title: Reorganization of actin in neurons after propofol exposure.
abstract: BACKGROUND
  It has previously been shown that propofol in clinically relevant concentrations induces a calcium-dependent conformational change in the cytoskeleton. The aim of this study was to further clarify the effect of propofol on the actin cytoskeleton and to determine if this conformational change is mediated by the interaction between the GABA(A)-receptor and propofol.
  
  
  METHODS
  Primary cultured cortical neurons from newborn rats were treated with propofol 3 microg x ml(-1) in a time-response titration, with and without preincubation with the GABA(A)-receptor antagonist, bicuculline. Actin-protein content was detected by Western blot analysis and the cellular content of F-actin measured by a spectrophotometric technique.
  
  
  RESULTS
  Propofol triggers a relatively slow statistically significant increase in the intracellular F-actin content, maximum after 20-min incubation (160%+/-16.3) (mean+/-SEM) P<0.05. The propofol-induced increase in F-actin was effectively blocked by bicuculline. The increase in intracellular actin content after exposure to propofol as well as the effect of bicuculline were verified by Western blot analysis.
  
  
  CONCLUSIONS
  The present study shows that propofol triggers a time-dependent change of actin. Since this reorganization can be blocked effectively by a GABA(A)-receptor antagonist, this suggests that the GABA(A)-receptor is involved in the pathway leading to cytoskeletal reorganization after propofol treatment. The actin polymerization reached its maximum after 20 min. Therefore, we believe that the propofol-induced changes might be connected with slower cellular responses such as cell-to-cell interaction and/or channel regulation.
authors.affiliation: Department of Anaesthesia/Intensive Care and Pharmacology, Linköping University Hospital, Linköping, Sweden.
authors.forename: A
authors.initials: A
authors.lastname: Oscarsson
authors.forename: R
authors.initials: R
authors.lastname: Massoumi
authors.forename: A
authors.initials: A
authors.lastname: Sjölander
authors.forename: C
authors.initials: C
authors.lastname: Eintrei
mesh_terms: D000199:Actins / Q000187:drug effects / Q000378:metabolism*; D018686:Anesthetics, Intravenous / Q000494:pharmacology*; D000818:Animals; D000831:Animals, Newborn; D001640:Bicuculline / Q000494:pharmacology; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000033:anatomy & histology; D004305:Dose-Response Relationship, Drug; D018756:GABA Antagonists / Q000494:pharmacology; D015151:Immunoblotting; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D015742:Propofol / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011963:Receptors, GABA-A / Q000502:physiology; D013050:Spectrometry, Fluorescence
chemical_list: D000199:Actins; D018686:Anesthetics, Intravenous; D018756:GABA Antagonists; D011963:Receptors, GABA-A; D001640:Bicuculline; D015742:Propofol