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

1983 ◽  
Vol 103 (3) ◽  
pp. 359-364 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Tsh Secretion ◽  
Pretreated Group ◽  
Basal Plasma ◽  
The Central Nervous System ◽  
Tsh Levels

Abstract. The effects of dynorphin (1-13) on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. Dynorphin (500 μg/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 haloperidolor 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.

β-Neoendorphin inhibits thyrotrophin secretion in rats

1983 ◽  
Vol 104 (4) ◽  
pp. 437-442 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Specific Radioimmunoassay ◽  
Tsh Secretion ◽  
Pretreated Group ◽  
The Central Nervous System ◽  
Tsh Levels

Abstract. The effects of β-neoendorphin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. β-neoendorphin (500 μg/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 β-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 β-neoendorphin, but the plasma TSH response to TRH was not. Naloxone partially prevented the inhibitory effect of β-neoendorphin on TSH release. In the haloperidol- or 5-hydroxytryptophan-pretreated group, the inhibitory effect of β-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 β-neoendorphin acts on the hypothalamus by inhibiting TRH release, which may be modified by amines of the central nervous system.

Effects of eledoisin on thyrotrophin secretion in rats

1985 ◽  
Vol 110 (1) ◽  
pp. 90-94
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori ◽  
De Heng Sun ◽  
Masahiro Chaya
Keyword(s):  
Central Nervous System ◽  
Thyroid Hormone ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Tsh Secretion ◽  
Pretreated Group ◽  
The Central Nervous System ◽  
Thyroid Hormone Levels ◽  
Tsh Levels

Abstract. The effect of peripheral administration of eledoisin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. Eledoisin (500 μg/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after eledoisin injection, whereas its plasma concentration tended to decrease, but not significantly. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. Plasma thyroid hormone levels did not change significantly. Plasma ir-TRH and TSH responses to cold were inhibited by eledoisin, but the plasma TSH response to TRH was not affected. In the pimozide- or para-chlorophenylalanine-pretreated group, the inhibitory effect of eledoisin on TSH levels was prevented, but not in the l-dopa- or 5-hydroxytryptophan-pretreated group. These drugs alone did not affect plasma TSH levels at the dose used. The inactivation of TRH immunoreactivity by plasma or hypothalamus in vitro after eledoisin injection did not differ from that of controls. These findings suggest that eledoisin acts on the hypothalamus to inhibit TRH release, and its effects are modified by amines of the central nervous system.

Bombesin inhibits thyrotrophin secretion in rats

1985 ◽  
Vol 108 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori ◽  
Masahiro Chaya
Keyword(s):  
Thyroid Hormone ◽  
Plasma Concentrations ◽  
Treated Group ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Tsh Secretion ◽  
The Central Nervous System ◽  
Thyroid Hormone Levels ◽  
Tsh Levels

Abstract. The effects of peripheral administration of bombesin on thyrotrophin-releasing hormone (TRH) and thvrotrophin (TSH) secretion in rats were studied. Bombesin (200 μg/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after bombesin injection, whereas plasma concentrations tended to decrease, but not significantly. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. Plasma thyroid hormone levels did not change significantly. Plasma ir-TRH and TSH responses to cold were inhibited by bombesin, but the plasma TSH response to TRH was not affected. In the pimozide- or para-chlorophenylalanine pre-treated group, the inhibitory effect of bombesin on TSH levels was prevented, but not in the l-Dopa- or 5-hydroxytryptophan pre-treated group. These drugs alone had no effect on plasma TSH levels in terms of the dose used. The inactivation of TRH immunoreactivity in plasma or hypothalamus in vitro after bombesin injection did not differ from that of the controls. These findings suggest that bombesin acts on the hypothalamus to inhibit TRH release, and that its effects are at least partially modified by amines of the central nervous system.

scholarly journals Thyrotrophin-releasing hormone receptor 1 and prothyrotrophin-releasing hormone mRNA expression in the central nervous system are regulated by suckling in lactating rats

2005 ◽  
Vol 152 (5) ◽  
pp. 791-803 ◽  
Author(s):  
Åse-Karine Fjeldheim ◽  
Per Ivar Høvring ◽  
Ole-Petter Løseth ◽  
Per Wiik Johansen ◽  
Joel C Glover ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mrna Expression ◽  
Physiological Role ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
The Central Nervous System ◽  
Plasma Prl

Background: The accepted function of the hypothalamic peptide, thyrotrophin-releasing hormone (TRH), is to initiate release of thyrotrophin (TSH) from the pituitary. A physiological role for TRH in lactating rats has not yet been established. Methods: Tissues were prepared from random-cycling and lactating rats and analysed using Northern blot, real time RT-PCR and quantitative in situ hybridisation. Results: This study demonstrates that TRH receptor 1 (TRHR1) mRNA expression is up-regulated in the pituitary and in discrete nuclei of the hypothalamus in lactating rats, while proTRH mRNA expression levels are increased only in the hypothalamus. The results were corroborated by quantitative in situ analysis of proTRH and TRHR1. Bromocriptine, which reduced prolactin (PRL) concentrations in plasma of lactating and nursing rats, also counteracted the suckling-induced increase in TRHR1 mRNA expression in the hypothalamus, but had an opposite effect in the pituitary. These changes were confined to the hypothalamus and the amygdala in the brain. Conclusions: The present study shows that the mechanisms of suckling-induced lactation involve region-specific regulation of TRHR1 and proTRH mRNAs in the central nervous system notably at the hypothalamic level. The results demonstrate that continued suckling is critical to maintain plasma prolactin (PRL) levels as well as proTRH and TRHR1 mRNA expression in the hypothalamus. Increased plasma PRL levels may have a positive modulatory role on the proTRH/TRHR1 system during suckling.

scholarly journals Hypothalamic gonadotropin-releasing hormone (GnRH) receptor neurons fire in synchrony with the female reproductive cycle

2015 ◽  
Vol 114 (2) ◽  
pp. 1008-1021 ◽  
Author(s):  
Christian Schauer ◽  
Tong Tong ◽  
Hugues Petitjean ◽  
Thomas Blum ◽  
Sophie Peron ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Firing Pattern ◽  
Gnrh Receptor ◽  
Gonadotropin Releasing Hormone ◽  
Burst Firing ◽  
Hypothalamic Nucleus ◽  
Hpg Axis ◽  
Releasing Hormone ◽  
The Central Nervous System

Gonadotropin-releasing hormone (GnRH) controls mammalian reproduction via the hypothalamic-pituitary-gonadal (hpg) axis, acting on gonadotrope cells in the pituitary gland that express the GnRH receptor (GnRHR). Cells expressing the GnRHR have also been identified in the brain. However, the mechanism by which GnRH acts on these potential target cells remains poorly understood due to the difficulty of visualizing and identifying living GnRHR neurons in the central nervous system. We have developed a mouse strain in which GnRHR neurons express a fluorescent marker, enabling the reliable identification of these cells independent of the hormonal status of the animal. In this study, we analyze the GnRHR neurons of the periventricular hypothalamic nucleus in acute brain slices prepared from adult female mice. Strikingly, we find that the action potential firing pattern of these neurons alternates in synchrony with the estrous cycle, with pronounced burst firing during the preovulatory period. We demonstrate that GnRH stimulation is sufficient to trigger the conversion from tonic to burst firing in GnRHR neurons. Furthermore, we show that this switch in the firing pattern is reversed by a potent GnRHR antagonist. These data suggest that endogenous GnRH acts on GnRHR neurons and triggers burst firing in these cells during late proestrus and estrus. Our data have important clinical implications in that they indicate a novel mode of action for GnRHR agonists and antagonists in neurons of the central nervous system that are not part of the classical hpg axis.

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