Stimulation of neurogenesis in rat nucleus of the solitary tract by ghrelin

Zhang, Weizhen; Hu, Yuexuan; Lin, Theodore R.; Fan, Yongyi; Mulholland, Michael W.

doi:10.1016/j.peptides.2005.04.023

Cited by 47 publications

(37 citation statements)

References 47 publications

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“…However, the phenotype of progenitor cell progeny in the DG after ulated neurogenesis is likely to be the consequence of increasing cell proliferation. Similar neuroproliferative effects of ghrelin were observed in fetal spinal cord [8], NTS [9], DMNV [10], and cultured adult hippocampal progenitor cells [11]. Conversely, in this study the BrdU incorporation was reduced in animals passive-immunized against ghrelin.…”

Section: Discussionsupporting

confidence: 82%

“…Ghrelin is also involved in neurogenesis of the rat fetal spinal cord [8]. In addition, in the nucleus of the solitary tract (NTS) [9] and the dorsal motor nucleus of vagus (DMNV) [10] in adult rats with cervical vagotomy, ghrelin promotes neural proliferation in vivo and in vitro. Moreover, very recently it has been reported that ghrelin increases cellular proliferation of adult rat hippocampal progenitor cells in vitro [11].…”

Section: Rapid Communicationmentioning

confidence: 99%

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Ghrelin Regulates Hippocampal Neurogenesis in Adult Mice

Moon¹,

Kim²,

Hwang³

et al. 2009

Endocr J

103

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Rapid CommuniCationis principally released from Gr cells in the oxyntic mucosa of the stomach [5]. In addition to stimulating GH release via the hypothalamus and direct pituitary pathways and inducing a positive energy balance by stimulating food intake while decreasing fat use through GH-independent mechanisms, ghrelin has been suggested to have numerous peripheral actions including direct effects on exocrine and endocrine pancreatic functions, carbohydrate metabolism, the cardiovascular system, gastric secretion, stomach motility, and sleep [6]. It has been reported that maternal ghrelin plays an important role in rat fetal development during pregnancy [7]. Ghrelin is also involved in neurogenesis of the rat fetal spinal cord [8]. In addition, in the nucleus of the solitary tract (NTS) [9] and the dorsal motor nucleus of vagus (DMNV) [10] in adult rats with cervical vagotomy, ghrelin promotes neural proliferation in vivo and in vitro. Moreover, very recently it has been reported that ghrelin increases cellular proliferation of adult rat hippocampal progenitor cells in vitro [11]. However, there is no report to date about the effect of ghrelin on neurogenesis in the adult mammalian SGZ of the DG in vivo. In the present study, we wanted to study the impact of systemically administered ghrelin. Therefore, the aim of this study was to investigate the proliferation and differentiation of Medicine, Seoul, Korea abstract. The aim of our study was to investigate the effect of the peripheral administration of ghrelin, a peptide hormone secreted from the stomach, on cellular proliferation and differentiation of progenitor cells in the adult hippocampus. Double immunohistochemical staining revealed that ki-67-positive hippocampal progenitor cells expressed ghrelin receptors. In mice treated with ghrelin (80 µg/kg, i.p.) for 8 days, bromodeoxyuridine incorporation and doublecortin-positive neuroblasts were significantly increased in the dentate subgranular zone. We also found that the numbers of bromodeoxyuridine-and doublecortin-immunoreactive cells were significantly reduced after anti-ghrelin antibody (10 µg/kg, i.p.) treatment for 8 days. Therefore, our results indicate that ghrelin induces proliferation and differentiation of adult hippocampal progenitors, suggesting an involvement of ghrelin in hippocampal neurogenesis.

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Section: Discussionsupporting

confidence: 82%

Section: Rapid Communicationmentioning

confidence: 99%

Ghrelin Regulates Hippocampal Neurogenesis in Adult Mice

Moon¹,

Kim²,

Hwang³

et al. 2009

Endocr J

103

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“…In vitro incubation of hypothalamic and brain stem cells with ghrelin induces proliferation with many of the resultant newborn cells acquiring a neuronal and/or glial phenotype (224,575,576). Insulin has also long been associated with brain development.…”

Section: Gene-environment Causes Of Obesitymentioning

confidence: 99%

Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity

Bouret

Levin

Ozanne

2015

Physiological Reviews

138

103

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LBouret S, Levin BE, Ozanne SE. Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity. Physiol Rev 95: 47-82, 2015; doi:10.1152/physrev.00007.2014.-Obesity and type 2 diabetes mellitus (T2DM) often occur together and affect a growing number of individuals in both the developed and developing worlds. Both are associated with a number of other serious illnesses that lead to increased rates of mortality. There is likely a polygenic mode of inheritance underlying both disorders, but it has become increasingly clear that the pre-and postnatal environments play critical roles in pushing predisposed individuals over the edge into a disease state. This review focuses on the many genetic and environmental variables that interact to cause predisposed individuals to become obese and diabetic. The brain and its interactions with the external and internal environment are a major focus given the prominent role these interactions play in the regulation of energy and glucose homeostasis in health and disease.

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“…Initially, ghrelin was known to increase neurogenesis in the rat fetal spinal cord (Sato et al 2006) and the nucleus of the solitary tract (Zhang et al 2005) and the dorsal motor nucleus of vagus in adult rats. We previously reported that systemic administration of ghrelin induces hippocampal neurogenesis in adult mice (Moon et al 2009b).…”

Section: Introductionmentioning

confidence: 99%

Multiple signaling pathways mediate ghrelin-induced proliferation of hippocampal neural stem cells

Chung

Kim

et al. 2013

Journal of Endocrinology

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Ghrelin, an endogenous ligand for the GH secretagogue receptor (GHS-R) receptor 1a (GHS-R1a), has been implicated in several physiologic processes involving the hippocampus. The aim of this study was to investigate the molecular mechanisms of ghrelin-stimulated neurogenesis using cultured adult rat hippocampal neural stem cells (NSCs). The expression of GHS-R1a was detected in hippocampal NSCs, as assessed by western blot analysis and immunocytochemistry. Ghrelin treatment increased the proliferation of cultured hippocampal NSCs assessed by BrdU incorporation. The exposure of cells to the receptor-specific antagonist D-Lys-3-GHRP-6 abolished the proliferative effect of ghrelin. By contrast, ghrelin showed no significant effect on cell differentiation. The expression of GHS-R1a was significantly increased by ghrelin treatment. The analysis of signaling pathways showed that ghrelin caused rapid activation of ERK1/2 and Akt, which were blocked by the GHS-R1a antagonist. In addition, ghrelin stimulated the phosphorylation of Akt downstream effectors, such as glycogen synthase kinase (GSK)-3b, mammalian target of rapamycin (mTOR), and p70 S6K. The activation of STAT3 was also caused by ghrelin treatment. Furthermore, pretreatment of cells with specific inhibitors of MEK/ERK1/2, phosphatidylinositol-3-kinase (PI3K)/Akt, mTOR, and Jak2/STAT3 attenuated ghrelin-induced cell proliferation. Taken together, our results support a role for ghrelin in adult hippocampal neurogenesis and suggest the involvement of the ERK1/2, PI3K/Akt, and STAT3 signaling pathways in the mediation of the actions of ghrelin on neurogenesis. Our data also suggest that PI3K/Akt-mediated inactivation of GSK-3b and activation of mTOR/p70 S6K contribute to the proliferative effect of ghrelin.

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Stimulation of neurogenesis in rat nucleus of the solitary tract by ghrelin

Cited by 47 publications

References 47 publications

Ghrelin Regulates Hippocampal Neurogenesis in Adult Mice

Ghrelin Regulates Hippocampal Neurogenesis in Adult Mice

Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity

Multiple signaling pathways mediate ghrelin-induced proliferation of hippocampal neural stem cells

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