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 spectra of pharmacological effects of ethanol and the benzodiazepine show a degree of overlap. Neurophysiological and neurochemical evidence indicates that both ethanol and benzodiazepines facilitate inhibitory neurotransmission mediated by GABA. Diazepam has been reported to inhibit both the tremor and mechanism of cerebellar cyclic GMP caused by harmaline by a neurotransmission in the cerebellum. Because of the similarities between ethanol and benzodiazepines, the effects of ethanol on harmaline-induced tremor and increase of cerebellar cyclic GMP were studied. Ethanol inhibited harmaline-induced tremor at doses as low as 0.1 g/kg. At this low dose, however, a dissociation between inhibition of harmaline tremor and inhibition of the harmaline-induced increase of cerebellar cyclic GMP was observed.
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PMID:Ethanol effects on harmaline-induced tremor and increase of cerebellar cyclic GMP. 631 33

Ethanol (1.5 g/kg i.v.) was found to decrease spontaneous complex spike (CS) activity in cerebellar Purkinje cells in urethane anaesthetized rats while not changing the threshold required to evoke a CS by juxtafastigial stimulation. Thus ethanol does not decrease CS activity by an action at the climbing fibre-Purkinje cell synapse. Tremor induced by harmaline (5 mg/kg i.v.) in unanaesthetized animals was markedly antagonized by ethanol (0.5-2.0 g/kg i.v.) in all animals tested. However, in nine urethane-anaesthetized animals, ethanol markedly reversed the effects of harmaline on Purkinje cells in only two cases and partially reversed the effects in another four cells. Thus, the depressant effects of ethanol on the inferior olive is not total responsible for the blockade of the harmaline tremor bur would account for the decrease in spontaneous CS activity.
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PMID:Ethanol effects on the olivocerebellar system. 710 48

Ethanol-oleic acid esterification by a free and microencapsulated lipase from Mucor miehei, using dodecane as solvent and phosphatidylcholine as surfactant, was studied. The initial esterification rate was influenced by the water content in the biphasic system. Kinetic studies with free and microencapsulated enzyme showed that the microencapsulation led to an increase of the kinetic parameters (Vmax and Km), probably due to an increase of the interfacial area. The reaction rate was also affected by the shaking rate, the temperature and the pH. The optimal temperature and pH achieved were, respectively, 40 degrees C and 4.5 using free enzyme, and 50 degrees C and 6 using microencapsulated enzyme.
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PMID:Kinetic studies of Mucor miehei lipase in phosphatidylcholine microemulsions. 776 31

Essential tremor (ET) is typically 4 to 12 Hz frequency, absent at rest, maximal during maintenance of a posture, attenuated during movement and often accentuated at the termination of movement. Prevalence in Americans is 300 to 415 per 100,000 population, and it is frequently disabling. There is controversy about the central or peripheral origin of ET. There is no specific diagnostic test for ET; the diagnosis is made clinically. Ethanol is the most effective suppressor of ET. Treatment is with beta-adrenergic blockers, primidone, and benzodiazepines. The first systematic description of essential tremor (ET) was 100 years ago by Dana in 1887, who regarded the disorder as a hereditary tremor that was a form of "motor neurosis." Most subsequent contributions to the English literature consisted predominantly of case reports until Critchley's exhaustive survey of the subject in 1949. The disorder has been variously termed essential, benign essential, hereditary, familial, idiopathic, juvenile, presenile or senile tremor.
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PMID:Essential tremor: an overview. 791 60

Ethanol reduces the size of essential tremor. We here show that, contrary to a recent report, ethanol also causes a large decrease in the size of physiological tremor. As in the case of essential tremor, the frequency is not changed. The reduction in tremor probably explains the well-known link between certain types of skilled activity and alcohol consumption.
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PMID:The effect of alcohol on physiological tremor. 800 13

We used H2 15O positron emission tomography (PET) to investigate the effect of ethyl alcohol on regional cerebral blood flow in 6 patients with alcohol-responsive essential tremor and 6 age-matched control subjects. The patients were scanned while at rest and during involuntary postural tremor of the extended right arm. Normal control subjects were scanned at rest and during passive wrist oscillation of the right arm at tremor frequency. Regional cerebral blood flow associated with these conditions was measured before and after oral administration of 2 to 3 units of alcohol. The mean blood alcohol level was 35.3 +/- 20.0 mg/dl in the patient group and caused marked suppression of tremor; it was 33.9 +/- 12.9 mg/dl in the control group. Similar to previous PET studies on essential tremor patients, tremor compared with rest was associated with bilateral cerebellar activation including the cerebellar vermis. This pattern of activation differed from passive wrist oscillation where ipsilateral cerebellar activation was observed. Ethanol ingestion led to bilateral decreases of cerebellar blood flow in both tremor patients and normal subjects, and this was associated with suppression of tremor in the patients. Alcohol-associated increases of regional cerebral blood flow were observed in the inferior olivary nuclei in the patients but not in the control subjects. We conclude that alcohol-induced suppression of essential tremor is mediated via a reduction of cerebellar synaptic overactivity resulting in increased afferent input to the inferior olivary nuclei.
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PMID:The effect of ethanol on alcohol-responsive essential tremor: a positron emission tomography study. 900 8

The importance of temporal factors on the presence and severity of ethanol withdrawal signs in the rat was quantified using rating scale, tremor, and acoustic startle paradigms. Ethanol dependence was induced in naive male Wistar rats by liquid diet administration (n = 21) or vapor inhalation (n = 13). Subjects were analyzed for intensity and duration of physiological ethanol dependence in repeated-measures trials conducted over 72 h post-ethanol withdrawal. Indices of dependence included CNS hyperexcitability manifested as observable withdrawal signs increased acoustic startle reactivity, and tremor activity. Data analysis revealed that withdrawal signs, observed and elicited, generally reached peak intensities between 12 and 24 h postwithdrawal and were more readily observed following vapor inhalation than liquid diet administration, probably because of the higher BALs attained with the inhalation procedure. Results suggest a difference in time course observed with the different behavioral paradigms. In particular, a possible sensitization to startle stimuli was exhibited independent of both startle intensity and dependence induction method. The neural substrates governing these behavioral time course differences remain to be determined.
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PMID:Time-dependent quantifiable withdrawal from ethanol in the rat: effect of method of dependence induction. 881 51

Ethanol is metabolized in the brain by catalase/H2O2 to yield acetaldehyde and by an ethanol-inducible form of cytochrome P450 (P450 IIE1) in a reaction that yields oxygen radicals. Within the cytoplasm of serotonergic axon terminals these metabolic pathways together provide conditions for the endogenous synthesis of 1-methyl-6-hydroxy-1,2,3,4-tetrahydro-beta-carboline (1), by reaction of acetaldehyde with unbound 5-hydroxytryptamine (5-HT), and for the oxygen radical-mediated oxidation of this alkaloid. The major initial product of the hydroxyl radical (HO.)-mediated oxidation of 1 in the presence of free glutathione (GSH), a constituent of nerve terminals and axons, is 8-S-glutathionyl-1-methyl-1,2,3,4-tetrahydro-beta-carboline-5,6-dione (6). When administered into the brains of mice, 6 is a potent toxin (LD50 = 2.9 microg) and evokes episodes of hyperactivity and tremor. Compound 6 binds at the GABA(B) receptor and evokes elevated release and turnover of several neurotransmitters. Furthermore, the GABA(B) receptor antagonist phaclofen attenuates the behavioral response caused by intracerebral administration of 6. These observations suggest that 6 might be an inverse agonist at the GABA(B) receptor site. Accordingly, it is speculated that ethanol drinking might potentiate formation of 6 that contributes to elevated release of several neurotransmitters including dopamine (DA) and endogenous opioids in regions of the brain innervated by serotonergic axon terminals. Subsequent interactions of DA and opioids with their receptors might be related to the initial development of dependence on ethanol. Redox cycling of 6 (and of several putative secondary metabolites) in the presence of intraneuronal antioxidants and molecular oxygen to produce elevated fluxes of cytotoxic reduced oxygen species might contribute to the degeneration of serotonergic pathways. Low levels of 5-HT in certain brain regions of the rat predisposes these animals to drink or augments drinking. Accordingly, 6, formed as a result of ethanol metabolism in the cytoplasm of certain serotonergic axon terminals, might contribute to the initial development of dependence on ethanol, by mediating DA and opioid release, and long-term preference and addiction to the fluid as a result of the progressive degeneration of these neurons.
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PMID:Putative oxidative metabolites of 1-methyl-6-hydroxy-1,2,3,4-tetrahydro-beta-carboline of potential relevance to the addictive and neurodegenerative consequences of ethanol abuse. 916 Jul 98

Cocaine remains a widely abused illicit substance in our society. Cocaine hepatotoxicity has been linked to cocaine metabolism. Cocaine can undergo hydrolytic inactivation via plasma and hepatic esterases or it can be N-oxidized by cytochrome P-450 and FAD-containing monooxygenases. Ethanol is frequently used in combination with cocaine. The presence of ethanol can affect the metabolism of other agents, depending on the dose and duration of exposure. In this investigation, hepatocytes isolated from male Sprague-Dawley rats were utilized to study the effect of ethanol exposure on cocaine metabolism. Hepatocytes were isolated using a two-step collagenase perfusion system. Hepatocytes (2 x 10(6) cells ml(-1)) were exposed to cocaine, ethanol or the combination of cocaine and ethanol for a 2-h period in a shaking water-bath at 30 oscillations per minute maintained at 37 degrees C. Sodium fluoride (NaF) was added to aliquots of cells which were removed from the incubation following 30, 60 and 120 min. The cells were homogenized on ice and immediately extracted for the quantification of cocaine, benzoylecognine, norcocaine and ethylcocaine by HPLC. Quantitative analysis revealed that there was a time-dependent increase in the disappearance of cocaine from hepatocytes. The rate of cocaine disappearance was not changed when ethanol was included in incubations containing cocaine. However, in the presence of ethanol there was a difference in the quantities of cocaine metabolites produced. When ethanol was included in incubations containing cocaine, the formation of norcocaine and benzoylecognine was less than that formed in hepatocytes exposed to cocaine alone. Additionally, when hepatocytes were exposed to cocaine in combination with ethanol, the formation of ethylcocaine was linear with time. This study revealed that in the presence of ethanol, cocaine qualitative metabolism is altered.
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PMID:Role of ethanol exposure on cocaine metabolism in rat hepatocytes. 918 53

Effects of agmatine, which is an endogenous polyamine metabolite formed by decarboxylation of L-arginine, have been investigated on the ethanol withdrawal syndrome in rats. Adult male Wistar rats were used in the study. Ethanol (7.2% v/v) was given to the rats by a liquid diet for 21 days. Agmatine (20, 40, 80 and 160 mg/kg) and saline were injected to rats intraperitoneally 30 min before ethanol withdrawal testing. After 30th min, 2nd and 6th h of ethanol withdrawal, rats were observed for 5 min, and withdrawal signs which included locomotor hyperactivity, agitation, stereotyped behavior, wet dog shakes and tremor were recorded or rated. A second series of injections was given at 6 h after the first one, and subjects were then tested for audiogenic seizures. Agmatine caused dose-dependent and significant inhibitory effects on stereotyped behaviors, wet dog shakes and tremors during the observation period. It did not cause any significant change in motor coordination of naive (not ethanol-dependent) rats. Our results suggest that agmatine attenuates withdrawal syndrome in ethanol-dependent rats; thus, this drug may be beneficial in the treatment of ethanol dependence.
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PMID:Effects of agmatine on ethanol withdrawal syndrome in rats. 1062 39


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