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Biomedical subjects

T Mitsuma

Publications and source records attributed to T Mitsuma.

At least 307 records · Page 17Linked to original sources
PubMed1983

Effects of leucine-enkephalin on hypothalamic-pituitary-thyroid axis in rats.

Basal thyrotropin (TSH) levels in plasma and the TSH response to thyrotropin-releasing hormone (TRH) were inhibited after Leucine-enkephalin (L-EK) administration iv in rats. TRH and TSH responses to cold were inhibited after L-EK administration. In the L-DOPA, haloperidol or 5-hydoxytryptophan-treated rats, the inhibitory effect of L-EK on TSH release was restored. Findings suggested that L-EK acted both the hypothalamus and pituitary. Its inhibitory effects on TRH and TSH release at least partially mediated by interaction with amines in the central nervous system.

Animals↗
PubMed1983

Distribution of immunoreactive thyrotropin-releasing hormone in the forebrain and hypophysis of the bullfrog, Rana catesbeiana.

The distribution of immunoreactive thyrotropin-releasing hormone (TRH) in the forebrain and hypophysis of Rana catesbeiana was studied by means of specific radioimmunoassay and immunohistochemistry based on peroxidase-antiperoxidase (PAP) techniques. A relatively high concentration of immunoassayable TRH is present in the hypothalamus. Immunoreactive TRH cell bodies are found in the anterior part of the preoptic nucleus, the dorsal infundibular nucleus, the nucleus of diagonal band of Broca, and the medial part of the amygdala. Immunoreactive nerve terminals are observed in the neurohypophysis and the external layer of the median eminence, where the terminals are in close contact with the capillary loops of the hypophyseal portal vessels. The possible role of TRH in the frog brain is discussed.

Animals↗
PubMed1983

Effects of serotonergic system on hypothalamic-pituitary-thyroid axis in rats.

The effects of the serotonergic system on the hypothalamic-pituitary-thyroid axis in rats were studied. Immunoreactive thyrotropin releasing hormone (ir-TRH) in plasma significantly increased 24 hours after para-chlorophenylalanine (PCPA) administration. Basal thyrotropin (TSH) levels in plasma significantly decreased after tryptophan or 5-hydroxytryptophan (5-HTP) administration, but not after PCPA administration. The plasma ir-TRH and TSH responses to cold were inhibited after tryptophan or 5-HTP administration, but not after PCPA treatment. In these treated groups, the TSH response to TRH did not differ from that of control. Thyroxine, 3,3',5-triiodothyronine showed no change after administration of these drugs. These data indicate that the serotonergic system might inhibit TRH and TSH release in rats.

Animals↗
PubMed1983

Effects of insulin on thyrotropin releasing hormone from frog skin.

Thyrotropin releasing hormone (TRH) is concentrated in the skin of Rana nigromacula. Its elution profile on Sephadex G-10 was identical to that of synthetic TRH. Insulin and noradrenaline stimulated TRH release from frog skin in a dose-related manner. The effects of insulin were not blocked by preincubation with phentolamine and they enhanced the noradrenaline effect. These data indicate that insulin stimulates directly TRH release from frog skin in other than the sympathetic pathway.

Animals↗
PubMed1983

Effects of calcium hopantenate on the hypothalamic-pituitary-thyroid axis in rats.

Effects of calcium hopantenate (HOPA) on the hypothalamic pituitary-thyroid axis in rats were studied. Basal plasma thyrotropin (TSH) levels significantly decreased from 277 +/- 24 to 167 +/- 24 ng/ml (p less than 0.01) at 20 min after HOPA administration. In the bicuculline-pretreated rats, the inhibitory effect of HOPA on TSH release was corrected. The plasma immunoreactive thyrotropin-releasing hormone (TRH) and TSH responses to cold were significantly inhibited after HOPA administration. The plasma TSH response to TRH was also significantly inhibited by HOPA. The plasma thyroxine and 3,3', 5-triiodothyronine levels did not change after HOPA administration. Findings suggest that HOPA acts both on the hypothalamus and pituitary gland, inhibiting TRH and TSH release.

Animals↗
PubMed1983

Dynorphin (1-13) effects on thyrotrophin-releasing hormone and thyrotrophin secretion in rats.

The effects of dynorphin (1-13) on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. Dynorphin (500 micrograms/kg) was injected iv, and the rats were serially decapitated. TRH and TSH, thyroxine (T4) and 3,3',5-triiodothyronine (T3) were measured by radioimmunoassay. The hypothalamic immunoreactive TRH did not change significantly after dynorphin injection. Basal plasma TSH levels significantly decreased in a dose-related manner with a nadir at 40 min after dynorphin injection. The effect of dynorphin on TSH release was partially prevented by naloxone. The plasma TSH response to cold was significantly inhibited by dynorphin. The plasma TSH response to TRH did not differ from that of the control. In the L-DOPA or 5-hydrotryptophan-pretreated group, the inhibitory effect of dynorphin on TSH release was prevented, but not in the haloperidol-or para-chlorophenylalanine-pretreated group. These drugs alone did not affect plasma TSH levels. The plasma T4 and T3 levels did not change significantly after dynorphin injection. The findings suggest that dynorphin acts on the hypothalamus by inhibiting TRH release, which may be modified by amines of the central nervous system.

Animals↗
PubMed1983

beta-Neoendorphin inhibits thyrotrophin secretion in rats.

The effects of beta-neoendorphin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. beta-neoendorphin (500 micrograms/kg) was injected iv, and the rats were decapitated serially. TRH, TSH, thyroxine (T4) and 3,3',5-triiodothyronine (T3) were measured by means of a specific radioimmunoassay for each. Hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after beta-neoendorphin injection, and plasma concentrations tended to decrease, but not significantly so. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min. Plasma T4 and T3 levels did not change after the injection. Plasma ir-TRH and TSH responses to cold were significantly inhibited by beta-neoendorphin, but the plasma TSH response to TRH was not. Naloxone partially prevented the inhibitory effect of beta-neoendorphin on TSH release. In the haloperidol- or 5-hydroxytryptophan-pretreated group, the inhibitory effect of beta-neoendorphin on TSH release was prevented, but not in the L-dopa- or para-chlorophenylalanine-pretreated group. These drugs alone did not affect plasma TSH levels at the dose used. These findings suggest that beta-neoendorphin acts on the hypothalamus by inhibiting TRH release, which may be modified by amines of the central nervous system.

Animals↗
PubMed1982

Effects of streptozotocin-induced diabetes mellitus on hypothalamic-pituitary-thyroid axis in rats.

The effects of streptozotocin-induced diabetes mellitus on the hypothalamic-pituitary-thyroid axis in rats were studied. Streptozotocin (60 mg/kg) was injected ip. Rats were decapitated at two and four weeks after the streptozotocin treatment. Thyrotropin releasing hormone (TRH), thyrotropin (TSH), thyroxine (T4), 3,3',5-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), 3,3'-diiodothyronine (3,3'-T2) and 3',5'-diiodothyronine (3',5'-T2) were measured by means of the specific radioimmunoassay for each. Immunoreactive TRH (ir-TRH) contents in the hypothalamus significantly decreased at four weeks (p less than 0.02). Basal TSH levels in plasma significantly decreased (p less than 0.005, p less than 0.001), and plasma ir-TRH and TSH responses to cold were significantly inhibited after the streptozotocin treatment (p less than 0.001). The plasma TSH response to TRH was decreased, but not significantly. The plasma T4 and T3 levels fell significantly. RT3 did not change throughout the experiment. 3,3'-T2 levels in plasma fell significantly, whereas 3',5'-T2 increased. Blood glucose levels rose significantly after streptozotocin treatment, but insulin treatment led to partial restoration. The findings suggest that streptozotocin-induced diabetes mellitus affects various sites of the hypothalamic-pituitary-thyroid axis in rats.

Animals↗
PubMed1982

Effects of dexamethasone on the hypothalamic-pituitary-thyroid axis in rats.

Effects of dexamethasone on the hypothalamic-pituitary-thyroid axis in rats were studied. Rats given saline (group A), 25 micrograms of dexamethasone/100 g body weight (group B) or 500 micrograms o dexamethasone/100 g body weight (group C) were serially decapitated and brain tissues and blood were obtained. TRH contents in the hypothalamus, plasma concentrations of TRH, TSH, T4, T3 and reverse T3 were measured by specific radioimmunoassay. TRH contents in the hypothalamus were significantly increased at 3 h in group B after dexamethasone treatment. In group C, however, they significantly increased for 1 to 3 h, but then decreased with the minimum at 20 h. TRH plasma levels significantly increased with the maximum at 4 h in group B and at 24 h in group C. TSH plasma levels were significantly decreased initially and then significantly increased with the maximum at 5 h in group B and at 24 h in group C. TSH responsiveness to TRH was significantly decreased at 1 to 3 h in group B, but in group C it was significantly decreased initially and the significantly increased. T3 plasma levels significantly decreased at 1 to 3 h in group B and at 1 to 18 h in group C. Reverse T3 plasma levels were significantly increased with the maximum at 3 h in group B and at 6 h in group C. The results demonstrate that dexamethasone may act on multiple sites of the hypothalamic-pituitary-thyroid axis in rats and that its effect depends on the dose used or the time interval after dexamethasone treatment.

Animals↗
PubMed1982

Tumor promoter 12-O-tetradecanoylphorbol 13-acetate: effect on complement and Epstein-Barr virus receptors in human lymphoblastoid cell lines.

The effect of the tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA) on the C3 and Epstein-Barr virus (EBV) receptors in various human lymphoblastoid cells was investigated with the use of the erythrocyte-antibody-complement (EAC) rosette formation method and a quantitative bioassay for EBV receptors. TPA caused a significant decrease of C3 receptors in the cultures of both Raji and SB4 cells (by approximately 50% of the C3 receptors in untreated cultures at 10 ng/ml). Kinetic studies revealed that the rate of reduction was rather moderate but progressive, reaching a maximum 5 days after treatment with TPA. Kinetic studies showed that EBV receptors also decreased, similar to the reduction seen with C3 receptors after TPA treatment. The effect of TPA on the reduction of C3 receptors was observed not only in these cells but also in other EBV-positive B-cells, subclones of SB4 cells, and MOLT-4 cells. However, in an EBV-negative B-cell line, BJAB, EAC rosette formation was significantly enhanced.

Burkitt Lymphoma↗
PubMed1981

Increase in plasma thyrotropin-releasing hormone in normal human pregnancy.

Maternal thyroid regulation in pregnancy was examined by measuring the concentrations of TRH, T4, T3, free T4 (by RIA), T4-binding globulin, TSH, PRL, and hCG in the sera of 30 normal pregnant women, 10 puerperally lactating women, and 10 normal pregnant women, 10 puerperally lactating women, and 10 normal nonpregnant female controls. Results showed that serum T4, T3, T4-binding globulin, PRL, and hCG, but not free T4 (by RIA), increased significantly during pregnancy. The plasma level of TRH was significantly higher (P less than 0.01) in the second trimester and significantly lower (P less than 0.05 1 month post partum than those values in nonpregnant controls. No significant correlations, however, were observed between the serum level of TRH and those of the thyroid hormones TSH, PRL, and hCG in pregnancy. The TRH-degrading activity of the plasma in the second trimester was normal. These results indicate that TRH secretion may be increased in the second trimester of pregnancy.

Adult↗