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)

Hindlimb tremor was produced in chronic cats by intracaudate microinjection of the monoamine oxidase (MAO) inhibitors tranylcypromine and harmaline throughout a range of doses (150-385 mug). Pargyline, however, was non-tremorgenic within the same range, suggesting that interference with MAO is not sufficient in itself to elicit tremor. Tranylcypromine tremors differed from those of harmaline by exhibiting a slower onset, longer duration and susceptibility to antagonism by hemicholinium. In contrast, ongoing cholinergic tremors following intracaudate physostigmine were variably suppressed by all three MAO inhibitors at comparable dose levels (175-200 mug); pargyline produced the most complete suppression. These results indicate that MAO inhibitors can modify tremor activities in a differential manner dependent both on the functional state of the caudate nucleus and on the ability of cartain MAO inhibitors to exert other local actions.
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PMID:Contrasting local effects of MAO inhibitors on caudate tremor activities. 112 76

Tranylcypromine (TCP) pretreatment was found to accelerate the tremorogenic activity of tremorine in rats. Conversely, reserpinization delayed the onset of induction of tremors, and a significant diminution in their intensity was observed in these rats. A comparative study of the antitremor activity of beta-adrenoceptor antagonists against this tremor-model showed that butoxamine (beta 2-antagonist) and propranolol (nonselective antagonist) were able to afford a rapid and powerful protection, whereas a weaker and delayed effect was observed in rats treated with the beta 1-antagonist, acebutolol. Furthermore, the antitremor activity of butoxamine and propranolol but not that of acebutolol was found to be potentiated and diminished in rats pretreated with reserpine and TCP, respectively. It was inferred that beta 2-receptor modulated the tremorogenic activity of tremorine, and that inhibition by propranolol or butoxamine of this subtype beta-adrenoceptor resulted in rapid and powerful suppression of tremors, and that the antiadrenergic activity of acebutolol was unlikely to have a role in its antitremor effect.
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PMID:The role of adrenergic mechanism in tremorine-induced tremors in rats: antitremor effect of beta-adrenoceptor antagonists. 288 20

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