• Alexander Nürnberg, Anja U Braüer, Nina Wettschureck, and Stefan Offermanns.
• Institute of Pharmacology, University of Heidelberg, Im Neuenheimer Feld 366, D-69120 Heidelberg, Germany.
• J. Biol. Chem. 2008 Dec 19;283(51):35526-31.

AbstractThe induction of neurite retraction and growth cone collapse via G-protein-coupled receptors is involved in developmental as well as regenerative processes. The role of individual G-protein-mediated signaling processes in the regulation of neurite morphology is still incompletely understood. Using primary neurons from brains lacking Galpha(q)/Galpha(11) or Galpha(12)/Galpha(13), we show here that G(12)/G(13)-mediated signaling is absolutely required for neurite retraction and growth cone collapse induced by the blood-borne factors lysophosphatidic acid and thrombin. Interestingly, the effects of lysophosphatidic acid were mediated mainly by G(13), whereas thrombin effects required G(12). Surprisingly, lack of Galpha(q)/Galpha(11) resulted in overshooting responses to both stimuli, indicating that G(q)/G(11)-mediated signaling most likely via activation of Rac antagonizes the effects of G(12)/G(13).

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