title: Xenon attenuates excitatory synaptic transmission in the rodent prefrontal cortex and spinal cord dorsal horn.
abstract: BACKGROUND
  The molecular mechanisms of the inhalational anesthetic xenon are not yet fully understood. Recently, the authors showed that xenon reduces both N-methyl-d-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated synaptic transmission in a brain slice preparation of the amygdala. In the current study, the authors examined the effects of xenon on synaptic transmission in the prefrontal cortex and the spinal cord dorsal horn (substantia gelatinosa).
  
  
  METHODS
  In rodent brain or spinal cord slice preparations, the authors used patch clamp technique to investigate the impact of xenon on NMDA and AMPA receptor-mediated excitatory postsynaptic currents, as well as on gamma-aminobutyric acid type A receptor-mediated inhibitory postsynaptic currents. The currents were either evoked upon electrical stimulation (NMDA-eEPSCs and AMPA-eEPSCs) or upon photolysis of caged L-glutamate (p-NMDA-Cs and p-AMPA-Cs). In addition, the authors investigated the effects of xenon on AMPA receptor-mediated miniature excitatory postsynaptic currents.
  
  
  RESULTS
  In both central nervous system regions, xenon had virtually no effect on inhibitory postsynaptic currents. In the prefrontal cortex (spinal cord), xenon reversibly reduced NMDA-eEPSCs to approximately 58% (72%) and AMPA-eEPSCs to approximately 67% (65%) of control. There was no difference in the xenon-induced reduction of NMDA-eEPSCs and p-NMDA-Cs, or AMPA-eEPSCs and p-AMPA-Cs. Xenon did not affect the frequency of miniature excitatory postsynaptic currents but reduced their amplitude.
  
  
  CONCLUSIONS
  In the current study, the authors found that xenon depresses NMDA and AMPA receptor-mediated synaptic transmission in the prefrontal cortex and the substantia gelatinosa without affecting gamma-aminobutyric acid type A receptor-mediated synaptic transmission. These results provide evidence that the effects of xenon are primarily due to postsynaptic mechanisms.
authors.affiliation: Department of Anesthesiology, Klinikum rechts der Isar, Technische Universität München, Ismaninger Strasse 22, 81675 Munich, Germany. haseneder@mpipsykl.mpg.de
authors.forename: Rainer
authors.initials: R
authors.lastname: Haseneder
authors.forename: Stephan
authors.initials: S
authors.lastname: Kratzer
authors.forename: Eberhard
authors.initials: E
authors.lastname: Kochs
authors.forename: Corinna
authors.initials: C
authors.lastname: Mattusch
authors.forename: Matthias
authors.initials: M
authors.lastname: Eder
authors.forename: Gerhard
authors.initials: G
authors.lastname: Rammes
mesh_terms: D018685:Anesthetics, Inhalation; D000818:Animals; D004558:Electric Stimulation; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010146:Pain / Q000503:physiopathology; D020671:Posterior Horn Cells / Q000187:drug effects*; D017397:Prefrontal Cortex / Q000187:drug effects*; D018091:Receptors, AMPA / Q000187:drug effects; D011963:Receptors, GABA-A / Q000187:drug effects; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects; D013116:Spinal Cord / Q000187:drug effects*; D009435:Synaptic Transmission / Q000187:drug effects*; D014978:Xenon
chemical_list: D018685:Anesthetics, Inhalation; D018091:Receptors, AMPA; D011963:Receptors, GABA-A; D016194:Receptors, N-Methyl-D-Aspartate; D014978:Xenon