Radiprodil, a selective GluN2B negative allosteric modulator, rescues audiogenic seizures in mice carrying the GluN2A(N615S) mutation

Br J Pharmacol. 2024 Jun;181(12):1886-1894. doi: 10.1111/bph.16361. Epub 2024 Mar 26.

Abstract

Background and purpose: GRIN-related disorders are neurodevelopmental disorders caused by mutations in N-methyl-D-aspartate receptor (NMDAR) subunit genes. A large fraction of these mutations lead to a 'gain of function' (GoF) of the NMDAR. Patients present with a range of symptoms including epilepsy, intellectual disability, behavioural and motor. Controlling seizures is a significant unmet medical need in most patients with GRIN-related disorders. Although several hundred GRIN mutations have been identified in humans, until recently none of the mouse models carrying Grin mutations/deletions showed an epileptic phenotype. The two recent exceptions both carry mutations of GluN2A. The aim of this study was to assess the efficacy of radiprodil, a selective negative allosteric modulator of GluN2B-containing NMDARs, in counteracting audiogenic seizures (AGS) in a murine model carrying the GluN2A(N615S) homozygous mutation (Grin2aS/S mice).

Experimental approach: Grin2aS/S mice were acutely treated with radiprodil at different doses before the presentation of a high-frequency acoustic stimulus commonly used for AGS induction.

Key results: Radiprodil significantly and dose-dependently reduced the onset and severity of AGS in Grin2aS/S mice. Surprisingly, the results revealed a sex-dependent difference in AGS susceptibility and in the dose-dependent protection of radiprodil in the two genders. Specifically, radiprodil was more effective in female versus male mice.

Conclusion and implications: Overall, our data clearly show that radiprodil, a GluN2B selective negative allosteric modulator, may have the potential to control seizures in patients with GRIN2A GoF mutations. Further studies are warranted to better understand the sex-dependent effects observed in this study.

Keywords: audiogenic seizures; dose–response curve; gain of function mutation; knock‐in mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Allosteric Regulation / drug effects
  • Animals
  • Anticonvulsants / administration & dosage
  • Anticonvulsants / pharmacology
  • Anticonvulsants / therapeutic use
  • Dose-Response Relationship, Drug
  • Epilepsy, Reflex / drug therapy
  • Epilepsy, Reflex / genetics
  • Female
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mutation*
  • Piperidines / administration & dosage
  • Piperidines / pharmacology
  • Piperidines / therapeutic use
  • Receptors, N-Methyl-D-Aspartate* / genetics
  • Seizures / drug therapy
  • Seizures / genetics

Substances

  • Receptors, N-Methyl-D-Aspartate
  • NR2B NMDA receptor
  • N-methyl D-aspartate receptor subtype 2A
  • Piperidines
  • Anticonvulsants