Augmentation of cognitive function by NS9283, a stoichiometry-dependent positive allosteric modulator of α2- and α4-containing nicotinic acetylcholine receptors

Br J Pharmacol. 2012 Sep;167(1):164-82. doi: 10.1111/j.1476-5381.2012.01989.x.

Abstract

Background and purpose: Positive allosteric modulation of α4β2 nicotinic acetylcholine (nACh) receptors could add a new dimension to the pharmacology and therapeutic approach to these receptors. The novel modulator NS9283 was therefore tested extensively.

Experimental approach: Effects of NS9283 were evaluated in vitro using fluorescence-based Ca(2+) imaging and electrophysiological voltage clamp experiments in Xenopus oocytes, mammalian cells and thalamocortical neurons. In vivo the compound was tested in models covering a range of cognitive domains in mice and rats.

Key results: NS9283 was shown to increase agonist-evoked response amplitude of (α4)(3) (β2)(2) nACh receptors in electrophysiology paradigms. (α2)(3) (β2)(2) , (α2)(3) (β4)(2) and (α4)(3) (β4)(2) were modulated to comparable extents, but no effects were detected at α3-containing or any 2α : 3β stoichiometry nACh receptors. Native nACh receptors in thalamocortical neurons similarly displayed DHβE-sensitive currents that were receptive to modulation. NS9283 had favourable effects on sensory information processing, as shown by reversal of PCP-disrupted pre-pulse inhibition. NS9283 further improved performance in a rat model of episodic memory (social recognition), a rat model of sustained attention (five-choice serial reaction time task) and a rat model of reference memory (Morris water maze). Importantly, the effects in the Morris water maze could be fully reversed with mecamylamine, a blocker of nACh receptors.

Conclusions and implications: These results provide compelling evidence that positive allosteric modulators acting at the (α4)(3) (β2)(2) nACh receptors can augment activity across a broad range of cognitive domains, and that α4β2 nACh receptor allosteric modulation therefore constitutes a promising therapeutic approach to symptomatic treatment of cognitive impairment.

MeSH terms

  • Allosteric Regulation / drug effects
  • Animals
  • Cell Line
  • Cell Line, Tumor
  • Cognition / drug effects
  • Female
  • HEK293 Cells
  • Humans
  • Male
  • Maze Learning / drug effects
  • Mice
  • Motor Activity / drug effects
  • Nicotine / pharmacology
  • Nicotinic Agonists / pharmacokinetics
  • Nicotinic Agonists / pharmacology*
  • Oocytes / drug effects
  • Oocytes / physiology
  • Oxadiazoles / pharmacokinetics
  • Oxadiazoles / pharmacology*
  • Protein Subunits / physiology*
  • Pyridines / pharmacokinetics
  • Pyridines / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Rats, Wistar
  • Receptors, Nicotinic / physiology*
  • Recognition, Psychology / drug effects
  • Xenopus laevis

Substances

  • 3-(3-(pyridine-3-yl)-1,2,4-oxadiazol-5-yl)benzonitrile
  • Nicotinic Agonists
  • Oxadiazoles
  • Protein Subunits
  • Pyridines
  • Receptors, Nicotinic
  • nicotinic receptor alpha4beta2
  • Nicotine