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 piperazine-type 5-hydroxytryptamine (5-HT) agonists 1-(m-trifluoromethylphenyl)piperazine (TFMPP), 1-(m-chlorophenyl)-piperazine (m-CPP), 1-(p-chlorophenyl)piperazine (p-CPP) and MK-212 [6-chloro-2-(1-piperazinyl)pyrazine], produced a dose-dependent suppression of spontaneous ambulatory behavior in rats. Pretreatment with the 5-HT antagonists metergoline, methysergide or mianserin, but not selective 5-HT2 or catecholamine antagonists, blocked the reduction of activity caused by TFMPP suggesting that the stimulation of 5-HT receptors was involved in causing this behavioral effect. Other behavioral signs of 5-HT receptor stimulation, such as the 5-HT behavioral syndrome or head-shaking behavior, were not observed in rats injected with TFMPP, m-CPP or MK-212 except at toxic doses. The ability of piperazine agonists to reduce locomotor activity in rats was altered by long-term changes in 5-HT neurotransmission. The destruction of 5-HT neurons by i.v.t. injection of the neurotoxin 5,7-dihydroxytryptamine potentiated the ability of m-CPP to inhibit ambulatory behavior. On the other hand, elevating 5-HT content by administering the monoamine oxidase inhibitors phenelzine or nialamide for 7 days reduced the ability of m-CPP to suppress locomotor activity. Acute administration of the monoamine oxidase inhibitors, or chronic administration of other antidepressants such as desmethylimipramine or iprindole, failed to alter m-CPPs activity-suppressant effects. These studies suggest that chronic changes in 5-HT neurotransmission produce compensatory changes which alter the behavioral response to these piperazine agonists. Taken together with other evidence that both TFMPP and m-CPP are agonists at 5-HT1B and 5-HT1C receptors, the effects of TFMPP and m-CPP on locomotor activity may be associated with the selective activation of 5-HT1C, or possibly 5-HT1B, receptors.
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PMID:Effect of 1-(m-chlorophenyl)piperazine and 1-(m-trifluoromethylphenyl)piperazine on locomotor activity. 270 29

The effect of beta-adrenoceptor antagonists, varying in lipophilicity and receptor selectivity, were studied on tremor elicited by L-5-hydroxytryptophan (L-5-HTP) in rats pretreated with a peripherally acting decarboxylase inhibitor and a monoamine oxidase inhibitor, or by the directly acting 5-HT agonist 5-methoxy-N,N-dimethyltryptamine (5-MeODMT). Plasma levels of the beta-adrenoceptor antagonists were determined simultaneously. The non-selective lipophilic adrenoceptor antagonist propranolol was found to dose-dependently reduce tremor intensity, whereas the non-selective hydrophilic adrenoceptor antagonist sotalol had no effect, indicating a central site of action. Furthermore, beta 1-selective blockade with the adrenoceptor antagonist metoprolol had no effect on tremor intensity, whereas the beta 2-selective antagonist ICI 118,551 dose-dependently suppressed tremor intensity, suggesting that the beta-adrenoceptor subtype involved is of the beta 2-type. These results suggest that blockade of centrally located beta 2-adrenoceptors are able to attenuate the tremor response following 5-hydroxytryptamine receptor activation.
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PMID:Blockade of central beta-adrenoceptors attenuates tremor induced by 5-hydroxytryptamine (5-HT)-receptor activation in rats. 288 12

A multicenter trial was conducted at 9 Neurology Departments to evaluate the action of L-Deprenyl, a specific monoamine oxidase-B inhibitor, combined with L-Dopa in the treatment of Parkinson disease. In all, 76 patients were treated, 33 women and 43 men, on stable treatment with L-Dopa+ aromatic decarboxylase inhibitors (DI) for at least 6 months. After a 50% reduction of the L-Dopa dose, all received L-Deprenyl 5 mg twice daily for 35 day. The combined treatment resulted in a definite improvement in rigidity, bradykinesia and, most of all, tremor. Further, at the end of treatment fewer patients had depressive symptoms and the total daily number of hours of wellbeing and normal movement increased. 12 patients presented modest side effects, in no case serious enough to warrant suspension of treatment. The trial shows that with the L-Deprenyl + L-Dopa combination the dose of L-Dopa needed to control the disease can be drastically reduced.
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PMID:Multicenter trial of L-Deprenyl in Parkinson disease. 308 93

SR 95191 [3-(2-morpholino-ethyl-amino)-4-cyano-6-phenyl-pyridazine], a novel compound, has been shown in preliminary experiments to inhibit type A monoamine oxidase (MAO). This report describes the activities of SR 95191 in behavioral experiments in mice and rats and shows that SR 95191 has the profile of a selective type A MAO inhibitor (MAOI). Moreover, SR 95191 also possesses dopamine (DA) stimulant properties. The activities of SR 95191 were compared to those of the MAOIs moclobemide, clorgyline, pargyline and l-deprenyl, as well as to those of the antidepressant drugs imipramine, nomifensine and indalpine and to those of the DAergic drugs (+)-amphetamine and apomorphine. SR 95191 p.o. antagonized the effects of reserpine in mice and rats, decreased immobility in the mouse despair test, antagonized haloperidol-induced catalepsy in rats and potentiated 5-hydroxytryptophan in mice and rats with an overall potency which was half that of imipramine. SR 95191, like moclobemide, did not potentiate yohimbine-induced lethality and did not antagonize oxotremorine-induced tremor. Like selective type A MAOIs, SR 95191 potentiated 5-hydroxytryptophan-induced tremor without affecting beta-phenethylamine-induced stereotypies in mice. SR 95191 did not antagonize 3-hydroxy-4-methyl-alpha-phenylethylamine-induced hyperthermia. Like all DA stimulant drugs, SR 95191 induced stereotypies in rats, which were blocked by haloperidol and alpha-methylparatyrosine, and induced contralateral turning in mice with a unilateral striatal 6-hydroxydopamine lesion. Based on these results, it is postulated that SR 95191 has a unique profile of activity combining the properties of a selective type A MAO inhibitor and those of an atypical DAergic drug.
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PMID:SR 95191, a selective inhibitor of type A monoamine oxidase with dopaminergic properties. I. Psychopharmacological profile in rodents. 310 Jul 70

The head shake reflex is a rapid rhythmic shaking of the head in a radial motion and is a prominent part of the behavior of most mammalian species. The administration of agonists at 5-hydroxytryptamine (5-HT) receptors to rats increases apparently-spontaneous head shaking behavior. The present study examined the relationship between the head shake reflex, elicited by stimulation of the aural ampullae with Tween 80, with a similar-appearing behavior, the head shake response caused by the administration of 5-HT agonists to rats. Head shaking was attenuated by the subcutaneous infiltration of the local anesthetic procaine into the posterior border of the external auditory meatus. However, the local anesthetic did not alter head shake behavior produced by administering either the 5-HT agonist quipazine or the 5-HT precursor 5-hydroxy-L-tryptophan (L-5-HTP). The magnitude of the head shake reflex was also diminished after habituation of the reflex by repeatedly applying Tween 80 to the ampullae, yet this treatment had no effect on the head shaking behavior caused by quipazine. In a complementary manner, pretreatment with the 5-HT2 receptor antagonist ketanserin potently blocked shaking behavior caused by quipazine without significantly altering the head shake reflex. Chronic administration of the atypical antidepressant drug iprindole to rats for 7 days reduced quipazine-induced shaking behavior without affecting the head shake reflex. In contrast, chronic administration of the monoamine oxidase inhibitor phenelzine to rats for 7 days reduced head shaking behavior caused by either stimulus, indicating that an attenuation of motor reflex activity could play a role in the reduced response to quipazine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of the aural head shake reflex in serotonin-mediated head shaking behavior. 311 Aug 36

Lithium has been used successfully to enhance the effectiveness of tricyclic and other antidepressants, monoamine oxidase inhibitors, and combinations of antipsychotics and antidepressants. The safety and efficacy of adding lithium to the treatment regimen was examined in 14 elderly patients with refractory depression. Seven of the 14 had a complete recovery, and three showed a partial response. Side effects, including peripheral weakness, severe fine tremor, and neurotoxicity, necessitated the discontinuation of lithium in three patients. In two other patients with side effects, lower dosages of lithium relieved their symptoms. Lithium augmentation appears to be a promising treatment for geriatric depressed patients who are unresponsive to or cannot tolerate other standard therapies.
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PMID:Lithium augmentation for treatment-resistant depression in the elderly. 315 Sep 26

The experiments characterized the dose- and time-dependence of parkinsonian motor signs induced by reserpine in rats and a standardized system of manipulation of animals, evaluation of symptoms and analysis of data was devised. The assay procedure yielded no more than 0.5, 4.5 and 0.0% false positives with the evaluation of tremor, rigidity and hypokinesia, respectively. A dose-dependent and often complete blockade of all three signs was obtained with L-DOPA plus carbidopa (10:1) as well as with other classes of pharmacological agents that are used in the treatment of Parkinson's disease, i.e. direct or indirect dopamine (DA) agonists (amantadine, pergolide, lisuride) and inhibitors of monoamine oxidase (MAO) (clorgyline, pargyline, deprenyl, tranylcypromine). The inhibitor of the uptake of DA, nomifensine, and anticholinergics, 5-hydroxytryptamine (5-HT) antagonists, histamine antagonists and tricyclic antidepressants exerted little or no effect. The effects of putative agonists and antagonists at alpha 1- and alpha 2-adrenoceptors were also examined. Yohimbine blocked tremor and rigidity, but not hypokinesia, at 0.66 and 0.28 mg/kg, respectively. It is suggested that alpha-adrenergic mechanisms and, in particular, alpha 2-adrenoceptors, may be involved in reserpine-induced tremor and rigidity. Noradrenergic and dopaminergic systems can conceivably interact to progressively generate these different motor signs.
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PMID:Pharmacological characteristics of tremor, rigidity and hypokinesia induced by reserpine in rat. 367 May 63

The responses of male and female rats to drugs causing the behavioural syndrome induced by 5-hydroxytryptamine (5-HT) were compared. Preliminary experiments showed that females had largely similar responses to the releaser of 5-HT, p-chloroamphetamine (PCA) and the 5-HT receptor agonist 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) at different stages of the oestrus cycle. The behavioural responses to 5-MeODMT (with and without the monoamine oxidase inhibitor pargyline) or to p-chloroamphetamine were not significantly different to those of males except for tremor after p-chloroamphetamine which was more marked in the females. However, concentrations of p-chloroamphetamine in brain in these animals, when killed immediately after behavioural recording were greater in the females. When rats, pretreated with the monoamine oxidase inhibitor, pargyline, were given the precursor of 5-HT, tryptophan, the females showed substantially greater hypothermia and larger scores for components of the 5-HT syndrome than the males. This sex difference may have been due to the moderately but significantly higher levels of 5-HT (and possibly tryptamine) in brain attained by the female rats, than by similarly-treated males. The results as a whole therefore suggest that the greater behavioural response of female rats to pargyline and tryptophan reflects a greater effect of this treatment on the synthesis of indoleamines than that occurring in males.
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PMID:5-Hydroxytryptamine-mediated behaviour in male and female rats. 374 24

The pharmacological properties of MO-8282 (1,2,3,4-tetrahydro-2-methyl-9H-dibenzo [3,4: 6,7]cyclohepta [1,2-c]pyridine maleate) as an antidepressant were investigated. At doses 10 times less than those of amitriptyline, MO-8282 showed similar potencies in reducing the duration of immobility during forced swimming in rats and in potentiating stereotype induced by L-DOPA. Intermediate doses of MO-8282 reduced the duration of immobility during forced swimming, in mice as well, suppressed muricide behavior of olfactory-bulbectomized rats and antagonized clonidine-induced suppression of exploratory activity in mice. MO-8282 moderately antagonized the ptosis but not the hypothermia induced by reserpine in mice. MO-8282 exhibited weak antagonism against the tremor, lacrimation and diarrhea induced by tremorine, but its activity was milder than that of amitriptyline. The uptake of noradrenaline into rat hypothalamic synaptosomes was inhibited by MO-8282 at concentrations 20 times less than equally effective doses of amitriptyline, but the uptake of dopamine or serotonin was unaffected by MO-8282. A single oral administration of MO-8282 at a dose of 30 mg/kg accelerated noradrenaline turnover, but did not affect dopamine and serotonin turnover in the rat brain. MO-8282 strongly inhibited noradrenaline-, histamine- or adenosine-sensitive adenylate cyclase activity of guinea pig brain. Its mode of action differed from that of imipramine, rather resembling that of mianserin. MO-8282 did not affect monoamine oxidase activity of rat liver. These results suggest that the pharmacological characteristics of MO-8282 are different from those of tricyclic antidepressants and rather similar to those of mianserin, but more potent. The results, therefore, indicate that MO-8282 is possibly a novel antidepressant.
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PMID:[Pharmacological properties of MO-8282, a novel antidepressant]. 379 61

Effects of intravenous administration of the serotonin precursor tryptophan (TRP) on serum prolactin, neuromotor function, subjective mood, and blood pressure and pulse were determined in nine depressed patients before and during placebo-controlled treatment with the monoamine oxidase inhibitor (MAOI) tranylcypromine. Tranylcypromine significantly increased the prolactin response to TRP. Four patients developed a distinctive neuromotor syndrome following TRP during tranylcypromine, but not placebo, treatment. Symptoms included hyperreflexia, ankle clonus, nystagmus, incoordination, tremor, myoclonic jerks, and nausea. There were no differences in peak prolactin, mood, or autonomic responses between patients with and without the syndrome, but those with the syndrome had received active tranylcypromine for a significantly shorter duration. Tranylcypromine had little effect on TRP-induced changes in mood or autonomic function, except for a modest enhancement of the TRP-induced rise in diastolic blood pressure. These results suggest that tranylcypromine treatment may enhance serotonin function in depression.
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PMID:Effects of tranylcypromine treatment on neuroendocrine, behavioral, and autonomic responses to tryptophan in depressed patients. 403 56


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