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)

Previous studies have suggested that racial differences may exist in beta-adrenoceptor-mediated responsiveness. However, no clear conclusions can be drawn based on these studies because of the confounding effect of the parasympathetic nervous system on responses to isoproterenol bolus doses. In this study, we blocked the effects of the parasympathetic nervous system with atropine, to determine whether racial differences exist in sensitivity to beta-adrenoreceptor stimulation and blockade. Sixteen healthy black and white men participated in the study. Atropine was administered before all studies to induce parasympathetic blockade. Isoproterenol sensitivity studies and treadmill exercise were then performed in the with and without beta-adrenoceptor blockade by propranolol. Responses measured included heart rate (HR), blood pressure (BP), and tremor. The average isoproterenol dose producing a 25-beat/min increase in HR was more than twofold higher in blacks than in whites (3.4 +/- 1.2 vs. 1.6 +/- 0.4 micrograms, respectively, p < 0.05). There were no racial differences in response to beta-adrenoreceptor blockade. Our results showed that during parasympathetic blockade blacks were less sensitive to the chronotropic effects of isoproterenol than whites. We conclude that these response differences are due to greater beta-adrenoceptor sensitivity in whites than in blacks.
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PMID:Racial differences in beta-adrenoceptor-mediated responsiveness. 772 60

Facial electromyography (EMG) coupled with visual observation was used to investigate spontaneous and drug induced perioral movements in freely moving rats. Four separate perioral behaviours were identified; facial tremor, purposeless chewing, gaping and yawning. Facial tremor, yawning and gaping but not purposeless chewing produced characteristic EMG signals. Normal rats displayed a low level of purposeless chewing, occasional bursts of facial tremor but not gaping or yawning. Each burst of facial tremor was accompanied by a transient increase in purposeless chewing. Administration of the D1 agonist SKF 38393 induced a dose related increase in bursts of facial tremors and consequently an increase in the total number of purposeless chews. Gaping and yawning were not induced by SKF 38393 administration. Administration of the cholinesterase inhibitor physostigmine (0.1-0.4 mg/kg) induced a dose related increase in the total number of purposeless chews, but primarily these were not associated with facial tremor. Administration of physostigmine also increased gaping and yawning. Administration of the D1 antagonist SCH 23390 almost abolished facial tremor in normal treated rats but only partially reduced that induced by SKF 38393 and physostigmine. SCH 23390 reduced purposeless chewing in SKF 38393 treated rats but not in normal or physostigmine treated animals. Administration of the cholinergic antagonist atropine almost abolished facial tremor in normal and physostigmine treated rats, but only reduced by 46% that induced by SKF 38393. Atropine reduced purposeless chewing in normal, physostigmine and SKF 38393 treated animals. Physostigmine induced gaping and yawning were abolished by atropine administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electromyographical differentiation of the components of perioral movements induced by SKF 38393 and physostigmine in the rat. 787 Oct 53

The potency of centrally administered non-selective (atropine and N-methyl scopolamine) and putatively selective muscarinic antagonists (pirenzepine, AF-DX 116 and 4-DAMP) in inhibition of oxotremorine-induced hypothermia, tremor and salivation in male mice has been compared with their potency in vitro in three functional systems, where muscarinic effects are mediated preferentially by M1 (i.e. superior cervical ganglion), M2 (i.e. atrium), and M3 (i.e. ileum) receptors. Atropine, N-methyl scopolamine and 4-DAMP potently abolished the effects of oxotremorine. Pirenzepine abolished tremor and salivation, whereas hypothermia was antagonized partially only. AF-DX 116 had but weak antagonistic effects. Atropine and N-methyl scopolamine were potent antagonists in all three in vitro test systems. High potency was also seen with 4-DAMP, in particular in the ileum preparation. Pirenzepine showed its highest potency in the ganglion preparation. AF-DX 116 was a weak and non-selective antagonist in all three in vitro preparations. Our studies indicate that the muscarinic induction of tremor and salivation may be preferentially mediated by M3 receptors whereas both M2 and M3 receptors may be involved in the mediation of hypothermia. However, the overall conclusion is that compounds with higher receptor subtype selectivity are needed.
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PMID:The involvement of muscarinic receptor subtypes in the mediation of hypothermia, tremor, and salivation in male mice. 815 35

This study examined the effects of acute and chronic desipramine, 24-h total sleep deprivation (TSD) and 96-h REM sleep deprivation (REMSD) on physostigmine-induced hypothermia, analgesia and behaviour. The effects of acute and chronic desipramine treatment on oxotremorine-induced hypothermia were also examined. Intraperitoneal administration of physostigmine (0.5 mg/kg i.p.) induced hypothermia, analgesia, purposeless chewing movements (chewing) and head tremors. While atropine given in a low dose (1.0 mg/kg i.p. 15 min prior) did not antagonize the hypothermia, chewing and head tremor associated with physostigmine (0.5 mg/kg i.p.), a higher dose of atropine (10 mg/kg i.p. 15 min prior) decreased physostigmine-induced hypothermia, chewing and head tremor behaviour. Chronic (10 or 20 mg/kg i.p. daily for 10 days and withdrawn 24 h prior, chronic DMI) and acute (10 mg/kg, i.p. + 60 min prior, acute DMI) desipramine treatments abolished physostigmine (0.5 mg/kg i.p.)-induced hypothermia compared with saline pretreatment. Interestingly atropine (1 mg/kg i.p. 15 min prior) reversed the inhibitory effect of chronic DMI on hypothermia induced by physostigmine. Acute but not chronic DMI decreased physostigmine-induced chewing and head tremor behaviour. Atropine (1 mg/kg i.p. 15 min prior) increased the inhibitory action of acute DMI on physostigmine-induced chewing behaviour. Acute DMI (10 mg/kg i.p.) decreased oxotremorine (0.1 mg/kg i.p.)-induced hypothermia, while chronic DMI increased the hypothermic effect of oxotremorine. TSD and REMSD did not alter physostigmine (0.5 mg/kg i.p.)-induced hypothermia; however, REMSD and stress decreased physostigmine-induced analgesia and chewing.It is suggested that chronic desipramine treatment decreased physostigmine-induced hypothermia by causing hypersensitivity of pre-synaptic muscarinic receptors, whereas acute desipramine decreased the sensitivity of post-synaptic muscarinic receptors
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PMID:Functional reactivity of central cholinergic systems following desipramine treatments and sleep deprivation. 1368 87

Tacrine is a potent and reversible inhibitor of acetylcholinesterase (AChE) in the brain. It produces tremor in animals, which is believed to be due to an increase in the brain acetylcholine level following AChE inhibition. The present study was undertaken to investigate the involvement, if any, of biogenic amines in the genesis of this motor dysfunction. Administration of tacrine (10-20 mg/kg, i.p.) produced dose- and time-dependent tremor in Balb/c mice. While in vivo inhibition of striatal AChE activity was observed only for the highest dose of tacrine, a dose-dependent increase in striatal choline acetyltransferase activity was obtained. Serotonin (5-HT) levels, as assayed following a sensitive HPLC-electrochemical procedure, were significantly increased in nucleus caudatus putamen, nucleus accumbens, substantia nigra, nucleus raphe dorsalis, olivary nucleus and the cerebellum. However, dopamine or norepinephrine levels remained unaltered in these areas of the brain. In animals treated with p-chlorophenylalanine, a specific tryptophan hydroxylase inhibitor and 5-HT depletor, tacrine failed to elevate the levels of 5-HT in the brain regions, and significantly attenuated tremor response to the drug. Tacrine-induced tremor was also significantly (83%) attenuated by 5-HT(2A/2C) receptor antagonist mianserin (5 mg/kg, i.p.), but methysergide (5 mg/kg, i.v.) could block tacrine-induced tremor only by 20%. Atropine (5 mg/kg, i.p.) antagonized tacrine-induced tremor by about 53%, but a combination of atropine and mianserin completely blocked the tremor response. These results indicate that the cholinergic tremor produced by tacrine in Balb/c mice is mediated via central serotonergic mechanisms, and stimulation of 5-HT(2A/2C) receptors plays a pivotal role in this motor dysfunction.
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PMID:Evidence for the involvement of central serotonergic mechanisms in cholinergic tremor induced by tacrine in Balb/c mice. 1599 Jan 78


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