Functional Modulation of Voltage-Gated Sodium Channels by a FGF14-Based Peptidomimetic

ACS Chem Neurosci. 2018 May 16;9(5):976-987. doi: 10.1021/acschemneuro.7b00399. Epub 2018 Feb 6.

Abstract

Protein-protein interactions (PPI) offer unexploited opportunities for CNS drug discovery and neurochemical probe development. Here, we present ZL181, a novel peptidomimetic targeting the PPI interface of the voltage-gated Na+ channel Nav1.6 and its regulatory protein fibroblast growth factor 14 (FGF14). ZL181 binds to FGF14 and inhibits its interaction with the Nav1.6 channel C-tail. In HEK-Nav1.6 expressing cells, ZL181 acts synergistically with FGF14 to suppress Nav1.6 current density and to slow kinetics of fast inactivation, but antagonizes FGF14 modulation of steady-state inactivation that is regulated by the N-terminal tail of the protein. In medium spiny neurons in the nucleus accumbens, ZL181 suppresses excitability by a mechanism that is dependent upon expression of FGF14 and is consistent with a state-dependent inhibition of FGF14. Overall, ZL181 and derivatives could lay the ground for developing allosteric modulators of Nav channels that are of interest for a broad range of CNS disorders.

Keywords: CNS drug discovery; Fibroblast growth factor 14 (FGF14); minimal functional domains; neurochemical probes; peptidomimetics; protein:protein interaction (PPI); voltage-gated sodium channels (Nav1.6).

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Fibroblast Growth Factors / genetics
  • Fibroblast Growth Factors / pharmacology*
  • HEK293 Cells
  • Hippocampus / drug effects*
  • Humans
  • Mice, Knockout
  • Peptidomimetics / pharmacology
  • Sodium / metabolism*
  • Voltage-Gated Sodium Channels / drug effects*

Substances

  • Peptidomimetics
  • Voltage-Gated Sodium Channels
  • fibroblast growth factor 14
  • Fibroblast Growth Factors
  • Sodium