Glycine receptors are pentameric ligand-gated ion channels that mediate fast inhibitory neurotransmission. They have recently emerged as targets for chronic pain therapies due to their role in nociceptive signalling. N-arachidonyl glycine is an endogenous lipid that has been shown to modulate glycine receptors [1] and produce analgesia in animal models [2], however its mechanism of action remains unknown.
The first aim of this study was to identify lipids that positively modulate glycine receptors and characterise their activity. A library of 35 acyl-amino acids was screened across human glycine receptors. Lipids containing a glycine head group conjugated to an unsaturated lipid tail cause significant potentiation when the cis-double bonds occurred in the central region of the tail [3]. From this, a second series of lipids containing a benzyl-moiety within the lipid tail were synthesised which improved the efficacy by up to 6-fold, and increased the potency of receptor activation by over 10-fold. (8-(2-octylphenyl)octanoyl)glycine (OPOG) caused the greatest receptor potentiation with an EC50 of 664 nM at the α1 receptor.
The second aim of this study was to identify lipid binding sites on the glycine receptor. Molecular dynamic simulations of OPOG binding to the α1 receptor were conducted and demonstrated binding within a cavity at the intracellular portion of transmembrane domains (TM) 1 and 4. A cryoEM structure of OPOG bound to the zebrafish glycine receptor was also obtained and identified binding to an inter-subunit cavity between the extracellular portions of TM1(-), TM2(-) and TM3(+). This cavity has previously been shown to bind the positive allosteric modulator ivermectin [4]. Mutagenesis of the residues within the site identified by molecular dynamics simulations suggest that this site is important for the stimulatory activity. Mutagenesis studies of the site identified by cryoEM are ongoing to establish the structural basis for lipid modulation.