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Differential Effects of a Full and Biased Ghrelin Receptor Agonist in a Mouse Kindling Model. / Buckinx, An; Van Den Herrewegen, Yana; Pierre, Anouk; Cottone, Eleonora; Ben Haj Salah, Khoubaib; Fehrentz, Jean-Alain; Kooijman, Ron; De Bundel, Dimitri; Smolders, Ilse.

In: International Journal of Molecular Sciences, Vol. 20, No. 10, 2480, 20.05.2019.

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Buckinx A, Van Den Herrewegen Y, Pierre A, Cottone E, Ben Haj Salah K, Fehrentz J-A et al. Differential Effects of a Full and Biased Ghrelin Receptor Agonist in a Mouse Kindling Model. International Journal of Molecular Sciences. 2019 May 20;20(10). 2480.

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@article{504adcee151346979d89868e67043713,
title = "Differential Effects of a Full and Biased Ghrelin Receptor Agonist in a Mouse Kindling Model",
abstract = "The ghrelin system has received substantial recognition as a potential target for novel anti-seizure drugs. Ghrelin receptor (ghrelin-R) signaling is complex, involving Gα q/11, Gα i/o, Gα 12/13, and β-arrestin pathways. In this study, we aimed to deepen our understanding regarding signaling pathways downstream the ghrelin-R responsible for mediating anticonvulsive effects in a kindling model. Mice were administered the proconvulsive dopamine 1 receptor-agonist, SKF81297, to gradually induce a kindled state. Prior to every SKF81297 injection, mice were treated with a ghrelin-R full agonist (JMV-1843), a Gα q and Gα 12 biased ligand unable to recruit β-arrestin (YIL781), a ghrelin-R antagonist (JMV-2959), or saline. Mice treated with JMV-1843 had fewer and less severe seizures compared to saline-treated controls, while mice treated with YIL781 experienced longer and more severe seizures. JMV-2959 treatment did not lead to differences in seizure severity and number. Altogether, these results indicate that the Gα q or Gα 12 signaling pathways are not responsible for mediating JMV-1843‘s anticonvulsive effects and suggest a possible involvement of β-arrestin signaling in the anticonvulsive effects mediated by ghrelin-R modulation.",
author = "An Buckinx and {Van Den Herrewegen}, Yana and Anouk Pierre and Eleonora Cottone and {Ben Haj Salah}, Khoubaib and Jean-Alain Fehrentz and Ron Kooijman and {De Bundel}, Dimitri and Ilse Smolders",
year = "2019",
month = "5",
day = "20",
language = "English",
volume = "20",
journal = "International Journal of Molecular Sciences",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "10",

}

RIS

TY - JOUR

T1 - Differential Effects of a Full and Biased Ghrelin Receptor Agonist in a Mouse Kindling Model

AU - Buckinx, An

AU - Van Den Herrewegen, Yana

AU - Pierre, Anouk

AU - Cottone, Eleonora

AU - Ben Haj Salah, Khoubaib

AU - Fehrentz, Jean-Alain

AU - Kooijman, Ron

AU - De Bundel, Dimitri

AU - Smolders, Ilse

PY - 2019/5/20

Y1 - 2019/5/20

N2 - The ghrelin system has received substantial recognition as a potential target for novel anti-seizure drugs. Ghrelin receptor (ghrelin-R) signaling is complex, involving Gα q/11, Gα i/o, Gα 12/13, and β-arrestin pathways. In this study, we aimed to deepen our understanding regarding signaling pathways downstream the ghrelin-R responsible for mediating anticonvulsive effects in a kindling model. Mice were administered the proconvulsive dopamine 1 receptor-agonist, SKF81297, to gradually induce a kindled state. Prior to every SKF81297 injection, mice were treated with a ghrelin-R full agonist (JMV-1843), a Gα q and Gα 12 biased ligand unable to recruit β-arrestin (YIL781), a ghrelin-R antagonist (JMV-2959), or saline. Mice treated with JMV-1843 had fewer and less severe seizures compared to saline-treated controls, while mice treated with YIL781 experienced longer and more severe seizures. JMV-2959 treatment did not lead to differences in seizure severity and number. Altogether, these results indicate that the Gα q or Gα 12 signaling pathways are not responsible for mediating JMV-1843‘s anticonvulsive effects and suggest a possible involvement of β-arrestin signaling in the anticonvulsive effects mediated by ghrelin-R modulation.

AB - The ghrelin system has received substantial recognition as a potential target for novel anti-seizure drugs. Ghrelin receptor (ghrelin-R) signaling is complex, involving Gα q/11, Gα i/o, Gα 12/13, and β-arrestin pathways. In this study, we aimed to deepen our understanding regarding signaling pathways downstream the ghrelin-R responsible for mediating anticonvulsive effects in a kindling model. Mice were administered the proconvulsive dopamine 1 receptor-agonist, SKF81297, to gradually induce a kindled state. Prior to every SKF81297 injection, mice were treated with a ghrelin-R full agonist (JMV-1843), a Gα q and Gα 12 biased ligand unable to recruit β-arrestin (YIL781), a ghrelin-R antagonist (JMV-2959), or saline. Mice treated with JMV-1843 had fewer and less severe seizures compared to saline-treated controls, while mice treated with YIL781 experienced longer and more severe seizures. JMV-2959 treatment did not lead to differences in seizure severity and number. Altogether, these results indicate that the Gα q or Gα 12 signaling pathways are not responsible for mediating JMV-1843‘s anticonvulsive effects and suggest a possible involvement of β-arrestin signaling in the anticonvulsive effects mediated by ghrelin-R modulation.

M3 - Article

VL - 20

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1661-6596

IS - 10

M1 - 2480

ER -

ID: 45765096