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 22-year old man with a goiter and clinical manifestations of mild thyrotoxicosis (finger tremor, palpitation, tachycardia) was diagnosed as a syndrome of inappropriate secretion of TSH. Serum concentrations of T4, free T4, T3 and TSH were 24.1 micrograms/100 ml, 4.07 ng/100 ml, 261 ng/100 ml and 1.72 microU/ml, respectively. Thyroidal 131I uptake at 24 hr was 80%. The BMR was within the normal range. He had a normal TSH response to TRH (500 micrograms) with a peak level of 23.8 microU/ml. The basal level of alpha-subunit of TSH was not elevated (0.35 ng/ml). Oral 1-T3 administration (75 and 150 micrograms daily) raised serum T3 concentration, reduced basal TSH and blunted TSH response to TRH. The diurnal variation of TSH was maintained. There was no evidence of abnormalities in the secretion of other pituitary hormones. These findings were compatible with thyroid hormone resistance. However, the presence of a microadenoma in the pituitary gland was suspected with CT scan. Bilateral and simultaneous venous sampling for TSH from inferior petrosal sinus showed no gradient in TSH concentration indicating that a TSH secreting pituitary tumor was unlikely. These data suggest that inappropriate TSH secretion in the present patient is resulted from resistance to thyroid hormone. In the present study selective venous sampling is useful to differentiate the thyroid hormone resistance from a TSH secreting tumor.
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PMID:A case of refetoff syndrome: selective venous sampling for TSH is useful in differentiating thyroid hormone resistance from TSH secreting tumor. 271 78

The Rolling mouse Nagoya (RMN), Staggerer, Weaver and Reeler, all of which show hereditary ataxia, were intraperitoneally injected with 25 mg/kg of thyrotropin-releasing hormone (TRH-T) or physiological saline, and changes in the motions of these animals were observed by an Animex II and an open field method. All four strains of mice with ataxia showed improvement of ataxia and an increase in the motion volume, but these changes were not necessarily consistent in degree. Improvement of ataxia was most marked in the RMN and the Staggerer, moderate in the Weaver and slight in the Reeler, which showed enhanced tremor. The relationship between the competence of transmitting information in the cerebellum and improvement of ataxia by the injection of TRH-T aroused our interest.
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PMID:The pharmacological effect of thyrotropin-releasing hormone on ataxic mutant mice. 308 1

Tremor induced by TRH and oxotremorine was recorded by a capacitance transducer, and its intensity and frequency were evaluated using power arrays. In mice treated with TRH (20 mg/kg, i.p.), the latency of tremor was 17.1 +/- 1.7 min (mean +/- S.E.) and the duration was 20.4 +/- 2.2 min, while the frequency was 13.7 +/- 0.3 Hz. In animals with oxotremorine (0.5 mg/kg, i.p.), the latency was 4.3 +/- 0.4 min and the duration was 18 +/- 2.2 min, while the frequency was 12.7 +/- 0.3 Hz. The latter frequency, however, was significantly shifted to a lower frequency as a function of time. In TRH-induced tremor, vertical movements appeared in the same degree as horizontal movements. In oxotremorine-induced tremor, the vertical movements were few, whereas the horizontal movements were observed in a degree similar to those of TRH. The TRH tremor was suppressed by haloperidol and propranolol, but not by atropine. On the contrary, the oxotremorine tremor was inhibited by atropine, but not by haloperidol or propranolol. These results suggest that mechanisms of tremor induced by TRH differ qualitatively from those by oxotremorine; dopaminergic and beta-adrenergic receptor mediated functions may be linked to the developments of tremor caused by TRH, while cholinergic systems have a little effect in mice. The apparatus used in this study and power spectral analysis with power arrays may provide a useful method for simultaneous evaluation of the latency, duration, intensity and frequency of tremors.
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PMID:[Power spectral analysis of tremor induced by TRH and oxotremorine in mice]. 309 4

The study reported here was undertaken to establish the degree to which a person in a preclinical state of hyperthyroidism, with (by definition) euthyroid T3 and T4 levels but suppressed TRH on testing, already exhibits psychological changes and clinical symptoms. Two groups of 20 patients each, with clear clinical and preclinical hyperthyroidism (as defined by laboratory parameters), were studied, as well as a group of 20 controls. The subjects' psychological state of mind was investigated using self-rating scales, including the state-trait-anxiety inventory (STAI), "Befindlichkeits"-Skala (Bf-S'), depression scale (D-S'), and a list of adjectives (EWL-K) with 14 different aspects of affective moods. Cognitive achievements were evaluated using the d2 test. Subjects were examined for somatic symptoms in accordance with Crooks' index of hyperthyroidism. The results clearly showed that typical psychological and somatic changes are already present in preclinical hyperthyroidism, these changes being partly identical with those of definite hyperthyroidism. In both patient groups, a significant increase in anxiety, a sense of not feeling well, and emotional irritability were found, as well as a tendency towards depressiveness, and an increased lack of vitality and activity. Attentiveness and concentration in both patient groups were lower than in the control group. Both patient groups showed the same prevalence of symptoms, such as palpitations, preference of cold over heat, excessive sweating, nervousness, fine digital tremor, and increased heart rate. With regard to the results, the diagnosis "preclinical hyperthyroidism" thus gains importance. Further prospective studies are required to answer the question whether antithyroidal treatment will influence the described psychological and somatic state of patients with preclinical hyperthyroidism.
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PMID:[Correlation of "latent hyperthyroidism" with psychological and somatic changes]. 358 69

While previous reports have immunocytochemically localized oxytocin and TRH in the spinal cord, the functional significance of these peptides is unclear. The present paper examined this issue and tested the effects of these peptides upon intrathecal administration. We found both peptides produced lasting motor and blood pressure changes. Oxytocin elicited prolonged jerks of the hindlimbs and the tail, while TRH produced an increase of hindlimb muscle tone and tail tremor. TRH in larger doses (5, 10 micrograms) also caused tail erections and whipping. The motor effects of both peptides were dose-dependent. Intrathecal oxytocin (0.75 or 1.5 IU) caused a transient drop in blood pressure followed by a rise, in 4 out of 7 rats. The other 3 only showed a hypertensive effect. In contrast, intrathecal TRH produced a rise in blood pressure in all the animals tested. These findings suggest that both oxytocin and TRH may play a role in the regulation of motor and automatic functioning at the spinal level.
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PMID:Differential motor and blood pressure effects of intrathecal oxytocin and TRH in the rat. 393 43

Administration of thyroliberin (TRH) to reserpinized mice causes tremor and counteracts the hypothermia in a dose-dependent fashion. The thyroliberin response is inhibited by gamma-hydroxybutyric acid (GHB) and baclofen, but not by other, more specific GABA-ergic agents, such as THIP, gamma-acetylenic GABA, and sodium valproate. Picrotoxin neither potentiates nor inhibits the thyroliberin actions. Nor are the thyroliberin effects dependent on cholinergic, monoaminergic or histaminergic mechanisms. The results repudiate a current hypothesis, that the peptide actions may be mediated by GABA-ergic pathways in the brain.
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PMID:Thermic and tremorogenic effects of thyroliberin (TRH) in reserpine-treated mice--the non-involvement of GABA-ergic mechanisms. 611 36

Ethanol (2.0-5.0 g/kg, IP) caused a dose-related impairment of the aerial righting reflex of mice 60 min after injection. Ethanol (3.5 g/kg, IP) given simultaneously with neurotensin (30 micrograms, IC), bombesin (30 micrograms, IC) or beta-endorphin (20 micrograms, IC) caused a greater impairment of the reflex than ethanol alone. Simultaneous treatment with ethanol (4.0 g/kg, IP) and thyrotropin-releasing hormone (TRH, 3.0-30 micrograms, IC) caused less impairment of this measure than ethanol alone. None of the peptides altered the height of aerial righting when administered alone, or when administered with ethanol no peptide altered blood or brain ethanol content. Unexpectedly, TRH (20 and 40 mg/kg, IP) potentiated the action of ethanol by increasing punished licking in water-deprived rats, rather than antagonizing this acute action of ethanol. Like ethanol (1.0 and 2.0 g/kg, IP), beta-endorphin (100 micrograms, IC) suppressed ethanol-withdrawal tremor and audiogenic-seizure susceptibility in ethanol-dependent rats. beta-Endorphin (1 microgram) and bombesin (10 and 30 micrograms, IC) reduced only audiogenic-seizure susceptibility. TRH (10-100 micrograms, IC, or 1-40 mg/kg, IV) and neurotensin (10-100 micrograms, IC) had no effect on these ethanol-withdrawal signs. These findings suggest that centrally active peptides may play a role in certain acute and chronic actions of ethanol. Because TRH, neurotensin, bombesin and beta-endorphin do not alter all actions of ethanol in the same way, an interaction of ethanol with many functionally independent neuronal circuits is suggested.
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PMID:Modification of the actions of ethanol by centrally active peptides. 626 62

Administration of TRH into the lateral ventricle of unanesthetized rats produced increases in the incidence of hippocampal theta (5.9-9.1 Hz) rhythm, locomotor activity and shaking behavior. The increase in theta rhythm produced by TRH was brief (less than 5 min) and was coincident with a brief, large increase in locomotor activity. Intracerebroventricular injection of either TRH or D-Ala2-metenkephalinamide (D-Ala2-ME) also induced episodes of shaking behavior. Shakes induced by D-Ala2-ME were associated with the occurrence of hippocampal epileptiform activity whereas those caused by TRH occurred in the absence of any recorded abnormalities in hippocampal activity. These results suggest that the increase in hippocampal theta rhythm after TRH is secondary to the increase in locomotor activity and, that in contrast to enkephalins, shaking behavior caused by TRH may not be related to an action on the electrographic activity of the hippocampus.
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PMID:Comparison of the effects of TRH and D-Ala2-metenkephalinamide on hippocampal electrical activity and behavior in the unanesthetized rat. 641 57

Dispersed rat anterior pituitary cells were allowed to reassociate into spherical aggregates by gyrotory shaking in serum-free chemically defined culture medium. When aggregates were superfused after being cultured for 5 days in this medium, stimulation of PRL release by TRH, VIP, angiotensin II and the beta-adrenergic agonist isoproterenol was comparable to that of aggregates cultured in serum-supplemented culture medium. Addition to the serum-free medium of 80 nM dexamethasone (Dex) resulted in a significant enhancement of the stimulation of PRL release by TRH, VIP and angiotensin II but not of the stimulation of PRL release by isoproterenol. Dex also failed to influence the inhibition of PRL release by 10 min exposure to 10 nM dopamine (DA). However, Dex significantly enhanced the post-DA rebound secretion of PRL. After 3 weeks in culture Dex provoked a similar potentiation of the response to angiotensin as at 5 days in culture but it abolished almost completely the stimulatory effect of isoproterenol. It is concluded that pituitary cell aggregates cultured in defined serum-free medium are a reliable system to study the multifactorial control of PRL release. The data show that peptidergic, dopaminergic and beta-adrenergic control at the pituitary level is differentially modulated by corticosteroids.
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PMID:Influence of corticosteroids on prolactin release from anterior pituitary cell aggregates cultured in serum-free medium. Differential effects on dopamine-induced inhibition, post-dopamine rebound and stimulation by TRH, vasoactive intestinal peptide (VIP), angiotensin II and isoproterenol. 642 98

Bombesin, vasoactive intestinal peptide (VIP) and neurotensin were found to suppress body shaking behavior caused by intracerebroventricular injection of TRH.
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PMID:Effects of bombesin, vasoactive intestinal peptide and neurotensin on TRH-induced body shaking in rats. 642 99


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