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)

Oxotremorine, 0.25 mg/kg, produces marked tremor in the rat, which is abolished by scopolamine, 0.5 mg/kg, and is substantially reduced in intensity and duration both by adrenalmedullectomy and by chemical sympathectomy with 6-hydroxydopamine. Oxotremorine increases plasma norepinephrine from 0.62 +/- 0.07 to 3.01 +/- 0.47 ng/ml and plasma epinephrine, from 0.82 +/- 0.14 to 3.42 +/- 0.48 ng/ml, in conscious unrestrained rats. l-Propranolol (0.5-2.5 mg/kg) reduces tremor, and at 2.5 mg/kg is more effective than either chemical sympathectomy or adrenal demedullation. d-Propranolol and sotalol are also active at 4 and 10 times the dose of l-propranolol, respectively. l-Propranolol does not prevent the rise in catecholamines induced by oxotremorine. It is suggested that stimulation of central muscarinic receptors causes tremor by a combination of two effects. There is an increase in cholinergic influence to motor efferents accompanied by an activation of the sympathoadrenal system to release catecholamines which augment tremor by stimulation of beta2 adrenoceptors.
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PMID:The role of peripheral catecholamines in oxotremorine tremor in the rat and its antagonism by beta adrenoceptor blocking agents. 2

Oxotremorine did not alter the level of 5-HT and 5-hydroxyindoleacetic acid in different brain regions. The content of 5-HT in the striatum was diminished by electrolytic lesions of the raphe system, by microinjection of the selective depletor 5,6-dihydroxytryptamine into the raphe system and inhibition of synthesis by pCPA or pCAM. The intensity of oxotremorine-induced tremor was reduced only in some experimental groups without clear-cut correlation to the decreased 5-HT levels. In pCPA-pretreated animals resoring of 5-HT concentration by intrastriatal microinjection of 5-HT and ip administration of 5-HT did not reestablish tremor intensity. There is no evidence that cholinergic tremor is triggered indirectly and depends upon an intact 5-HT system.
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PMID:Serotonin content in the central nervous system of rats and cholinergic tremor. 12 45

Oxotremorine, a specific stimulant of central muscarinic acetylcholine receptors, inhibited lateral hypothalamic self-stimulation at a dose-level less than one-tenth of that necessary to produce body tremor. Tremor induced by oxotremorine (0.5 mg/kg) was inhibited by pretreatment with hyoscine (scopolamine) (0.3 mg/kg) or propranolol (20 mg/kg) but not by methylhyoscine (0.3 mg/kg) or apomorphine (0.3 mg/kg). Inhibition of self-stimulation by oxotremorine (.03 mg/kg) was prevented by hyoscine (0.3 mg/kg) but not by any other of the drugs tested and thus constitutes a uniquely specific in vivo model for assessing central antimuscarinic activity. The results confirm the presence of centrally situated ACh receptors eleciting tremor and inhibiting self-stimulation but provide no evidence of an effect on tremor by central adrenergic beta-receptors.
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PMID:Central cholinergic mechanisms in electrical self-stimulation and in drug-induced tremor in rats. 53 51

1. The effect of various agents injected into the cerebral ventricles of the mouse, upon the tremor and hypothermia produced by oxotremorine (0.5 mg/kg i.p.) was studied. 2. Acetylcholine (0.1-10 mug) produced a dose-dependent potentiation of oxotremorine tremor in contrast to the multiphasic effect it had on the accompanying hypothermia. Both tremor and hypothermia were antagonised by very small doses (0.1-10 ng) of atropine. 3. Dopamine and apomorphine (0.1-10 mug) had no significant effect on oxotremorine tremor. A dose-dependent potentiation of hypothermia was, however, observed. 4. Noradrenaline (0.1-10 mug), phentolamine and propranolol (0.1-10 mug) produced no significant effect on tremor and inconsistent results were obtained on hypothermia. 5. Neither tremor nor hypothermia were affected by 5-hydroxytryptamine (1-20 mug). 6. Oxotremorine tremor appears to be due solely to the activation of cholinergic pathways, whereas the production of hypothermia is brought about via a system involving both cholinergic and dopaminergic components. 5-Hydroxytryptamine is not involved.
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PMID:Modification of oxotremorine tremor and hypothermia by injections of drugs into the cerebral ventricles of the mouse. 101 35

The effects of levocabastine (R 50 547; CAS 79516-68-0) on the central nervous system were studied in comparison with those of diphenhydramine, ketotifen and azelastine. At high doses, levocabastine caused a decrease in locomotor activity, prolongation of thiopental-induced sleep, depression of acetic acid-induced writhing in mice and inhibition of active avoidance response in rats, but these adverse effects were much less potent than those seen in diphenhydramine, ketotifen and azelastine. Oxotremorine-induced tremor and salivation in mice were delayed after extremely high dosage of levocabastine; however, these were much less effective than those seen after diphenhydramine and ketotifen. Levocabastine did not affect the tonic extensor seizure induced by maximal electroshock in mice which is different from that of diphenhydramine. In EEG analysis, levocabastine at a dose of 20 mg/kg caused no significant changes in the EEG recorded from the frontal cortex, occipital cortex, hippocampus and amygdala in rats with chronic electrodes.
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PMID:Central effect of the potent long-acting H1-antihistamine levocabastine. 198 50

Oxotremorine-induced tremor activity in mice was suppressed by pretreatment with either L-dopa or atropine. Additional pretreatment with the opiate receptor blocker naloxone significantly potentiated the antitremor effect of L-dopa but not that of atropine. These findings indicate a selectivity of drug interaction between naloxone and L-dopa.
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PMID:A selective potentiation by naloxone of L-dopa but not atropine suppression of oxotremorine-induced tremor in mice. 286 96

Previous work in our laboratory has shown that the aziridinium ion of BM 123 (N-[4(2-chloroethylmethylamino)-2-butynyl]-2 pyrrolidone) is a potent and selective muscarinic agonist and binds irreversibly to muscarinic receptors (mAChR). The present series of experiments was designed to study the effects of BM 123 on behavioral and physiological variables known to be sensitive to manipulations of the cholinergic neurotransmitter system. BM 123 was injected into the tail vein of Sprague-Dawley rats, reducing mAChR to approximately 10% of normal as judged by [3H](-)QNB binding. Oxotremorine was injected IV for purposes of comparison. Behavioral and physiological variables were measured daily for 26 days. Physiological variables (e.g., tremor, chromodacryorrhea, salivation, and temperature) showed effects in less than 5 min after injection and returned to their pretreatment baselines within minutes. Nociceptive thresholds, dependent on sensory-perceptual processes, showed peak changes of approximately +230% and returned to normal within hours. Motoric responses, i.e., drinking and general activity, recovered in 3-4 days. Learned responses and those requiring temporal discrimination took 8-11 days to recover and were the only responses paralleling the return of the mAChRs to their normal levels. Changes elicited by oxotremorine recovered more rapidly than those elicited by BM 123. The results suggest that the different variables measured are dependent on different densities of functional receptors. Implications for a theoretical model are discussed.
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PMID:Behavioral and physiological effects associated with changes in muscarinic receptors following administration of an irreversible cholinergic agonist (BM 123). 309 16

Oxotremorine (0.125 mg/kg) produces a significant increase in total acetylcholine content in whole pigeon brain. The contribution of different regions to this increase varies. The largest increase occurs in the nucleus basalis (paleostriatum augmentatum), a region which is highly involved in motor control. The mechanism by which oxotremorine increases the acetylcholine content of brain and the causal relationship between the rise in acetylcholine content and tremor are discussed.
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PMID:Effect of oxotremorine on the acetylcholine content of whole brain and various brain regions in the pigeon. 509 Nov 63

1. The relationship between tremor and change in brain acetylcholine concentration after the injection of tremorine or oxotremorine has been investigated in rats.2. Tremorine produced a significant increase in whole brain acetylcholine and in tremor 5 min after injection. After this time tremor subsided but brain acetylcholine continued to increase.3. Oxotremorine produced tremor within 30 sec. This became maximal within 5 min of injection and then declined rapidly. The brain acetylcholine concentration showed a significant increase 5 min after injection and continued to increase until 30 min afterwards.
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PMID:The relationship between tremor and change in brain acetylcholine concentration produced by injection of tremorine or oxotremorine in the rat. 577 44

Sensitivity of central cholinergic (muscarinic) receptors was studied in rats after application of single and repeated (once daily for 7 days) electroconvulsive shocks (ECS). Oxotremorine-induced tremor was significantly enhanced after single as well as chronic exposure to ECS; [3H]QNB binding in frontal cortex was also significantly increased by chronic ECS. The results indicate that ECS develops supersensitivity in central muscarinic receptors.
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PMID:Effect of electroconvulsive shock on central cholinergic (muscarinic) receptors. 710 97


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