Biomedical subjects
Publications and source records attributed to T Mitsuma.
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Effects of thyrotropin-releasing hormone (TRH) on the plasma beta-endorphin-like immunoreactivity (beta-Ep-LI) levels in rats have been studied. TRH (10 mg/kg) were injected i.v., and the animals were serially decapitated. The plasma beta-Ep-LI levels were measured by radioimmunoassay. Effects of TRH on beta-Ep-LI release from the anterior pituitary were also investigated by means of an in vitro experiment. The beta-Ep-LI content in the hypothalamus, pituitary gland or adrenal gland did not change significantly after TRH injection. The plasma beta-Ep-LI levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. In the hypophysectomized rats, the plasma beta-Ep-LI levels were lower than that of the control, and did not change significantly after TRH injection. beta-Ep-LI release from anterior pituitary in vitro significantly decreased after the addition of TRH to medium. These findings suggest that TRH may act on the pituitary gland to reduce plasma beta-Ep-LI levels in rats.
Effects of growth hormone-releasing hormone (GRH) and corticotropin-releasing hormone (CRH) on the release of immunoreactive thyrotropin-releasing hormone (ir-TRH) from the rat hypothalamus in vitro were studied. The rat hypothalamus was incubated in medium 199 with 1.0 mg/ml of bacitracin (pH 7.4) for 20 min. The amount of ir-TRH release into the medium was measured by radioimmunoassay. The ir-TRH release from the rat hypothalamus was inhibited significantly in a dose-related manner with the addition of GRH or CRH. These findings suggest that GRH and CRH inhibit ir-TRH release from the rat hypothalamus in vitro.
The effects of calcium hopantenate (HOPA), a GABA agonist, on the release of thyrotropin-releasing hormone (TRH) from the rat adrenal gland were studied in vitro. The adrenal glands were incubated in medium 199 with 1.0 mg/ml of bacitracin (pH 7.4) (medium) for 20 min. The amount of TRH release into the medium was measured by radioimmunoassay. The TRH release from the rat adrenal gland was inhibited significantly in a dose-related manner with the addition of HOPA to the medium. HOPA's effects on TRH release from the adrenal gland were blocked with the addition of bicuculline, a GABA receptor inhibitor. The elution profile of methanol-extracted rat adrenal gland TRH was identical to that for synthetic TRH. The findings suggest that HOPA inhibits TRH release from the rat adrenal gland, and that its effects are mediated via the GABA receptor.
The effects of dopamine on the release of thyrotropin-releasing hormone (TRH) from the rat adrenal gland were studied in vitro. The rat adrenal glands were incubated in medium 199 with 1.0 mg/ml of bacitracin and 100 micrograms/ml of ascorbic acid (pH 7.4) (medium) for 20 min. The amount of TRH release into the medium was measured by radioimmunoassay. The immunoreactive TRH (ir-TRH) release from the rat adrenal gland was inhibited significantly in a dose-related manner with the addition of dopamine and enhanced with the addition of pimozide or domperidone to the medium. Dopamine's effects on ir-TRH release from the adrenal gland were blocked with the addition of pimozide or domperidone. The elution profile of methanol-extracted rat adrenal gland was identical to that of synthetic TRH. The findings suggest that the dopaminergic system inhibits TRH release from the rat adrenal gland.
Morphometric evaluation was performed on myelinated fibers of the corticospinal tract at the seventh thoracic spinal cord segment from three patients with Shy-Drager syndrome (SDS), six patients with amyotrophic lateral sclerosis (ALS), and five patients with nonneurologic symptoms. In SDS, small-sized myelinated fibers were nearly completely depleted, while large-sized myelinated fibers were considerably well preserved. In ALS, on the contrary, large myelinated fibers were predominantly decreased. These results suggested that selective vulnerability of axonal loss depends on fiber size and should be considered in interpretation of pathology of corticospinal tracts.
Central effect of thyrotropin releasing hormone (TRH) on gastric acid output and mucosal blood flow (MBF) was examined in urethane anesthetized rats. TRH, microinjected into the dorsal vagal complex [the dorsal motor nucleus of the vagus (NDV), the nucleus tractus solitarius and area postrema] induced dose-dependent (0.5-50 pmole) increases in gastric acid output and MBF. In contrast, 5 pmole TRH microinjected into various hypothalamic regions had no effect on these gastric parameters. Administration of TRH intraventricularly (i.c.v.) also increased these gastric parameters; however, about a 10 times higher dose of TRH was required to obtain the same order of excitatory effects seen with microinjection to the dorsal vagal complex. Application of anti-TRH serum to the dorsal vagal complex inhibited the increases in gastric acid output and MBF induced by TRH (i.c.v.). The effect of TRH applied to the dorsal vagal complex and i.c.v. were not modified by a concomitant administration of atropine. These results suggests that NDV is probably the site of action of TRH in inducing gastric hyper-functions. The mode of action of TRH seems to be independent of cholinergic muscarinic mechanisms present in the NDV.
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The effect of histamine and related compounds on the plasma beta-endorphin-like immunoreactivity (beta-En-Li) levels in rats were studied. Histamine (2.5 mg/kg), mepyramine (10 mg/kg) or famotidine (5.0 mg/kg) was injected i.p., and the animals were serially decapitated. The plasma beta-En-Li levels were measured by radioimmunoassay. Effects of histamine, mepyramine and famotidine on beta-En-LI release from the anterior pituitary were also investigated by means of an in vitro experiment. The beta-En-LI content in the hypothalamus and pituitary gland did not change significantly after histamine, mepyramine and famotidine injection. The plasma beta-En-LI levels increased significantly in a dose-related manner with a zenith at 20 min after histamine injection and decreased significantly after mepyramine injection, but did not change significantly after famotidine injection. Effects of histamine on plasma beta-En-LI levels were prevented with the pretreatment of mepyramine. The beta-En-LI release from the anterior pituitary was enhanced with the addition of histamine to the medium, and histamine's effects were blocked with an addition of mepyramine to the medium. These findings suggest that histamine acts as to stimulate beta-En-LI release from the anterior pituitary, and that histamine's effects may be mediated via H1-receptor.
The effects of calcium hopantenate (HOPA) on plasma beta-endorphin-like immunoreactivity (beta-En-LI) levels in rats have been studied. HOPA (1.5 g/kg) was injected ip, and the animals were serially decapitated. The plasma beta-En-LI levels were measured by radioimmunoassay. Effects of HOPA on beta-En-LI release from the anterior pituitary were also investigated by means of an in vitro experiment. The beta-En-LI content in the hypothalamus and pituitary gland did not change significantly after HOPA injection. The plasma beta-En-LI levels increased significantly in a dose-related manner with a zenith at 30 min after HOPA injection. Effects of HOPA on plasma beta-En-LI levels were prevented with the pretreatment of bicuculline. The beta-En-LI release from the anterior pituitary was enhanced with the addition of HOPA to the medium, and HOPA's effects were blocked with an addition of bicuculline to the medium. These findings suggest that HOPA acts on the anterior pituitary to stimulate beta-En-LI release, and its effects are mediated via GABA receptor.
The effects of histamine and its blocker on the release of thyrotropin releasing hormone (TRH) from the rat adrenal gland were studied in vitro. Rat adrenals were incubated in medium 199 with 1.0 mg ml-1 of bacitracin and 100 micrograms ml-1 of ascorbic acid (pH 7.4) for 20 min and TRH released into the medium was measured by radio-immunoassay. The immunoreactive TRH (ir-TRH) release from the rat adrenal gland was inhibited significantly in a dose-related manner by the addition of histamine and enhanced by the addition of famotidine. The effect of histamine on ir-TRH release from the rat adrenal gland was blocked by the addition of famotidine to the medium, but not by that of mepyramine. The elution profile of methanol extracted adrenal gland on Sephadex G-10 was identical to that of synthetic TRH. The findings suggest that histamine inhibits TRH release from the rat adrenal gland and that its effects may be mediated via H2-receptor.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
By using indirect immunofluorescence, galactocerebroside (galC) was detected on the surface of Schwann cells cultured from unmyelinated fibers of 10- to 12-day-old rat cervical sympathetic nerve trunk. By day 4 in vitro, galC-positive cells disappeared from the culture. When the 4-day cultures were treated with 1 mM 8-bromo cyclic AMP or dibutyryl cyclic AMP, galC reappeared in 72 h. The proportion of Schwann cells expressing galC was dependent on the concentration of cyclic AMP derivatives used.
Concentrations of thyrotropin-releasing hormone (TRH) were studied in the brain of the Weaver ataxic mouse, the Purkinje cell degenerative ataxic mouse (pcd-ataxic mouse) and the cytosine arabinoside (ara-C)-induced ataxic mouse. The brain tissue was dissected into 4 parts, e.g., hypothalamus, cerebrum, cerebellum and brain stem. TRH concentrations in each part of the brain were measured by radioimmunoassay. TRH concentrations in the brain of Weaver ataxic mice were significantly higher in the cerebellum and brain stem than in the controls. In pcd-ataxic mice, the TRH concentrations in the brain were significantly higher in the cerebrum and brain stem. In ara-C-induced ataxic mice, the concentrations were significantly higher in the cerebrum, cerebellum and brain stem. TRH levels in the hypothalamus of ataxic mice did not differ from those of controls. The elution profile of methanol-extracted cerebellum of ataxic mice on Sephadex G-10 was identical to that of synthetic TRH. These findings suggest that changes in the TRH concentrations in the brain play a pathophysiological role in ataxic mice.
Concentrations of thyrotropin-releasing hormone (TRH) were measured by a specific radioimmunoassay in the brain of 11 patients with amyotrophic lateral sclerosis (ALS) and 6 controls (myocardial infarction, gastric cancer, multiple myeloma, cerebrovascular disease, amyloid neuropathy). TRH was found in all parts of the dissected brain tissues (pedunculus cerebri, corpus callosum, capsula interna, motor area) in patients with ALS and controls. The TRH concentrations in the brain of patients with ALS were significantly lower in the pedunculus cerebri, compared with controls, and tended to decrease in the motor area and corpus callosum, but not significantly. Changes in TRH concentrations did not always correlate with pathohistological changes. These findings suggest that TRH is widely distributed in the human brain and decreases in some part of the ALS brain.