BDNF up-regulates pre-pro-TRH mRNA expression in the fetal/neonatal paraventricular nucleus of the hypothalamus. Properties of the transduction pathway

Ubieta, Raimundo; Uribe, R.M.; González, José Antonio García-Cruces; Vázquez, Arlene Iskra García; Pérez‐Monter, Carlos; Pérez-Martı́nez, Leonor; Joseph‐Bravo, Patricia; Charlí, Jean-Louis

doi:10.1016/j.brainres.2007.08.026

Cited by 18 publications

(14 citation statements)

References 58 publications

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“…The ERK1/2 pathway can be stimulated by growth factors as BDNF [25], that increases TRH mRNA levels in immature hypothalamic cultures and this effect is antagonized by PD98059 [62,63]. In vivo, stress increases BDNF expression in the PVN in a fast and transient manner [64], which could activate TRH neurons expressing TrkB receptor [63].…”

Section: Discussionmentioning

confidence: 98%

The PKC and ERK/MAPK Pathways Regulate Glucocorticoid Action on TRH Transcription

et al. 2008

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Biosynthesis of TRH, a neuropeptide involved in energy homeostasis, is modulated by glucocorticoids. TRH mRNA and peptide levels are increased upon incubation of hypothalamic cells with dexamethasone or with cAMP analogs but when combined, a mutual antagonism is observed. These effects are observed at the transcriptional level and on binding of glucocorticoid receptor (GR) or pCREB to the composite GRE (cGRE) and CRE-2 sites of TRH promoter. The present work studied the involvement of PKC and MAPK pathways on the effect of dexamethasone and on its interaction with cAMP signaling in hypothalamic cell cultures. PKC or MEK inhibition abolished dexamethasone-stimulatory effect on TRH mRNA levels, as well as its interference with the stimulatory effect of 8Br-cAMP. Binding of nuclear extracts from hypothalamic or neuroblastoma cells stimulated with dexamethasone or 8Br-cAMP to oligonucleotides containing the CRE or cGRE sites of TRH gene promoter was decreased if cells were preincubated with PKC or MEK inhibitors. Mutations on the AP-1 or the GRE half sites of cGRE showed that GR binds as an heterodimer on cGRE, and PKC or MEK inhibitors diminish binding at the AP-1 site. PKC and ERK signaling thus modulate GR activity and its interaction with CREB or AP-1 at the TRH gene promoter.

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Section: Discussionmentioning

confidence: 98%

The PKC and ERK/MAPK Pathways Regulate Glucocorticoid Action on TRH Transcription

et al. 2008

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“…BDNF increases, while T 3 decreases expression of BDNF, leptin receptor, proopiomelanocortin (POMC), TRH, and agouti-related protein (AgRP) (35). Through TrkB receptor signaling, BDNF increases the expression of the TRH precursor pre-pro-TRH mRNA in PVN neurons (260). Thus, in the PVN, BDNF may, in part, contribute to negative energy balance via increasing TRH, or, conversely, TRH may affect energy balance by increasing BDNF.…”

Section: Bdnf and The Central Regulation Of Energy Metabolismmentioning

confidence: 99%

“…In recent years, studies have identified additional sites of BDNF action regulating energy balance, including the DVC, hypothalamic PVN and VMN, the VTA, amygdala, and possibly the hippocampus (17, 18, 32, 52, 57, 58, 266 -270, 272). In regulating energy balance, BDNF interacts with several other neuropeptides, including melanocortin (18,39,196,255,284), leptin (17,18,40,137,268,269,272), corticotrophin-releasing hormone (CRH) (35,39,40,251,271), and thyrotropin releasing hormone (TRH) (35,233,260).…”

Section: Bdnf and The Central Regulation Of Energy Metabolismmentioning

confidence: 99%

The lighter side of BDNF

Noble

Billington

Kotz³

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

237

168

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Brain-derived neurotrophic factor (BDNF) mediates energy metabolism and feeding behavior. As a neurotrophin, BDNF promotes neuronal differentiation, survival during early development, adult neurogenesis, and neural plasticity; thus, there is the potential that BDNF could modify circuits important to eating behavior and energy expenditure. The possibility that "faulty" circuits could be remodeled by BDNF is an exciting concept for new therapies for obesity and eating disorders. In the hypothalamus, BDNF and its receptor, tropomyosin-related kinase B (TrkB), are extensively expressed in areas associated with feeding and metabolism. Hypothalamic BDNF and TrkB appear to inhibit food intake and increase energy expenditure, leading to negative energy balance. In the hippocampus, the involvement of BDNF in neural plasticity and neurogenesis is important to learning and memory, but less is known about how BDNF participates in energy homeostasis. We review current research about BDNF in specific brain locations related to energy balance, environmental, and behavioral influences on BDNF expression and the possibility that BDNF may influence energy homeostasis via its role in neurogenesis and neural plasticity. food intake; body weight; ventromedial hypothalamus; paraventricular nucleus; brain-derived neurotrophic factor BRAIN-DERIVED NEUROTROPHIC factor (BDNF) is a member of the neurotrophin family of growth factors (151), along with nerve growth factor (152), and neurotrophin (NT) 3 (67, 163), NT 4/5 (28), and NT 6 (88). Neurotrophins are synthesized as 32-35-kDa pro-isoforms, which are later cleaved to mature forms that dimerize after translation and then act as receptor ligands (136). Whereas the precursor forms of other neurotrophins are constitutively secreted, the 32-kDa pro-BDNF is packaged into vesicles of a regulated pathway and is secreted in an activitydependent manner (87). Pro-BDNF may be secreted as is (48), cleaved by the extracellular protease plasmin (202), or interact with the pan-neurotrophin receptor p75 NTR and other receptors that cause an independent biological effect (244). Alternatively, pro-BDNF is processed to the mature form intracellularly by furin or proconvertases, where it forms C-terminal dimers (212, 226).Mature BDNF is considered the biologically active form, which has a high affinity for the tropomyosin-related kinase B (TrkB) receptor (130). Both BDNF and TrkB are present in presynaptic axon terminals and postsynaptic dendritic compartments of neurons, and they are capable of bidirectional release and activity [for review, see Tyler et al. (259)]. Typical of the neurotrophic factors, BDNF stimulates the development and differentiation of new neurons (3, 131) and promotes long-term potentiation (LTP) (139,140,205), and neuron survival (97,105,116). BDNF is abundantly expressed throughout the developing and mature CNS and in many peripheral tissues, including muscle, liver, and adipose (42,159,182,261). Regional differences between BDNF mRNA levels and protein concentrations in the CNS a...

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“…For example, comparison between lean and fat rats (Lou/C versus Wistar (Veyrat-Durebex et al 2013)) or selectively bred chickens (Byerly et al 2009) show increased Trh mRNA but also increased Npy and Agrp together with decreased Pomc in the lean animals which would seem to contradict the effects of these peptides on TRH expression in the PVN (Fekete & Lechan 2014). Although it is not possible to delineate the hypothalamic regions where these reported changes occur, coincident changes in these two species include the enhanced expression of brain-derived neurotrophic factor (BDNF) which in vitro increases Trh mRNA levels (Ubieta et al 2007). BDNF and its receptor TRKB are expressed in several hypothalamic nuclei including TRHergic cells of the PVN (Ubieta et al 2007).…”

Section: Hypothalamic Trh Neuronal Populationsmentioning

confidence: 99%

“…Although it is not possible to delineate the hypothalamic regions where these reported changes occur, coincident changes in these two species include the enhanced expression of brain-derived neurotrophic factor (BDNF) which in vitro increases Trh mRNA levels (Ubieta et al 2007). BDNF and its receptor TRKB are expressed in several hypothalamic nuclei including TRHergic cells of the PVN (Ubieta et al 2007). BDNF regulates neurogenesis, neuronal plasticity, and support during development and throughout the animal's life-span (Jeanneteau & Chao 2013).…”

Section: Hypothalamic Trh Neuronal Populationsmentioning

confidence: 99%

Regulation of TRH neurons and energy homeostasis-related signals under stress

Joseph‐Bravo

Jaimes-Hoy

Charlí

2015

Journal of Endocrinology

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Energy homeostasis relies on a concerted response of the nervous and endocrine systems to signals evoked by intake, storage, and expenditure of fuels. Glucocorticoids (GCs) and thyroid hormones are involved in meeting immediate energy demands, thus placing the hypothalamo-pituitary-thyroid (HPT) and hypothalamo-pituitary-adrenal axes at a central interface. This review describes the mode of regulation of hypophysiotropic TRHergic neurons and the evidence supporting the concept that they act as metabolic integrators. Emphasis has been be placed on i) the effects of GCs on the modulation of transcription of Trh in vivo and in vitro, ii) the physiological and molecular mechanisms by which acute or chronic situations of stress and energy demands affect the activity of TRHergic neurons and the HPT axis, and iii) the less explored role of non-hypophysiotropic hypothalamic TRH neurons. The partial evidence gathered so far is indicative of a contrasting involvement of distinct TRH cell types, manifested through variability in cellular phenotype and physiology, including rapid responses to energy demands for thermogenesis or physical activity and nutritional status that may be modified according to stress history.

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BDNF up-regulates pre-pro-TRH mRNA expression in the fetal/neonatal paraventricular nucleus of the hypothalamus. Properties of the transduction pathway

Cited by 18 publications

References 58 publications

The PKC and ERK/MAPK Pathways Regulate Glucocorticoid Action on TRH Transcription

The PKC and ERK/MAPK Pathways Regulate Glucocorticoid Action on TRH Transcription

The lighter side of BDNF

Regulation of TRH neurons and energy homeostasis-related signals under stress

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