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Biochim Biophys Acta Biomembr. 2017 Apr;1859(4):598-604. doi: 10.1016/j.bbamem.2016.10.016. Epub 2016 Oct 29.

Sphingolipids modulate the function of human serotonin1A receptors: Insights from sphingolipid-deficient cells.

Author information

1
CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad 500 007, India.
2
CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad 500 007, India. Electronic address: amit@ccmb.res.in.

Abstract

Sphingolipids are essential components of eukaryotic cell membranes and are known to modulate a variety of cellular functions. It is becoming increasingly clear that membrane lipids play a crucial role in modulating the function of integral membrane proteins such as G protein-coupled receptors (GPCRs). In this work, we utilized LY-B cells, that are sphingolipid-auxotrophic mutants defective in sphingolipid biosynthesis, to monitor the role of cellular sphingolipids in the function of an important neurotransmitter receptor, the serotonin1A receptor. Serotonin1A receptors belong to the family of GPCRs and are implicated in behavior, development and cognition. Our results show that specific ligand binding and G-protein coupling of the serotonin1A receptor exhibit significant enhancement under sphingolipid-depleted conditions, which reversed to control levels upon replenishment of cellular sphingolipids. In view of the reported role of sphingolipids in neuronal metabolism and pathogenesis of several neuropsychiatric disorders, exploring the role of serotonin1A receptors under conditions of defective sphingolipid metabolism assumes relevance, and could contribute to our overall understanding of such neuropsychiatric disorders. This article is part of a Special Issue entitled: Lipid order/lipid defects and lipid-control of protein activity edited by Dirk Schneider.

KEYWORDS:

GPCR; LY-B cells; Lipid-protein interactions; Serotonin(1A) receptor; Sphingolipids

PMID:
27984018
DOI:
10.1016/j.bbamem.2016.10.016
[Indexed for MEDLINE]
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