groups: beta-adrenergic stimulants including specific beta-2 receptor agonists (salbutamol, terbutaline, fenoterol) which are the agents of this group used in everyday practice, theophylline and its derivatives, and atropine-like drugs (ipratropium bromide). Bronchodilators act chiefly upon the spasm observed at the bronchial level in reversible obstructive phenomena (mainly asthma), their effect upon inflammation and hypersecretion being slight or controversial. Beta-stimulants have a relatively specific mode of action at the bronchial level in the setting of use in pneumology; they exhibit cardiac effects only at high doses and when used by oral or parenteral routes. Relative to isoprenaline, they also have the advantage of being active orally and over a longer period of time. They are given in maintenance treatment of asthma, by parenteral or oral routes or as aerosols. Main side effects of adrenergic beta-stimulants are tremor with oral administration, and tachycardia with very high doses by parenteral or oral routes; when given as aerosols these agents may fail to control severe attacks. The bronchodilating properties of theophylline have been known for a long time; late advances concerning this drug result from better knowledge of its pharmacokinetics. Recent studies have discriminated between serum levels correlated with therapeutic effectiveness and those accompanied with mild or severe side effects; in addition, it has been clearly shown that the half life of this alkaloid varies from one person to another and with various physiopathologic (age, dietary habits, liver failure, heart failure...) or pharmacologic (drug interactions with enzyme inductors or inhibitors...) factors; these recent advances have led to improved individual adjustment of theophylline dosage using serum concentration assays if needed. Theophylline is used in acute attacks and in maintenance therapy of asthma. Main side effects are digestive intolerance and, with toxic doses, neurologic disorders. Atropine-like drugs inhibit the effects of the parasympathetic reflex which results from stimulation of receptors by irritation of the respiratory tract, through the action of mediators. In this group, ipratropium is the only drug given in aerosols; this, together with its pharmacologic specificity, contributes to its tolerance. In some instances, the bronchodilating effect of ipratropium bromide is comparable to that of sympathomimetics.
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PMID:[Bronchodilators]. 632 Apr 43

The effects of anticholinergic and dopaminergic drugs used for Parkinson's disease were studied on the tremor induced by physostigmine (0.3-3.0 mg/kg) in rats. For the measurement of tremor a new electronic device was employed. Atropine (0.3-1.2 mg/kg) and biperiden (0.01-1.0 mg/kg) reduced the physostigmine-induced tremor in a dose-related manner and could abolish it. Biperiden was less potent than atropine. Methylatropine in a dose of 1.2 mg/kg slightly inhibited the tremor. Amantadine (0.3-3.0 mg/kg) reduced the tremor but only to a certain degree. Bromocriptine (0.1-10.0 mg/kg) reduced it in a manner that was not dose-related. Pimozide potentiated the tremor in the dose of 0.2 mg/kg but not in larger doses. At the onset of the tremor, a small decrease in rectal temperature occurred. The hypothermia lasted significantly longer than the tremor. Neither the anticholinergic nor the dopaminergic anti-Parkinson drugs altered the hypothermic effect of physostigmine. The results show that those anti-Parkinson drugs, which act by increasing the dopaminergic activity can counteract the tremor induced by physostigmine. However, these drugs are clearly less active than th anticholinergic anti-Parkinson drugs.
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PMID:Drugs for Parkinson's disease reduce tremor induced by physostigmine. 662 15

Nicotine (4; 8 mg/kg) given intraperitoneally to mice had a marked hypothermic effect with a duration of more than 2 hours. Mecamylamine (0.5; 2.5 mg/kg) prevented the hypothermic effect of 2 mg/kg nicotine but had no effect on 4 mg/kg nicotine. Atropine (5 mg/kg) did not affect the hypothermia produced by nicotine. Other symptoms induced by nicotine (0.5-4 mg/kg) were convulsions, rigidity, tremor and decrease in motor activity. Pretreatment with mecamylamine (0.5 mg/kg) prevented convulsions but had only a slight effect on the decreased motor activity. Atropine pretreatment was ineffective. It thus seems as if the effects of nicotine at least to some part are mediated by nicotine-like receptors. When a tracer dose of labelled choline (3H-Ch) was given to mice treated with nicotine (4 mg/kg) a marked increase (+100%) in the biosynthesis of labelled acetylcholine (ACh) in the striatum was found when the animals were killed by decapitation. If the mice were killed by a more rapid technique, microwave irradiation of the head, no change in 3H-ACh formation was observed in comparison to controls. The findings indicate that nicotine can preserve a very labile pool of newly synthesized ACh in the striatum.
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PMID:Pharmacodynamic effects of nicotine and acetylcholine biosynthesis in mouse brain. 688 Jul 69

Rats were injected unilaterally into the rostral substantia nigra pars compacta with 8 micron of 6-OHDA. Those animals that conformed to be behavioral criteria for an effective nigrostriatal dopamine lesion by turning ipsilaterally to the injected side upon IP amphetamine, and contralaterally upon apomorphine injection were bilaterally detelencephalized (neocrotex, hippocampus, striatum, septum, amygdaloid complex were removed). Most detelencephalized animals exhibited spontaneous turning to the contralateral side, i.e. no longer behaved like 6-OHDA-lesioned rats, but instead, acted like animals with nigral kainic acid or electrolytic lesions. Amphetamine (2-3 mg/kg) increased general activity but no longer influenced turning. Apomorphine in doses of 2-3 mg/kg completely suppressed all motility. In small doses (0.1-0.2 mg/kg) it reversed the spontaneous contraversive turning. This effect could be blocked by haloperidol (0.1 mg/kg) pretreatment. High doses of haloperidol (5.0-7.5 mg/kg) reversed the direction of circling from contraversive to ipsiversive. Arecoline (10-12 mg/kg) induced tremor as in normal animals. Atropine (50-100 mg/kg) did not affect turning, but increased activity level in the thalamic rats.
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PMID:The influence of unilateral 6-OH-dopamine lesions of the substantia nigra in the absence of the telencephalon. 747 Sep 60


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