Pharmacological stimulation of GAL1R but not GAL2R attenuates kainic acid-induced neuronal cell death in the rat hippocampus
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- 作者：Kristin Weblingb ; 1 ; kristin.webling@neurochem.su.se" class="auth_mail" title="E-mail the corresponding author ; Jessica L. Groves-Chapmana ; 1 ; Johan Runessonb ; Indrek Saarc ; Andreas Langd ; Rannar Sillardb ; Erik Jakovenkob ; Barbara Koflerd ; Philip V. Holmesa ; Ü ; lo Langelb ; c
- 关键词：CHO cells ; Chinese hamster ovary cells ; DMEM ; Dulbecco's modified essential medium ; FBS ; fetal bovine serum ; GAL1R ; galanin receptor subtype 1 ; GAL2R ; galanin receptor subtype 2 ; GAL3R ; galanin receptor subtype 3 ; HEK cells ; human embryonic kidney cells ; KA ; kainic acid ; TFA ; trifluoroacetic acid
- 刊名：Neuropeptides
- 出版年：2016
- 出版时间：August 2016
- 年：2016
- 卷：58
- 期：Complete
- 页码：83-92
- 全文大小：1143 K
文摘
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A new protocol for evaluating novel GPCR ligands using real-time impedance based technology showed similar or slightly lower EC50 values when compared to previously published galanin ligands
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M1154, a novel GAL1/2R selective agonist was designed and its ability to significantly reduce the excitotoxicity of i.c.v. administered KA was evaluated.
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Our data indicate, that M617 (GAL1R selective ligand) and M1154 (GAL1/2R selective ligand), but not M1145 (GAL2R selective ligand), significantly reduced neuronal cell death, in the KA-excitoxicity model.
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Our findings suggest that the neuroprotective effect of pharmacological stimulation of galanin receptors in vivo after I.c.v. administration of KA in the CA3 region is mediated through GAL1R.