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The effect of propofol on actin, ERK-1/2 and GABA(A) receptor content in neurones

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Author

Summary, in English

Aim: Interaction with the gamma-aminobutyric acid receptor (GABA(A)R) complex is recognized as an important component of the mechanism of many anaesthetic agents, including propofol. The aims of this study were to investigate the effect of propofol on GABA(A)R, to determine whether exposure of neurones to propofol influences the localization of GABA(A)R within the cell and to look for cytoskeletal changes that may be connected with activation, such as the mitogen-activated protein kinase (MAPK) pathway. Methods: Primary cortical cell cultures from rat, with and without pre-incubation with the GABA(A)R antagonist bicuculline, were exposed to propofol. The cells were lysed and separated into membrane and cytosolic fractions. Immunoblot analyses of filamentous actin (F-actin), the GABA(A) beta(2)-subunit receptor and extracellular signal-regulated kinase-1/2 (ERK-1/2) were performed. Results: Propofol triggers an increase in GABA(A)R, actin content and ERK-1/2 phosphorylation in the cytosolic fraction. In the membrane fraction, there is a decrease in GABA(A) beta(2)-subunit content and an increase in both actin content and ERK-1/2 phosphorylation. The GABA(A)R antagonist bicuculline blocks the propofol-induced changes in F-actin, ERK and GABA(A) beta(2)-subunit content, and ERK-1/2 phosphorylation. Conclusion: We believe that propofol triggers a dose-dependent internalization of the GABA(A) beta(2)-subunit. The increase in internal GABA(A) beta(2)-subunit content exhibits a close relationship to actin polymerization and to an increase in ERK-1/2 activation. Actin contributes to the internalization sequestering of the GABA(A) beta(2)-subunit.

Publishing year

2007

Language

English

Pages

1184-1189

Publication/Series

Acta Anaesthesiologica Scandinavica

Volume

51

Issue

9

Document type

Journal article

Publisher

Wiley-Blackwell

Topic

  • Anesthesiology and Intensive Care

Keywords

  • propofol
  • mitogen-activated protein kinase (MAPK)
  • actin
  • extracellular signal-regulated kinase-1/2 (ERK-1/2)
  • gamma-aminobutyric
  • acid receptor.

Status

Published

Research group

  • Cell Pathology, Malmö

ISBN/ISSN/Other

  • ISSN: 0001-5172