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.

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.

scholarly journals Yolk sac-derived Pdcd11-positive cells modulate zebrafish microglia differentiation through the NF-κB-Tgfβ1 pathway

2020 ◽  
Vol 28 (1) ◽  
pp. 170-183
Author(s):  
Ruimeng Yang ◽  
Ming Zhan ◽  
Miaomiao Guo ◽  
Hao Yuan ◽  
Yiqin Wang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Susceptibility Gene ◽  
Physiological Role ◽  
Vital Role ◽  
Yolk Sac ◽  
Cerebral White Matter ◽  
Neuron Development ◽  
Mature Brain ◽  
The Central Nervous System

AbstractMicroglia are the primary immune cells in the central nervous system, which plays a vital role in neuron development and neurodegenerative diseases. Microglial precursors in peripheral hematopoietic tissues colonize the central nervous system during early embryogenesis. However, how intrinsic and extrinsic signals integrate to regulate microglia’s differentiation remains undefined. In this study, we identified the cerebral white matter hyperintensities susceptibility gene, programmed cell death protein 11 (PDCD11), as an essential factor regulating microglia differentiation. In zebrafish, pdcd11 deficiency prevents the differentiation of the precursors to mature brain microglia. Although, the inflammatory featured macrophage brain colonization is augmented. At 22 h post fertilization, the Pdcd11-positive cells on the yolk sac are distinct from macrophages and neutrophils. Mechanistically, PDCD11 exerts its physiological role by differentially regulating the functions of nuclear factor-kappa B family members, P65 and c-Rel, suppressing P65-mediated expression of inflammatory cytokines, such as tnfα, and enhancing the c-Rel-dependent appearance of tgfβ1. The present study provides novel insights in understanding microglia differentiation during zebrafish development.

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