2009
DOI: 10.1111/j.1460-9568.2009.06770.x
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Growth hormone‐releasing peptide 6 protection of hypothalamic neurons from glutamate excitotoxicity is caspase independent and not mediated by insulin‐like growth factor I

Abstract: Treatment of the fetal hypothalamic neuronal cell line RCA-6 with growth hormone-releasing peptide 6, an agonist of the ghrelin receptor, or insulin-like growth factor I activates intracellular signalling cascades associated with anti-apoptotic actions. Abnormally high concentrations of glutamate provoke over-excitation of neurons leading to cell damage and apoptosis. Thus, the aim of this study was to investigate whether the administration of growth hormone-releasing peptide 6 and insulin-like growth factor I… Show more

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Cited by 21 publications
(13 citation statements)
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References 50 publications
(99 reference statements)
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“…GHRP-6 is capable of preventing this glutamate-induced cell death in both the hypothalamus and cerebellum (Delgado-Rubín de Célix et al, 2006). Moreover, MSG also induces cell death in the neuronal cell line RCA-6 by activating the intrinsic pathway of apoptosis through caspase-9 and -3/7 (Delgado-Rubín et al, 2009), which is in agreement with previous studies indicating that neurons and the neuroblastoma cell lines B50 and SH-SY5Y use the intrinsic pathway to undergo apoptotic cell death in response to excitotoxicity (Henshall et al, 2001; Mattson, 2003). However, although GHRP-6 partially inhibits MSG-induced cell death in RCA-6 neurons, it does not modify caspase-9 or -3/7 activities (Delgado-Rubín et al, 2009).…”
Section: The Neuroprotective Actions Of Ghrelin and Ghssupporting
confidence: 89%
“…GHRP-6 is capable of preventing this glutamate-induced cell death in both the hypothalamus and cerebellum (Delgado-Rubín de Célix et al, 2006). Moreover, MSG also induces cell death in the neuronal cell line RCA-6 by activating the intrinsic pathway of apoptosis through caspase-9 and -3/7 (Delgado-Rubín et al, 2009), which is in agreement with previous studies indicating that neurons and the neuroblastoma cell lines B50 and SH-SY5Y use the intrinsic pathway to undergo apoptotic cell death in response to excitotoxicity (Henshall et al, 2001; Mattson, 2003). However, although GHRP-6 partially inhibits MSG-induced cell death in RCA-6 neurons, it does not modify caspase-9 or -3/7 activities (Delgado-Rubín et al, 2009).…”
Section: The Neuroprotective Actions Of Ghrelin and Ghssupporting
confidence: 89%
“…This is not related to an increase in the number of excitatory synapses as shown previously [111]. The glutamate release induced by ghrelin also stimulates the uptake of glutamate by astrocytes in order to prevent excess excitability and excitotoxicity to neighboring cells [127,128,129,130]. …”
Section: Ghrelin and Astrocytes In Metabolic Controlmentioning
confidence: 55%
“…Other studies report that ghrelin exerts its neuroprotective effects through stimulation of the protein kinase A and C pathways [151]. GHRP-6 is capable of preventing glutamate-induced neuronal death in both the hypothalamus and cerebellum [129] and also in the hypothalamic neuronal cell line RCA-6 [127]. Ghrelin has a neuroprotective role in hippocampal neurons against KA-induced excitotoxicity [161] via activation of the PI3K/AKT pathway and inhibition of the mitochondrial apoptotic pathway.…”
Section: Ghrelin and Astrocytes In Neuroprotectionmentioning
confidence: 99%
“…Treatment with GHRP-6 did not increase GFAP levels but stimulated proliferation in the hypothalamus and hippocampus. GHRP-6 and ghrelin stimulate the proliferation of a wide number of cells including osteoblasts (Kim et al 2005), cardiomyocytes (Pettersson et al 2002), somatotrophs (Dieguez & Casanueva 2000), endothelial cells (Rossi et al 2009) and adipocytes (Thompson et al 2004) and may also affect the CNS by protecting neurons from apoptosis (Frago et al 2002, 2011, Delgado-Rubin de Célix et al 2006, Delgado-Rubin et al 2009). We also evaluated the possible effect of GH and GHRP-6 on neuron number and did not observed any changes in the levels of Tuj1 in the hypothalamus or hippocampus.…”
Section: Discussionmentioning
confidence: 99%
“…GRLN-R1a activation leads to an increase in intracellular levels of Ca 2C via phosphatidylinositol-specific phospholipase C (Camiña et al 2003, Muccioli et al 2007). Ghrelin and GHRP-6 stimulate proliferation of different cell types (Dieguez & Casanueva 2000, Pettersson et al 2002, Thompson et al 2004, Rossi et al 2009) and may also affect the CNS by protecting neurons from apoptosis (Frago et al 2002, 2011, Delgado-Rubin de Célix et al 2006, Delgado-Rubin et al 2009). …”
Section: Introductionmentioning
confidence: 99%