Activity of 2,3-benzodiazepines at native rat and recombinant human glutamate receptors in vitro: stereospecificity and selectivity profiles

Neuropharmacology. 1996;35(12):1689-702. doi: 10.1016/s0028-3908(96)00156-6.

Abstract

The activity and selectivity of the glutamate receptor antagonists belonging to the 2,3-benzodiazepine class of compounds have been examined at recombinant human non-NMDA glutamate receptors expressed in HEK293 cells and on native rat NMDA and non-NMDA receptors in vitro. The racemic 2,3-benzodiazepines GYKI52466, LY293606 (GYKI53405) and LY300168 (GYKI53655) inhibited AMPA (10 microM)-mediated responses in recombinant human GluR1 receptors expressed in HEK293 cells with approximate IC50 values of 18 microM, 24 microM and 6 microM, respectively and AMPA (10 microM) responses in recombinant human GluR4 expressing HEK293 cells with approximate IC50 values of 22 microM, 28 microM and 5 microM, respectively. GYKI 52466, LY293606 and LY300168 were non-competitive antagonists of AMPA receptor-mediated responses in acutely isolated rat cerebellar Purkinje neurons with approximate IC50 values of 10 microM, 8 microM and 1.5 microM, respectively. The activity of racemic compounds LY293606 and LY300168 was established to reside in the (-) isomer of each compound. At a concentration of 100 microM, GYKI52466, LY293606 and LY300168 produced < 30% inhibition of kainate-activated currents evoked in HEK293 cells expressing either human homomeric GluR5 or GluR6 receptors or heteromeric GluR6+KA2 kainate receptors. The activity of the 2,3-benzodiazepines at 100 microM was weak at kainate receptors, but was stereoselective. Similar levels of inhibition were observed for kainate-induced currents in dorsal root ganglion neurons. Intact tissue preparations were also used to examine the stereoselective actions of the 2,3-benzodiazepines. In the cortical wedge preparation, the active isomer of LY300168, LY303070, produced a non-competitive antagonism of AMPA-evoked depolarizations with smaller changes in depolarizations induced by kainate and no effect on NMDA-dependent depolarizations. LY303070 was also effective in preventing 30 microM AMPA-induced depolarizations in isolated spinal cord dorsal roots with an approximate IC50 value of 1 microM. Synaptic transmission in the hemisected spinal cord preparation was stereoselectively antagonized by the active isomers of LY300168 and LY293606. In summary, these results indicate that 2,3-benzodiazepines are potent, selective and stereospecific antagonists of the AMPA subtype of the non-NMDA glutamate receptor.

MeSH terms

  • Animals
  • Anti-Anxiety Agents*
  • Benzodiazepines / chemistry
  • Benzodiazepines / metabolism
  • Benzodiazepines / pharmacology*
  • Benzothiadiazines / pharmacology
  • Cell Line
  • Cerebellum / physiology
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / physiology
  • Excitatory Amino Acid Antagonists / chemistry
  • Excitatory Amino Acid Antagonists / metabolism
  • Excitatory Amino Acid Antagonists / pharmacology*
  • Ganglia, Spinal / physiology
  • Humans
  • Kidney
  • Membrane Potentials / drug effects
  • Molecular Structure
  • Neurons / drug effects
  • Neurons / physiology*
  • Purkinje Cells / drug effects
  • Purkinje Cells / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, AMPA / biosynthesis
  • Receptors, AMPA / drug effects
  • Receptors, AMPA / physiology*
  • Recombinant Proteins / drug effects
  • Recombinant Proteins / metabolism
  • Spinal Cord / physiology
  • Structure-Activity Relationship
  • Transfection
  • alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / pharmacology

Substances

  • Anti-Anxiety Agents
  • Benzothiadiazines
  • Excitatory Amino Acid Antagonists
  • Receptors, AMPA
  • Recombinant Proteins
  • GYKI 52466
  • Benzodiazepines
  • GYKI 53655
  • alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
  • talampanel
  • cyclothiazide
  • glutamate receptor ionotropic, AMPA 1