title: Propofol and etomidate depress cortical, thalamic, and reticular formation neurons during anesthetic-induced unconsciousness.
abstract: BACKGROUND
  The sites where anesthetics produce unconsciousness are not well understood. Likely sites include the cerebral cortex, thalamus, and reticular formation. We examined the effects of propofol and etomidate on neuronal function in the cortex, thalamus, and reticular formation in intact animals.
  
  
  METHODS
  Five cats had a recording well and electroencephalogram screws placed under anesthesia. After a 5-day recovery period, the cats were repeatedly studied 3 to 4 times per week. Neuronal (single-unit) activity in the cerebral cortex (areas 7, 18 and 19), thalamus (ventral posterolateral and ventral posteromedial nuclei and medial geniculate body), and reticular formation (mesencephalic reticular nucleus and central tegmental field) was recorded before, during, and after infusion of either propofol or etomidate. Cortical neuronal action potentials were analyzed separately as either regular spiking neurons or fast spiking neurons.
  
  
  RESULTS
  Propofol and etomidate decreased the spontaneous firing rate of cortical neurons by 37% to 41%; fast spiking neurons and regular spiking neurons were similarly affected by the anesthetics. The neuronal firing rate in the thalamus and reticular formation decreased 30% to 49% by propofol and etomidate. The electroencephalogram shifted from a low-amplitude, high-frequency pattern to a high-amplitude, low-frequency pattern during drug infusion suggesting an anesthetic effect; peak power occurred at 12 to 13 Hz during propofol infusion. There were 2 major peaks during etomidate anesthesia: one at 12 to 14 Hz and another at 7 to 8 Hz. The cats were heavily sedated, with depressed corneal and whisker reflexes; withdrawal to noxious stimulation remained intact.
  
  
  CONCLUSIONS
  These data show that neurons in the cortex, thalamus, and reticular formation are similarly depressed by propofol and etomidate. Although anesthetic depression of neuronal activity likely contributes to anesthetic-induced unconsciousness, further work is needed to determine how anesthetic effects at these sites interact to produce unconsciousness.
authors.affiliation: Department of Anesthesiology and Pain Medicine, University of California, Davis, Davis, CA 95616, USA.
authors.forename: Jason
authors.initials: J
authors.lastname: Andrada
authors.forename: Preetha
authors.initials: P
authors.lastname: Livingston
authors.forename: Bong Jae
authors.initials: BJ
authors.lastname: Lee
authors.forename: Joseph
authors.initials: J
authors.lastname: Antognini
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D018685:Anesthetics, Inhalation / Q000008:administration & dosage; D018686:Anesthetics, Intravenous; D000818:Animals; D002415:Cats; D002540:Cerebral Cortex / Q000187:drug effects* / Q000502:physiology; D005045:Etomidate / Q000008:administration & dosage*; D005260:Female; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D015742:Propofol / Q000008:administration & dosage*; D012154:Reticular Formation / Q000187:drug effects* / Q000502:physiology; D013788:Thalamus / Q000187:drug effects* / Q000502:physiology; D014474:Unconsciousness / Q000139:chemically induced* / Q000503:physiopathology
chemical_list: D018685:Anesthetics, Inhalation; D018686:Anesthetics, Intravenous; D015742:Propofol; D005045:Etomidate