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)

A behavioral study was performed in an attempt to understand the neuronal mechanisms involved in wet dog body shaking in rats induced by the administration of thyrotropin-releasing hormone (TRH). The body shaking evoked by TRH (10 mg/kg, i.p.) was not affected by pretreatment with methysergide, scopolamine, levallorphan or phentolamine, but was inhibited by clonidine, haloperidol and reserpine. Body shaking behavior was also elicited by injection of levallorphan to morphine-dependent rats. The morphine-withdrawal body shaking was antagonized by pretreatment with TRH in the doses (10, 20 mg/kg, i.p.) which alone induced body shaking. A dose of TRH (10 mg/kg, i.p.) which induces body shaking in control rats, was without effect in morphine-dependent rats that had undergone withdrawal. The present results imply that TRH-induced body shaking is not associated with the increased activity of serotonergic, cholinergic and enkephalinergic neurons in the brain, and also its mechanisms seem to be different from that of morphine-withdrawal body shaking.
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PMID:Behavioral studies of shaking behavior induced by thyrotropin-releasing hormone and morphine withdrawal in rats. 630 93

The effects of thyrotropin-releasing hormone (TRH) and an analog of this hormone, MK-771, were determined on body shaking behavior and on biochemical estimates of the activity of dopamine (DA) neurons in the rat. Both compounds elicited dose-related episodes of "wet-dog shakes". A dose of TRH (20 mg/kg, i.p.) which caused marked shaking behavior did not alter the steady-state concentration of DA in any brain region, but, after an injection of alpha-methyltyrosine did enhance the rate of decline of DA in the nucleus accumbens, but not in the striatum of olfactory tubercle. The same dose of TRH increased the concentration of dihydroxyphenylacetic acid selectively in the nucleus accumbens, and caused a marked increase in the rate of synthesis of DA (accumulation of DOPA after the administration of a decarboxylase inhibitor) in the nucleus accumbens, and a modest and inconsistent increase in the striatum and olfactory tubercle. A single injection of MK-771 (3-100 mg/kg, i.p.) failed to change the rate of synthesis of DA in any brain region, while two injections of this compound (20 mg/kg, i.p.) slightly increased the rate of synthesis of DA in the striatum. These results suggest that TRH selectively increases the activity of DA neurons which terminate in the nucleus accumbens whereas its synthetic analog, MK-771, lacks this property. Since both compounds elicit similar body shaking behavior, it would appear that this behavior is not causally related to the actions of TRH on mesolimbic DA neurons which terminate in the nucleus accumbens.
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PMID:Effects of behaviorally active doses of thyrotropin-releasing hormone and its analog MK-771 on dopaminergic neuronal systems in the brain of the rat. 643 20

To more clearly characterize the neuroanatomical substrates mediating thyrotropin-releasing hormone (TRH) induced shaking and antagonsim of pentobarbital hypothermia, TRH was microinjected into 140 individual sites of the rat forebrain and brainstem. Previously determined threshold dosages of 10 ng TRH for the temperature response and 50 ng TRH for the shaking response were used. A clear distinction in regional sensitivity between the two TRH-induced effects was observed. The shaking response was most consistently observed with microinjection of TRH into the floor of the 4th ventricle and the periventricular posterior diencephalon, including the posterior hypothalamus and rostral periventricular grey. In contrast, the temperature response was most effectively induced by TRH administered in the interpeduncular nucleus and the rostral preoptic region located medial to, and including the diagonal band of Broca. The sensitivity of some brain areas to nanogram doses of TRH supports the possiblity that TRH may have a physiological function in the initiation of shaking behavior and/or thermogenesis. If such a function does exist, the brain regions identified in this study as most sensitive to exogenous TRH are likely neuroanatomical substrates for endogenous TRH.
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PMID:Neuroanatomical dissociation of thyrotropin-releasing hormone induced shaking behavior and thermogenic mechanisms. 678 7

The authors investigated the possibility of a thyrotropin-releasing hormone-related mechanism in a 43-year-old Japanese woman with Hashimoto's encephalopathy who experienced three relapses closely associated with the menstrual cycle. Her symptoms began at ovulation, worsened during the luteal phase, and improved during the menstruation phase. No abnormalities were found by brain magnetic resonance imaging and cerebral angiography. Intravenous administration of thyrotropin-releasing hormone induced symptoms of myoclonus and tremor similar to those observed during an exacerbation. The intensity and duration of involuntary movements induced by thyrotropin-releasing hormone were dose-dependent. The patient's symptoms were controlled effectively by thyroxine replacement therapy. On the basis of these findings, thyrotropin-releasing hormone may have an important role in Hashimoto's encephalopathy.
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PMID:Case report: thyrotropin-releasing hormone-induced myoclonus and tremor in a patient with Hashimoto's encephalopathy. 748 24

We studied the effect of various kinds of beta-adrenergic blockers on oxotremorine-, harmaline- and thyrotropin-releasing hormone (TRH)-induced tremors in mice. To investigate what property of beta-blockers plays the main role in suppressing tremor, we employed five beta-blockers (propranolol, atenolol, butoxamine, pindolol, and arotinolol). All drugs suppressed oxotremorine-induced tremors but none reduced harmaline-induced tremors. Even though TRH-induced tremors were decreased significantly only by propranolol and high doses of arotinolol, all drugs had a tendency to reduce the tremor. We concluded that neuropharmacological mechanisms underlying to harmaline-induced tremors were different from those of TRH- and oxotremorine-induced tremors and that features of beta-blockers (beta 1- or beta 2-selectivity, intrinsic sympathomimetic activity, and membrane stabilizing activity) did not primarily contribute to the suppression of tremors.
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PMID:Effects of beta-adrenergic blockers on drug-induced tremors. 809 22

The acute toxicity studies of taltirelin tetrahydrate (TA-0910), a new thyrotropin-releasing hormone (TRH) analogue, were performed in Slc:ddY mice, Slc:Wistar rats and beagle dogs of both sexes. The drug was administered to mice and rats by oral (p.o.), intravenous (i.v.) and subcutaneous (s.c.) routes, and to dogs by the p.o. and i.v. routes. LD50 values were more than 5,000 mg/kg in mice and rats of both sexes by the p.o. and s.c. routes. Some mice and rats died immediately after i.v. injection, the LD50 values were more than 2,000 mg/kg in mice of both sexes and calculated as 799 and 946 mg/kg in male and female rats, respectively. The minimum lethal doses were more than 2000 mg/kg in dogs of both sexes by the p.o. route. Though all dogs treated intravenously with 1000 mg/kg could survive during the observation period, a female dog with 500 mg/kg died on the day after administration. In general condition, hyperactivity, tremor and straub tail, that reflected central stimulatory effects of TA-0910, were observed in mice and rats, and also wet dog shaking in only rats. Vomiting and hyperactivity were seen in dogs by the p.o. route, and exaltation (during the dosing) and sedation by the i.v. route. In addition, salivation and transient tachycardia were observed in the both routes. In blood chemical examination, the transient changes of glucose, protein, lipid and/or serum enzyme were shown. In autopsy, no notable changes were seen in mice, rats and dogs.
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PMID:[Acute toxicity studies of taltirelin tetrahydrate in mice, rats, and dogs]. 943 92

Four-, 13- and 52-week repeated dose toxicity studies of taltirelin tetrahydrate(TA-0910), a thyrotropin-releasing hormone(TRH) analogue, were carried out in rats. Through the three studies, TA-0910 solution was administered orally at doses of 3, 30 and 300 mg/kg/day. The animals receiving TA-0910 showed hyperlocomotion, grooming and wet dog shaking which were attributable to the central effects similar to those of TRH, but there was no death nor obvious deterioration of health caused by the treatment. Body weights decreased in males of 300 mg/kg group, and food consumption was on the upward trend in females in 300 mg/kg group. In 13- and 52-week studies, females receiving 300 mg/kg showed elongated estrous cycle, although it was not an evident change. Blood examinations revealed increases in erythrocyte count, hemoglobin and hematocrit in 300 mg/kg group. Reductions in serum(plasma) proteins and lipids, and drug-metabolizing enzyme activity of the liver were regarded as non-specific changes, as they were sporadic and slight in 300 mg/kg group. Salivary gland and adrenal weights increased in 300 mg/kg group. For the thyroid, weights increased in 300 mg/kg group in the 4- and 13-week studies, and increases of microfollicles and cell debris were observed microscopically in each treated group in the 52-week study. These changes seemed to be related with hormonal action of TA-0910, but the effects on animals were judged slight from plasma TSH and thyroid hormone levels after 4 weeks of dosing. The non-toxic dose was estimated to be 30 mg/kg/day, through the rat repeated dose toxicity studies. All the above changes were alleviated or abolished by 4-week recovery period.
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PMID:[Repeated dose toxicity studies of taltirelin tetrahydrate(TA-0910) by oral administration to rats]. 943 93


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