Investigation of the presence of ghrelin in the central nervous system of the rat and mouse

Furness, John B.; Hunne, Billie; Matsuda, Norifumi; Yin, Lei; Russo, Diana da Silva; Kato, Ikuo; Fujimiya, Mineko; Patterson, Michael; McLeod, Julie; Andrews, Zane B.; Bron, Romke

doi:10.1016/j.neuroscience.2011.07.063

Cited by 109 publications

(93 citation statements)

References 49 publications

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“…Earlier immunocytochemical studies suggested the presence of ghrelin in some brain areas, such as the hypothalamus [38] and the cortex [39]. However, it has been reported that no ghrelin-specific staining is found and ghrelin receptor-expressing neurons do not have adjacent ghrelin immunoreactive terminals in the brain or spinal cord of the rat and mouse [40]. Recently, Cabral et al [41] provided a comprehensive review of all available data related to the distribution of ghrelin in the CNS and concluded that there are no indisputable and reliable evidences to support the idea that ghrelin is present in the brain at physiologically significant levels.…”

Section: Figmentioning

confidence: 99%

Ghrelin protects adult rat hippocampal neural stem cells from excessive autophagy during oxygen-glucose deprivation

2018

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Abstract. Ghrelin functions as a neuroprotective agent and saves neurons from various insults include ischemic injury. However, it remains to be elucidated whether ghrelin protects neuronal cells against ischemic injury-induced excessive autophagy. Autophagy is required for the maintenance of neural stem cell homeostasis. However, regarding autophagic cell death, it is commonly assumed that excessive autophagy leads to self-elimination of mammalian cells. The purpose of this study was to investigate the potential neuroprotection effects of ghrelin from excessive autophagy in adult rat hippocampal neural stem cells (NSCs). Oxygen-Glucose Deprivation (OGD) strongly induces autophagy in adult rat hippocampal NSCs. Ghrelin treatment inhibited OGD-induced cell death of adult rat hippocampal NSCs assessed by cell-counting-kit-8 assay. Ghrelin also suppressed OGD-induced excessive autophagy activity. The protective effect of ghrelin was accompanied by an increased expression levels of Bcl-2, p-62 and decreased expression level of LC3-II, Beclin-1 by Western blot. Furthermore, ghrelin reduced autophagosome formation and number of GFP-LC3 transfected puncta. In conclusion, our data suggest that ghrelin protects adult rat hippocampal NSCs from excessive autophagy in experimental stroke (oxygen-glucose deprivation) model. Regulating autophagic activity may be a potential optimizing target for promoting adult rat hippocampal NSCs based therapy for stroke.

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Section: Figmentioning

confidence: 99%

Ghrelin protects adult rat hippocampal neural stem cells from excessive autophagy during oxygen-glucose deprivation

2018

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“…Ghrelin-positive processes have also been reported outside of the hypothalamus, including the bed nucleus of stria terminalis, medial, central, and cortical amygdalae, the thalamic paraventricular nucleus, and the lateral habenula (Cowley et al, 2003). Some laboratories have also argued against the presence of ghrelin in the CNS (Furness et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Ghrelin Increases GABAergic Transmission and Interacts with Ethanol Actions in the Rat Central Nucleus of the Amygdala

Cruz

Herman

Cote

et al. 2012

Neuropsychopharmacol

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The neural circuitry that processes natural rewards converges with that engaged by addictive drugs. Because of this common neurocircuitry, drugs of abuse have been able to engage the hedonic mechanisms normally associated with the processing of natural rewards. Ghrelin is an orexigenic peptide that stimulates food intake by activating GHS-R1A receptors in the hypothalamus. However, ghrelin also activates GHS-R1A receptors on extrahypothalamic targets that mediate alcohol reward. The central nucleus of the amygdala (CeA) has a critical role in regulating ethanol consumption and the response to ethanol withdrawal. We previously demonstrated that rat CeA GABAergic transmission is enhanced by acute and chronic ethanol treatment. Here, we used quantitative RT-PCR (qRT-PCR) to detect Ghsr mRNA in the CeA and performed electrophysiological recordings to measure ghrelin effects on GABA transmission in this brain region. Furthermore, we examined whether acute or chronic ethanol treatment would alter these electrophysiological effects. Our qRT-PCR studies show the presence of Ghsr mRNA in the CeA. In naive animals, superfusion of ghrelin increased the amplitude of evoked inhibitory postsynaptic potentials (IPSPs) and the frequency of miniature inhibitory postsynaptic currents (mIPSCs). Coapplication of ethanol further increased the ghrelin-induced enhancement of IPSP amplitude, but to a lesser extent than ethanol alone. When applied alone, ethanol significantly increased IPSP amplitude, but this effect was attenuated by the application of ghrelin. In neurons from chronic ethanol-treated (CET) animals, the magnitude of ghrelin-induced increases in IPSP amplitude was not significantly different from that in naive animals, but the ethanol-induced increase in amplitude was abolished. Superfusion of the GHS-R1A antagonists D-Lys3-GHRP-6 and JMV 3002 decreased evoked IPSP and mIPSC frequency, revealing tonic ghrelin activity in the CeA. D-Lys3-GHRP-6 and JMV 3002 also blocked ghrelin-induced increases in GABAergic responses. Furthermore, D-Lys3-GHRP-6 did not affect ethanol-induced increases in IPSP amplitude. These studies implicate a potential role for the ghrelin system in regulating GABAergic transmission and a complex interaction with ethanol at CeA GABAergic synapses.

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“…21 However, published descriptions of the distributions of ghrelin-like immunoreactivity in the CNS are inconsistent. 22 Peripherally, the GHS-R1a gene is expressed in the stomach, intestine, pancreas, thyroid, gonads, adrenal, kidney, heart and vasculature, as well as several endocrine tumours and cell lines, and have been found to express GHS-R1a with negligible binding found in the parathyroid, pancreas, placenta, mammary gland, prostate, salivary gland, stomach, colon and spleen. 23 This wide distribution of GHS-R1a indicates that the ghrelin and synthetic GHS possess broader functions beyond the control of GH release and food intake.…”

Section: Ghrelin Receptors and Their Distributionmentioning

confidence: 99%

Ghrelin – Physiological Functions and Regulation

Abdalla

2015

European Endocrinology

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Ghrelin is an orexigenic peptide predominantly secreted from the stomach and stimulates appetite and growth hormone (GH) release.Studies have provided evidence that ghrelin exercises a wide range of functions, including regulation of food intake and energy metabolism, modulation of cardiovascular function, stimulation of osteoblast proliferation and bone formation and stimulation of neurogenesis and myogenesis. In the gastrointestinal system, ghrelin affects multiple functions, including secretion of gastric acid, gastric motility and pancreatic protein output. Most of these functions have been attributed to the actions of acylated ghrelin. The balance among its secretion rate, degradation rate and clearance rate determines the circulating level of ghrelin. This review explains what ghrelin is, its physiological functions and the factors that influence its level. KeywordsGhrelin, food intake, obesity, lipolysis, ghrelin receptors, regulation Disclosure: Mona Mohamed Ibrahim Abdalla has no conflicts of interest to declare. Acknowledgement:A note of appreciation to Research Management Centre of MAHSA University, Malaysia for funding publication of this article.

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Investigation of the presence of ghrelin in the central nervous system of the rat and mouse

Cited by 109 publications

References 49 publications

Ghrelin protects adult rat hippocampal neural stem cells from excessive autophagy during oxygen-glucose deprivation

Ghrelin protects adult rat hippocampal neural stem cells from excessive autophagy during oxygen-glucose deprivation

Ghrelin Increases GABAergic Transmission and Interacts with Ethanol Actions in the Rat Central Nucleus of the Amygdala

Ghrelin – Physiological Functions and Regulation

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