Figure - available from: Brain Structure and Function
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TRH-IR elements in the human hypothalamus. Periventricular and perifornical TRH neurons are typically bipolar (a). TRH-IR axon varicosities often form fiber baskets surrounding neurons that are obviously not TH or TRH immunoreactive in the periventricular (b) and perifornical region (c). Occasionally, these fiber baskets can also be observed in the lateral hypothalamic area (d). Multipolar TRH-IR neurons can be found often in the lateral hypothalamus. In the median eminence, dense TRH-IR fiber network surrounds dopaminergic neurons. Magnification: a–e 400x; f 100x
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Thyrotropin-releasing hormone (TRH) has a critical role in the central regulation of thyroid-stimulating hormone (TSH) from the anterior pituitary, and subsequently, thyroid hormone secretion from the thyroid gland. In addition to its role in the regulation of HPT axis, TRH is a potent regulator of prolactin (PRL) secretion by stimulating PRL secre...
Citations
... Another association between PRL and NDs is TRH, which is a well-known regulator of PRL secretion in tuberoinfundibular dopamine neurons [70,71]. Like other hormones, such as PRL, TRH administration has been studied in neuroprotection [72]. ...
Prolactin (PRL) is a peptide and pleiotropic hormone with more than 300 associated functions such as maternal behavior, lactation, osmoregulation, angiogenesis, and the immune system. It is associated with several functions in the brain, including lactation, cognition and memory, maternal behavior, and neurogenesis. PRL reportedly plays an important role in neuroprotection against excitotoxicity caused by glutamate (Glu) and kainic acid (KA) damage in vitro and in vivo models. However, the molecular mechanisms involved in the neuroprotective effects of PRL are unclear. Despite this, data suggest the involvement of PI3K/AKT, and GSK3β/NF-κB signaling pathways, which are involved in neuroprotection. In addition, PRL inhibits Glu- and KA-induced increase by intracellular Ca2+ concentration, leading to neuronal survival. We also discuss current knowledge on the role of PRL in neurodegenerative diseases. New avenues of research into the protective mechanisms of PRL and its potential therapeutic effects on the brain under pathological and physiological conditions are needed.
... In another study, which utilized the technique of in situ hybridization histochemistry, researchers identified a specific subtype of TRH-R1 mRNA that was predominantly expressed in hypothalamic regions, including the arcuate nucleus [59]. Additionally, TRH neurons make synaptic contact with TIDA neurons [60]. TRH binding sites are found in TIDA neurons, and TRH potently and robustly increases DA release and intracellular calcium concentrations in these cells [61]. ...
Tuberoinfundibular dopamine (TIDA) neurons have cell bodies located in the arcuate nucleus of the mediobasal hypothalamus. They project to the external zone of the median eminence, and the dopamine (DA) released there is carried by the hypophysial portal vasculature to the anterior pituitary. The DA then activates D2 receptors to inhibit prolactin (PRL) secretion from lactotrophs. The TIDA neuronal population is the principal regulatory factor controlling PRL secretion. The neuroendocrine role subserved by TIDA neurons sets them apart from other dopaminergic populations like the nigrostriatal and mesolimbic DA neurons. TIDA neurons exhibit intrinsic oscillatory fluctuations in their membrane potential that give rise to phasic firing and bursting activity. TIDA neuronal activity is sexually differentiated and modulated by gonadal hormones and PRL, as well as an array of small molecule and peptide neurotransmitters. This review covers these characteristics.
... Some of these downregulated signaling pathways are associated with inhibition of prolactin secretion. It has been reported that TRH can regulate the activity of dopaminergic neurons through neurosynapses and subsequently regulate prolactin secretion [50]. Intracerebroventricular angiotensin administration decreases the level of prolactin in the plasma [51]. ...
Prolactin (PRL) is an important hormone that is secreted by the pituitary gland and plays an important role in the growth, development and reproduction of organisms. Thyrotropin-releasing hormone (TRH) is a common prolactin-releasing factor that regulates the synthesis and secretion of prolactin. In recent studies, microRNAs (miRNAs) have been found to play a key role in the regulation of pituitary hormones. However, there is a lack of systematic studies on the regulatory role that TRH plays on the pituitary transcriptome, and the role of miRNAs in the regulation of PRL synthesis and secretion by TRH lacks experimental evidence. In this study, we first investigated the changes in PRL synthesis and secretion in the rat pituitary gland after TRH administration. The results of transcriptomic analysis after TRH treatment showed that 102 genes, including those that encode Nppc, Fgf1, PRL, Cd63, Npw, and Il23a, were upregulated, and 488 genes, including those that encode Lats1, Cacna2d1, Top2a, and Tfap2a, were downregulated. These genes are all involved in the regulation of prolactin expression. The gene expression of miR-126a-5p, which regulates the level of PRL in the pituitary gland, was screened by analysis prediction software and by a dual luciferase reporter system. The data presented in this study demonstrate that TRH can regulate prolactin synthesis and secretion through miR-126a-5p, thereby improving our understanding of the molecular mechanism of TRH-mediated PRL secretion and providing a theoretical basis for the role of miRNAs in regulating the secretion of pituitary hormones.
... Finally, although many studies have shown that TRH acts directly on lactotrophs, it is relevant to note that numerous TRH fibers enter the Arc (Péterfi et al. 2018). TRH terminals abut on tuberoinfudibular dopaminergic (TIDA) neurons in rats (Lyons et al. 2010) and humans (Dudas and Merchenthaler 2020), coincident with the expression of the TRH receptor in Arc (Heuer et al. 2000), but the TRH neurons of origin are not known. In hypothalamic slices, TRH provokes a transition from phasic to tonic firing of the TIDA neurons that control PRL secretion (Lyons et al. 2010). ...
Hypophysiotropic neurons of the paraventricular nucleus of the hypothalamus
that express thyrotropin-releasing hormone (TRH) control the synthesis and
release of thyrotropin, the pituitary hormone that regulates the synthesis and
release of thyroid hormones. Thyroid hormones are pleiotropic hormones with
multiple functions involved in growth, development, and energy homeostasis.
The TRH neuroendocrine cells receive neuronal inputs from different parts of the
brain, as well as local and hormonal signals, and integrate and transduce the
information as a hormone (TRH) output. They are glutamatergic neurons; most
co-express cocaine- and amphetamine-regulated transcripts; however, their
transcriptomic characterization is still in its infancy but suggests functional
diversity. Transcription of the Trh gene is rapidly but transiently increased by
multiple signals, some of which also cause the release of TRH. This review
summarizes the basic mechanisms involved in the generation of TRH in
hypophysiotropic neurons and turnover in median eminence, and recapitulates
the multiple factors that regulate Trh synthesis and the amount of TRH that
reaches thyrotropes, the physiological conditions and environmental stressors
that alter TRH neurons and thyroid axis status during development and in adult
animals, as well as critical sex differences
