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

In mice, Arecoline in vivo dose-dependently increased the cGMP concentrations of the cerebellum and the "cereberum" (= parts of cortex, hippocampus, hypothalamus, thalamus, striatum and midbrain) without influencing thecAMP levels. The cholinesterase inhibitors paraoxon and physostigmine caused an elevation only in "cerebrum", whereas the cGMP content of the cerebellum even decreased. Pretreatment with atropine prevented the rise in cGMP levels as well as the symptoms of cholinergic stimulation elicited by arecoline or paraoxon. Diazepam reduced cGMP levels below control values and blocked the effect of arecoline, while typical symptoms due to arecoline, e.g., tremor and salivation remained unaffected. The tripeptide prolyl-leucyl-glycinamide (MIF) had no effect on either cGMP values or the peripheral signs of cholinergic stimulation elicited by arecoline. The results show that elevation of cGMP in the central nervous system caused by cholinomimetic agents can be prevented not only by cholinolytics, blocking muscarinic receptors but also by influencing other mechanisms to be discussed.
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PMID:Effects of arecoline and cholinesterase inhibitors on cyclic guanosine 3',5'-monophosphate and adenosine 3'.5'-monophosphate in mouse brain. 24 44

The ability of four central cholinomimetics to reverse a scopolamine-induced spatial memory impairment or to improve visual recognition memory in primates was examined. Physostigmine (0.04-0.08 mg/kg IM) fully reversed the effects of scopolamine (0.03 mg/kg). Coadministration of pilocarpine (3.0-5.0 mg/kg) caused partial reversal of the scopolamine impairment after intermediate or long retention intervals (10 or 20 s). Treatment with arecoline (0.1-1.8 mg/kg) or nicotine (1.0-2.0 mg/kg) generally did not reverse the effects of scopolamine. A task in which memory could be taxed by increasing the number of visual stimuli presented appeared more sensitive to the effects of cholinomimetics on cognition than the scopolamine reversal model. In this paradigm treatment with physostigmine (0.001, 0.01 or 0.03 mg/kg) increased choice accuracy from about 55 to 70% correct. Arecoline improved performance at one dose only (0.1 mg/kg) which also induced marked adverse side-effects (salivation and tremor). Pilocarpine improved performance in the dose range 0.125-0.35 mg/kg, but not at higher doses which also induced marked salivation. Treatment with nicotine (0.001-2.0 mg/kg tended to improve performance but this did not reach statistical significance. The relevance of these findings for studies in man and for animal models of dementia is discussed.
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PMID:Comparison of the effects of four cholinomimetic agents on cognition in primates following disruption by scopolamine or by lists of objects. 250 53

Tremor in rats withdrawn from repeated ethanol administration was analyzed using an electronic device. The ethanol withdrawal tremor appeared in bursts during the first and second day of withdrawal and subsided at the third day of withdrawal. The frequency analysis showed that the mean frequency of withdrawal tremor was 6-7 Hz during the 48 hr observation period used. The frequency spectra of tremor induced by physostigmine (0.7 or 0.9 mg/kg) in control rats revealed that the tremoring frequency encompassed only a narrow peak, which temporarily decreased from 13 Hz to 11 Hz during the tremoring period. Arecoline (25 mg/kg) also induced tremor with a peak frequency at 13 Hz, but this tremor did not show any temporary decrease in peak frequency. The frequency analysis of tremor in ethanol withdrawn rats treated with physostigmine showed that the rats trembled at two frequencies, 6-7 Hz and 13 Hz. These two frequencies, each characteristic for one of the treatments, remained separate during the 48 hr observation period. As these two tremors did not interact with each other, it is suggested that these tremors are mediated by different mechanisms in the central nervous system. Thus it seems unlikely that the central muscarinic cholinergic system is involved in the genesis of tremor during ethanol withdrawal.
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PMID:Ethanol withdrawal tremor does not interact with physostigmine-induced tremor in rat. 404 28

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

Magnesium (Mg) has been proposed to take part in biochemical dysregulation contributing to psychiatric disorders. The aims of this study was to estimate acute behavioural responses to clonidine (0.1 mg/kg i.p.), d-amphetamine (5 mg/kg, i.p), arecoline (15 mg/kg i.p), nicotine (6 mg/kg i.p.), apomorphine (1.5 mg/kg i.p.) and L-5-hydroxytryptophan (300 mg/kg i.p.) in rats fed with Mg-deprivated diet for 49 days and then treated with organic and inorganic Mg salts (50 mg Mg per kg) ether alone or in combination with pyridoxine (5 mg vitamin B6 per kg). In our study Mg-deficient rats were more sensitive to d-amphetamine-induced motor stereotypes compared with control rats; time of onset of the stereotypies insignificantly decreased by 14.89% and duration of the stereotypies significantly increased by 19.44% (320.36 +/- 19.90 vs. 268.23 +/- 8.17 minutes; p = 0.043). Mg deficiency did not modulate sensitivity to nicotine-induced seizure. The time between nicotine injection and emergence of clonic seizure (seizure latency) in the controls and Mg-deficient rats were 0.80 +/- 0.26 and 0.96 +/- 0.21 minutes respectively. Duration of the seizures in the controls and Mg-deficient rats were 64.93 +/- 7.20 and 79.32 +/- 8.13 minutes. In our study, Mg deficiency did not affect on clonidine- and apomorphine-induced hypothermia. Clonidine produced similar decreases in rectal temperature in controls and Mg-deficient group. In experiments using apomorphine, values of hypothermia were similar to those observed with clonidine. Mg deficiency antagonized 5-hydroxytryptophan-induced head-twitch response. The number of head twitches produced by 5-hydroxytryptophan was significantly (p = 0.49) decreased: twofold in magnesium-deficient rats (1.23 +/- 0.44 per minute) as compared with controls (2.42 +/- 0.52 per minute). Arecoline-induced tremor was comparably less expressed in Mg-deficient rats than in controls. The time between arecoline injection and time of onset of the tremor in the controls and Mg-deficient rats were 92.75 +/- 19.35 and 245.17 +/- 121.86 seconds respectively (p < or = 0.035). Duration of the tremors in the controls and Mg-deficient rats were 1175.58 +/- 127.87 and 703.83 +/- 89.33 seconds (p = 0.015). Magnesium salts (Mg chloride, Mg L-aspartate alone and in combination with B6) were administered through gastric tube during twenty days up to complete compensation oferythrocyte and plasma Mg levels in all experimental groups. In our study administration of Mg salts resulted in normalization of acute behavioural responses in Mg-deficient rats to d-amphetamine, arecoline, and L-5-hydroxytryptophan. Behavioural responses in rats treated with both Mg chloride and Mg L-aspartate in combinations with B6 were comparable with those observed in MagneB6 treatment.
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PMID:[The characterization of central neuromediation in rats fed with magnesium-deprived diet before and after magnesium replenishment]. 1876 95