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)

Both TRH and quipazine (2.5-25 mg/kg) were found to restore and to intensify the oxotremorine-induced tremor in mice when injected i.p. 60 min after oxotremorine 0.5 mg/kg s.c. This phenomenon does not seem to be due to an increase in body temperature or muscle tone. Also other dopaminergic drugs, e.g. amphetamine, methylphenidate, nomifensine and apomorphine had a significant but lesser effect than TRH or quipazine. Haloperidol and methysergide both antagonized the effect of quipazine but not that of TRH. Neither propranolol, phenoxybenzamine, alpha-methyl-p-tyrosine, nor p-chlorophenylalanine inhibited the activity of TRH or quipazine. The restoration of oxotremorine-induced tremor could be prevented by atropine but not by methylatropine. It is concluded that quipazine exerts its effect by direct stimulation of serotoninergic and dopaminergic receptors, whereas TRH receptors may represent separate entities and TRH may function as a neurotransmitter or neuromodulator.
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PMID:Thyrotropin releasing hormone (TRH): restoration of oxotremorine tremor in mice. Comparison with quipazine, a serotoninergic and dopaminergic stimulant. 1 78

Administration of 10 mg/kg TRH to mice was found to reduce the sleep and hypothermia induced by 4.7 g/kg ethanol. However, TRH did not reduce the sleep of mice that were given gamma-hydroxybutyric acid (GHBA), baclophen, or aminooxyacetic acid (AOAA) in combination with 3 g/kg/ ethanol. TRH also failed to reverse the hypothermia induced by the combination of ethanol and baclophen or GHBA, and the characteristic neurological effects of TRH e.g. tremor, increased muscle tone, and increased respiratory rate were reduced. In addition, TRH-induced locomotor stimulation was prevented by pretreatment with small doses of the GABA-ergic agents, and while 30 mg/kg TRH reduced the hypothermia produced by large doses of the GABA-ergic drugs, it did not antagonize the locomotor retardation produced by baclophen or GHBA. A hypothesis that the analeptic effects of TRH may be medicated via an inhibition of GABA systems is discussed.
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PMID:Antagonism of the analeptic activity of thyrotropin-releasing hormone (TRH) by agents which enhance GABA transmission. 1 50

20 microgram TRH injected bilaterally into the caudate-putamen, tuberculum olfactorium, nucleus accumbens, amygdala, lateral ventricles, midbrain or cerebral cortex failed to induce any increase in locomotor activity (measured using photocells), although other behavioural changes were observed after each injection, and included body shakes, limb tremor, repetitive head and limb movements, biting, scratching and an alert appearance. These behavioural changes could result in positive readings from equipment used to measure locomotor activity, but careful investigations focussing on the nucleus accumbens used photocell boxes, activity wheels and Animex recorders to emphasise the inability of intracerebral TRH (10--40 microgram) to enhance locomotor activity. Intraaccumbens TRH also failed to enhance amphetamine hyperactivity or reduce the motor depression caused by haloperidol and analeptic drugs. The data do not support a central locomotor stimulant action of TRH.
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PMID:A study of the changes in motor behaviour caused by TRH on intracerebral injection. 10 33

In hyperthyroidism we differentiate two main forms: (1) hyperthyroidism due to Basedow's (Graves') disease, always characterized by endocrine eye signs, frequently with goiter; (2) hyperthyroidism due to nodular goiter or to Plummers' disease, without endocrine exophthalmos. The clinical diagnosis includes typical complaints (e.g., weight loss, heat intolerance, sweating) and findings (e.g., tachycardia, tremor, soft-warm skin). The technical diagnosis includes in vivo (scintigraphy, RI-uptake, X-ray examination) and in vitro (T3-RIA, T4-assay, TRH response to TRH) tests.
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PMID:[Hyperthyroidism: diagnosis (author's transl)]. 10 1

TRH and a new TRH analog (all L-pyro-2-aminoadipyl-histidyl-thiazolidine-4-carboxamide, MK-771) have been compared with several other peptides for their "analeptic" activity and their ability to enhance the excitatory actions of microiontophoretically applied acetylcholine (ACh) on cerebral cortical neurons of rats. TRH and MK-771 offset the narcosis induced by pentobarbital in mice, whereas the C-terminal free acid derived from TRH, melanostatin, somatostatin and pyroglutamyl-histidineamide have been found inactive. Similarly, of these peptides only TRH and MK-771 induced a tremor of the forepaws in pentobarbital-anesthetized mice. Employing comparable ejection currents and durations, only TRH and MK-771, applied by microiontophoresis, enhanced the excitatory actions of ACh on spontaneously active cortical neurons in anesthetized rats. Based on these findings and other recent data, it is suggested that the interactions of TRH and MK-771 with cholinergic mechanisms may underlie some of the actions, including their anti-anesthetic effects, of these peptides.
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PMID:Studies on the neuropharmacology of thyrotropin releasing hormone (TRH) and a new TRH analog. 41 61

The relative potencies of TRH analogs in provoking a shaking response in rats were determined. Bilateral administration of 0.011-2.0 mug TRH analog into the periaqueductal-fourth ventricular spaces of the barbiturate-anesthetized rat showed that N3im-methyl TRH was approximately 10X more potent than TRH, whereas N1im-methyl TRH was approximately 10X less potent than TRH. These results indicate that the potencies of the TRH analogs in inducing shaking parallel their thyrotropin-releasing activities.
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PMID:Potency of the N3im-methyl analog of TRH in the induction of shaking movements in the rat. 81 58

A rare case of simultaneous hypersecretion of thyroid stimulating hormone (TSH) and growth hormone (GH) in a pituitary adenoma is reported. A 59-year-old male complaining of general fatigue, dyspnea on exertion and finger tremor was admitted. Examination on admission, he revealed with hyperthyroidism and hypersecretion of TSH and thyroid hormones. Administration of TRH did not further increase serum TSH level, and administration of T3 also had no effect on TSH secretion. CT scan showed a pituitary macroadenoma 13mm in diameter. MRI demonstrated a homogenously hypointense mass with Gd-DTPA enhancement in the left side of the sella turcica. The entire chromophobic adenoma was removed by trans-sphenoidal surgery. Immunostaining of the specimen showed that the cytoplasm of the adenoma cells was positive for both TSH and GH. Double immunostaining using avidin-biotin-peroxidase complex (ABC) method and immunogold silver staining (IGSS) method, showed that the adenoma cells had been secreting both GH and TSH at the same time. After the adenomectomy, the hyperthyroidism disappeared, and all altered indicators of pituitary function returned to normal.
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PMID:[A case of pituitary adenoma with simultaneous secretion of TSH and GH detected by double immunostaining method]. 193 Dec 60

The behavioral effects of the TRH analogue RX77368, dimethyl proline-TRH (3, 10 and 30 mg/kg IP), in 5-, 10- and 20-day-old rat pups were investigated. The peptide induced shaking behavior and increased locomotion as early as 5 days after birth. At 20 days RX77368 also produced rearing, stereotyped mounting and grooming (mainly licking and chewing of the forepaws). Additionally, RX77368 produced hypothermia and antinociception in the infant rats. These responses, which were generally, although not always, comparable with those found in adults, agree with biochemical studies showing high levels of TRH receptors in the brain and spinal cord in the first three weeks following birth.
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PMID:Behavioral profile of the TRH analogue RX77368 in developing rats. 212 22

Pituitary apoplexy is characterized by a wide spectrum of clinical features. A quite rare case of painless thyroiditis, hypopituitarism and central diabetes insipidus (DI) followed by pituitary apoplexy was presented. A 61-year-old woman was admitted to our hospital in May, 1986 because of marked general malaise, polydipsia and weight loss which became progressively worse. Four months earlier she had experienced episodes of abrupt onset of severe headache associated with nausea and blurring vision. Physical examinations revealed a fine tremor, dry skin and nervousness. The thyroid gland was not palpable. Visual fields were intact. Her blood pressure was 105/64 mmHg with variable tachycardia. The routine laboratory studies were normal or negative except for hypoalbuminemia, hypocholesterolemia and hypernatremia. Erythrocyte sedimentation rate was 12 mm/hr. An impairment in corticotropin secretion was suspected from the low plasma cortisol and the low urinary excretion of 17-OHCS and the sufficient response to ACTH. Basal levels of GH and gonadotropin were also low, and responses to the stimulation tests (Insulin-stress, L-DOPA, and LH-RH) were all blunted. Brain computed tomographic scan and magnetic resonance imaging demonstrated a suprasellar mass that, after infusion, developed peripheral ring-like enhancement and large hyperintense pituitary mass, respectively. A diagnosis of pituitary apoplexy with anterior pituitary failure was made. However, the initial levels of thyroid hormones showed elevated as follows: Free T3 7.6 pg/ml, Free T4 3.3 ng/dl and T3-resin uptake 41.1%. TSH responses to TRH were all suppressed. TSH receptor antibody (TBII) was negative. Both antithyroglobulin and antimicrosomal antibodies were repeatedly positive. A thyroid scan with 99mTc revealed no uptake in the thyroid area. These findings led us to the diagnosis of "painless autoimmune thyroiditis". She had become hypothyroid without any medication. At that time radioactive 99mTc and 123I uptakes increased significantly. When hydrocortisone was substituted, daily urine output abruptly increased to about 10 liters with low osmolality, and the presence of DI was suspected. This diagnosis was confirmed by water deprivation and hypertonic saline infusion tests and subsequent pitressin test. She is currently quite well on L-thyroxine, hydrocortisone and desmopressin (1988). This association with pituitary apoplexy must be a rare occurrence, as a literature search has failed to find a similar case. The pathogenetic trigger of "painless thyroiditis" in this case may be responsible for some immunological change due to secondary adrenal insufficiency after pituitary apoplexy.
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PMID:[An unusual association of transient resolving thyrotoxicosis due to painless thyroiditis, hypopituitarism and central diabetes insipidus associated with spontaneous pituitary apoplexy]. 230 57

An 11-year-old girl with diffuse goiter is presented. She had no clinical evidence of thyrotoxic symptoms or signs of palpitation, excessive sweating, tachycardia or finger tremor. Both the serum T4 (24.0 micrograms/dl) and T3 (282ng/dl) were high, and thyroid 131I uptake rate (63.2%) was significantly elevated, but T3/T4 ratio was not elevated (11.8). BMR was measured three times and remained within normal limits. Her serum TSH was 1.9 microU/ml, and a TRH stimulation test resulted in a normal rise of serum TSH (13.4 microU/ml). The TSH secretion was not suppressed by medication (p.o.) of 75 micrograms of L-triiodothyronine given for 8 days. The autoantibodies of T4, T3 and TSH were negative. No sign of pituitary tumor was observed by plain X-ray film. No defect in her sight-field was found. From these clinical figures and data, Refetoff's syndrome was suspected. She was eumetabolic without any treatment, but the goiter gradually enlarged and dysphagia developed. A large dose of L-thyroxine (450 micrograms/day) was given for a period of one year and four months. She has been eumetabolic. Her goiter disappeared and the dysphagia completely subsided. After she was given large doses of L-T4, her serum TSH was reduced to 0.07 microU/ml and was slightly elevated to 0.24 microU/ml at 30 min after i.v. infusion of 500 micrograms TRH. Thyroid 123I uptake rate was suppressed to 8.3%. According to Refetoff's papers, this case was classified as being in the group with generalized resistance to thyroid hormone.
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PMID:[A case report of Refetoff's syndrome]. 259 12


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