{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Buckinx A"],"funding":["Geneeskundige Stichting Koningin Elisabeth","Fonds Wetenschappelijk Onderzoek"],"pagination":["E2480"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6567032"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(10)"],"pubmed_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 Gαq/11, Gαi/o, Gα12/13, 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 Gαq and Gα12 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 Gαq or Gα12 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."],"journal":["International journal of molecular sciences"],"pubmed_title":["Differential Effects of a Full and Biased Ghrelin Receptor Agonist in a Mouse Kindling Model."],"pmcid":["PMC6567032"],"funding_grant_id":["N/A","1S84218N","ING-prize"],"pubmed_authors":["Buckinx A","Kooijman R","De Bundel D","Ben Haj Salah K","Fehrentz JA","Van Den Herrewegen Y","Pierre A","Smolders I","Cottone E"],"additional_accession":[]},"is_claimable":false,"name":"Differential Effects of a Full and Biased Ghrelin Receptor Agonist in a Mouse Kindling Model.","description":"The ghrelin system has received substantial recognition as a potential target for novel anti-seizure drugs. Ghrelin receptor (ghrelin-R) signaling is complex, involving Gαq/11, Gαi/o, Gα12/13, 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 Gαq and Gα12 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 Gαq or Gα12 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.","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 May","modification":"2024-11-20T18:35:46.341Z","creation":"2019-07-24T07:18:02Z"},"accession":"S-EPMC6567032","cross_references":{"pubmed":["31137460"],"doi":["10.3390/ijms20102480"]}}