scholarly journals Ecdysone-dependent feedback regulation of prothoracicotropic hormone controls the timing of developmental maturation

Development ◽  
2020 ◽  
Vol 147 (14) ◽  
pp. dev188110 ◽  
Author(s):  
Christian F. Christensen ◽  
Takashi Koyama ◽  
Stanislav Nagy ◽  
E. Thomas Danielsen ◽  
Michael J. Texada ◽  
...  
Keyword(s):  
Larval Development ◽  
Feedback Regulation ◽  
Neuroendocrine System ◽  
Ecdysone Receptor ◽  
Feedback Circuit ◽  
Steroid Production ◽  
Prothoracicotropic Hormone ◽  
Adult Transition ◽  
Developmental Maturation

ABSTRACTThe activation of a neuroendocrine system that induces a surge in steroid production is a conserved initiator of the juvenile-to-adult transition in many animals. The trigger for maturation is the secretion of brain-derived neuropeptides, yet the mechanisms controlling the timely onset of this event remain ill-defined. Here, we show that a regulatory feedback circuit controlling the Drosophila neuropeptide Prothoracicotropic hormone (PTTH) triggers maturation onset. We identify the Ecdysone Receptor (EcR) in the PTTH-expressing neurons (PTTHn) as a regulator of developmental maturation onset. Loss of EcR in these PTTHn impairs PTTH signaling, which delays maturation. We find that the steroid ecdysone dose-dependently affects Ptth transcription, promoting its expression at lower concentrations and inhibiting it at higher concentrations. Our findings indicate the existence of a feedback circuit in which rising ecdysone levels trigger, via EcR activity in the PTTHn, the PTTH surge that generates the maturation-inducing ecdysone peak toward the end of larval development. Because steroid feedback is also known to control the vertebrate maturation-inducing hypothalamic-pituitary-gonadal axis, our findings suggest an overall conservation of the feedback-regulatory neuroendocrine circuitry that controls the timing of maturation initiation.

The Neuroendocrine System and General Mechanisms of Endocrine Disruption

2017 ◽  
Author(s):  
Heather B. Patisaul ◽  
Scott M. Belcher
Keyword(s):  
Feedback Regulation ◽  
Neuroendocrine System ◽  
Negative Feedback Regulation ◽  
Adrenal Hormone ◽  
Aryl Hydrocarbon ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Environmental Sensor ◽  
Exogenous Compounds ◽  
Primary Focus

The neuroendocrine system is the interface between the endocrine and nervous systems. This chapter presents an overview of the neuroendocrine system and endogenous hormones, with a primary focus on the hypothalamic-pituitary-gonadal (HPG) axis, the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-thyroid axis (HPT). The importance of impacts of exogenous compounds, both natural and man-made, on the neuroendocrine system is discussed, with a focus on endocrine-disruptive actions of plant-derived phytoestrogens and the role of the aryl hydrocarbon receptor as an environmental sensor. The impacts of EDCs on feed-forward and negative feedback regulation of neuroendocrine functions, including those mediated by estrogen, androgen, and thyroid pathways, as well as other less studied pathways of hormonal signaling that involve disruption of neurosteroids, peptide hormones, and adrenal hormone signaling are also presented.

scholarly journals Ecdysone receptor isoforms play distinct roles in larval–pupal–adult transition in Leptinotarsa decemlineata

2019 ◽  
Vol 27 (3) ◽  
pp. 487-499 ◽  
Author(s):  
Qing‐Yu Xu ◽  
Pan Deng ◽  
Qiong Zhang ◽  
Ang Li ◽  
Kai‐Yun Fu ◽  
...  
Keyword(s):  
Leptinotarsa Decemlineata ◽  
Ecdysone Receptor ◽  
Adult Transition ◽  
Receptor Isoforms

scholarly journals Forward and feedback regulation of cyclic steroid production in Drosophila melanogaster

Development ◽  
2014 ◽  
Vol 141 (20) ◽  
pp. 3955-3965 ◽  
Author(s):  
J.-P. Parvy ◽  
P. Wang ◽  
D. Garrido ◽  
A. Maria ◽  
C. Blais ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Feedback Regulation ◽  
Steroid Production

Influence of neonatal hemicastration on in-vitro secretion of inhibin, gonadotrophins and testicular steroids in male rats

1985 ◽  
Vol 106 (2) ◽  
pp. 259-265 ◽  
Author(s):  
A. M. Ultee-van Gessel ◽  
F. G. Leemborg ◽  
F. H. de Jong ◽  
H. J. van der Molen
Keyword(s):  
Sertoli Cells ◽  
Leydig Cells ◽  
Feedback Regulation ◽  
Male Rats ◽  
Steroid Production ◽  
Pituitary Secretion ◽  
Lh Releasing Hormone ◽  
Testicular Steroids

ABSTRACT Pituitary secretion of FSH in male animals is regulated, at least partly, by a protein hormone, inhibin, which is produced by Sertoli cells in the testes. To establish at which age the role of testicular inhibin in the regulation of FSH secretion becomes apparent, groups of male rats were hemicastrated or sham-operated on day 1 of life and pituitary and testicular function were investigated in vitro at 21, 42 or 63 days of age. Testis weights were increased in hemicastrated rats at all ages studied. Peripheral concentrations of gonadotrophins generally showed a good correlation with the concentrations of FSH and LH measured in the medium of hemipituitary glands which were incubated in vitro at 37 °C in the absence or presence of LH-releasing hormone. Peripheral testosterone concentrations in hemicastrated animals were not significantly different from those in sham-operated rats at all ages studied. Steroid production by Leydig cells in vitro was not significantly influenced by hemicastration. The secretion of inhibin by Sertoli cells from 21-day-old hemicastrated rats was decreased while Sertoli cells from 42- and 63-day-old hemicastrated animals secreted slightly but not significantly more inhibin than Sertoli cells from sham-operated rats. It is concluded that although compensatory increases of testosterone and inhibin production at later ages make it difficult to draw conclusions about the relative importance of inhibin in the feedback regulation of FSH secretion at different ages, it is likely that inhibin plays a role in the feedback of FSH in immature, rather than in mature male rats. J. Endocr. (1985) 106, 259–265

scholarly journals Neurotransmitters Affect Larval Development by Regulating the Activity of Prothoracicotropic Hormone-Releasing Neurons in Drosophila melanogaster

2021 ◽  
Vol 15 ◽  
Author(s):  
Shun Hao ◽  
Julia Yvonne Gestrich ◽  
Xin Zhang ◽  
Mengbo Xu ◽  
Xinwei Wang ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Larval Development ◽  
Ex Vivo ◽  
Dependent Manner ◽  
Larval Metamorphosis ◽  
Prothoracicotropic Hormone ◽  
Bidirectional Regulation ◽  
And Control ◽  
Ach Receptors

Ecdysone, an essential insect steroid hormone, promotes larval metamorphosis by coordinating growth and maturation. In Drosophila melanogaster, prothoracicotropic hormone (PTTH)-releasing neurons are considered to be the primary promoting factor in ecdysone biosynthesis. Recently, studies have reported that the regulatory mechanisms of PTTH release in Drosophila larvae are controlled by different neuropeptides, including allatostatin A and corazonin. However, it remains unclear whether neurotransmitters provide input to PTTH neurons and control the metamorphosis in Drosophila larvae. Here, we report that the neurotransmitters acetylcholine (ACh) affect larval development by modulating the activity of PTTH neurons. By downregulating the expression of different subunits of nicotinic ACh receptors in PTTH neurons, pupal volume was significantly increased, whereas pupariation timing was relatively unchanged. We also identified that PTTH neurons were excited by ACh application ex vivo in a dose-dependent manner via ionotropic nicotinic ACh receptors. Moreover, in our Ca2+ imaging experiments, relatively low doses of OA caused increased Ca2+ levels in PTTH neurons, whereas higher doses led to decreased Ca2+ levels. We also demonstrated that a low dose of OA was conveyed through OA β-type receptors. Additionally, our electrophysiological experiments revealed that PTTH neurons produced spontaneous activity in vivo, which provides the possibility of the bidirectional regulation, coming from neurons upstream of PTTH cells in Drosophila larvae. In summary, our findings indicate that several different neurotransmitters are involved in the regulation of larval metamorphosis by altering the activity of PTTH neurons in Drosophila.

scholarly journals A novel Tweak/ Stat1/ Snhg3 positive feedback circuit contributes to the glial cell activation in temporal lobe epilepsy mice

2019 ◽  
Author(s):  
Li Chen ◽  
Rui Shi ◽  
Xin Zhang ◽  
Chen Hou ◽  
Xiaohui Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Temporal Lobe Epilepsy ◽  
Glial Cell ◽  
Temporal Lobe ◽  
Cell Activation ◽  
Feedback Regulation ◽  
Inflammatory Factor ◽  
Feedback Circuit ◽  
Glial Cell Activation ◽  
Factor Secretion

Abstract Gliosis is an important feature of temporal lobe epilepsy (TLE), but the regulatory mechanism of glial cell activation remains unclear. Small nucleolar RNA host gene 3 (Snhg3) has been reported to be involved in cell proliferation and migration in various cancers. However, its role in the development of TLE has been hardly explored. Here, we established a mouse TLE model by injecting intraperitoneally with pilocarpine, and found that Tweak expression was significantly induced in TLE mice. Inhibiting Tweak expression by the injection of siRNA notably rescued the glial cell activation, neuroinflammatory cytokine secretion and cognitive behavior disorder in TLE mice. Molecular mechanism studies showed that cell proliferation, migration, inflammatory factor secretion, Stat1 pathway activation and Snhg3 expression were promoted after we incubated Tweak recombinant protein (rTweak) with mouse astrocytes (MAs). The Tweak neutralizing antibody (anti-Tweak) showed the opposite effect to that of rTweak. In subsequent researches, we found that Stat1 directly bound to Snhg3 promoter and they elevated the expression of each other. Moreover, both of them boosted cell proliferation, migration, inflammatory factor secretion and Tweak expression. Thus, we found a feedback regulation loop consisting of Tweak/Fn14, Stat1/ p-Stat1 and Snhg3 in the MAs, which increased cell activation. In vivo experiment demonstrated that the reduction of Snhg3 inhibited glial cell activation induced by TLE, and Tweak/Stat1/Snhg3 feedback circuit also existed in TLE mice. In short, our research testified a feedback regulation loop consisting of Tweak/Stat1/Snhg3, which was involved in the activation of hippocampal glial cells in TLE mice.

Sign in / Sign up

Export Citation Format

Share Document