Characterization of a novel high-potency positive modulator of K(v)7 channels

Eur J Pharmacol. 2013 Jun 5;709(1-3):52-63. doi: 10.1016/j.ejphar.2013.03.039. Epub 2013 Apr 3.

Abstract

K(v)7 channel activators decrease neuronal excitability and might potentially treat neuronal hyperexcitability disorders like epilepsy and mania. Here we introduce NS15370 ((2-(3,5-difluorophenyl)-N-[6-[(4-fluorophenyl)methylamino]-2-morpholino-3-pyridyl]acetamide)hydrochloride, an in vitro high-potency chemical analogue of retigabine, without effects on GABA(A) receptors. NS15370 activates recombinant homo- and heteromeric K(v)7.2-K(v)7.5 channels in HEK293 cells at sub-micromolar concentrations (EC₅₀~100 nM, as quantified by a fluorescence based Tl⁺-influx assay). In voltage clamp experiments NS15370 exhibits a complex, concentration-dependent mode-of-action: At low concentrations it accelerates voltage-dependent activation rates, slows deactivations, and increases steady-state current amplitudes. Quantified by the peak-tail current method, the V½ value of the steady-state activation curve is shifted towards hyperpolarized potentials at concentrations ~100 times lower than retigabine. However, in contrast to retigabine, NS15370 also introduces a distinct time-dependent current decrease, which eventually, at higher concentrations, causes suppression of the current at depolarized potentials, and an apparent "cross-over" of the voltage-activation curve. In brain slices, NS15370 hyperpolarizes and increases spike frequency adaptation of hippocampal CA1 neurons and the compound reduces the autonomous firing of dopaminergic neurons in the substantia-nigra pars compacta. NS15370 is effective in rodent models of hyperexcitability: (i) it yields full protection against mouse 6 Hz seizures and rat amygdala kindling discharges, two models of partial epilepsia; (ii) it reduces (+)-MK-801 hydrogen maleate (MK-801)-induced hyperactivity as well as chlordiazepoxide (CDP)+d-amphetamine (AMP)-induced hyperactivity, models sensitive to classic anti-psychotic and anti-manic treatments, respectively. Our findings with NS15370 consolidate neuronal K(v)7 channels as targets for anti-epileptic and psychiatric drug development.

MeSH terms

  • Aminopyridines / pharmacology
  • Aminopyridines / therapeutic use*
  • Animals
  • Anticonvulsants / pharmacology
  • Anticonvulsants / therapeutic use*
  • Antimanic Agents / pharmacology
  • Antimanic Agents / therapeutic use*
  • Antipsychotic Agents / pharmacology
  • Antipsychotic Agents / therapeutic use*
  • Benzeneacetamides / pharmacology
  • Benzeneacetamides / therapeutic use*
  • Bipolar Disorder / drug therapy
  • Bipolar Disorder / metabolism
  • CA1 Region, Hippocampal / drug effects
  • CA1 Region, Hippocampal / metabolism
  • Disease Models, Animal*
  • Dopaminergic Neurons / drug effects*
  • Dopaminergic Neurons / metabolism
  • Epilepsies, Partial / drug therapy
  • Epilepsies, Partial / metabolism
  • Female
  • GABAergic Neurons / drug effects*
  • GABAergic Neurons / metabolism
  • HEK293 Cells
  • Humans
  • In Vitro Techniques
  • KCNQ1 Potassium Channel / agonists*
  • KCNQ1 Potassium Channel / genetics
  • KCNQ1 Potassium Channel / metabolism
  • Male
  • Membrane Transport Modulators / pharmacology
  • Membrane Transport Modulators / therapeutic use
  • Mice
  • Nerve Tissue Proteins / agonists
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism
  • Psychotic Disorders / drug therapy
  • Psychotic Disorders / metabolism
  • Rats
  • Recombinant Proteins / metabolism
  • Substantia Nigra / drug effects
  • Substantia Nigra / metabolism

Substances

  • 2-(3,5-difluorophenyl)-N-(6-((4-fluorophenyl)methylamino)-2-morpholino-3-pyridyl)acetamide
  • Aminopyridines
  • Anticonvulsants
  • Antimanic Agents
  • Antipsychotic Agents
  • Benzeneacetamides
  • KCNQ1 Potassium Channel
  • Membrane Transport Modulators
  • Nerve Tissue Proteins
  • Recombinant Proteins