GAP-43 AUGMENTS G-PROTEIN-COUPLED RECEPTOR TRANSDUCTION IN XENOPUS-LAEVIS OOCYTES

The neuronal protein GAP-43 is thought to play a role in determining g rowth-cone motility, perhaps as an intracellular regulator of signal t ransduction, but its molecular mechanism of action has remained unclea r. We find that GAP-43, when microinjected into Xenopus laevis oocytes , increases the oocyte response to G protein-coupled receptor agonists by 10- to 100-fold. Higher levels of GAP-43 cause a transient current flow, even without receptor stimulation. The GAP-43-induced current, like receptor-stimulated currents, is mediated by a calcium-activated chloride channel and can be desensitized by injection of inositol 1,4, 5-trisphosphate. This suggests that neuronal GAP-43 may serve as an in tracellular signal to greatly enhance the sensitivity of G protein-cou pled receptor transduction.