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Akt Activation Is Necessary for Growth Factor–Induced Trafficking of Functional K_Ca Channels in Developing Parasympathetic Neurons

Department of Biology and Biochemistry, University of Houston, Houston, Texas

Submitted 4 August 2004; accepted in final form 21 October 2004

The protein kinase Akt is a crucial regulator of neuronal survival and apoptosis. Here we show that Akt activation is necessary for mobilization of large-conductance K_Ca channels in ciliary ganglion (CG) neurons evoked by -neuregulin-1 (NRG1) and transforming growth factor-1 (TGF1). Application of NRG1 to embryonic day 9 (E9) CG neurons increased Akt phosphorylation, as observed previously for TGF1. NRG1- and TGF1-evoked stimulation of K_Ca is blocked by inhibitors of PI3K by overexpression of a dominant-negative form of Akt, by overexpression of CTMP, an endogenous negative regulator of Akt, and by application of the Akt inhibitor 1L-6-hydroxymethyl-chiro-inositol 2-(R)-2-O-methyl-3-O-octadecylcarbonate (HIMO). Conversely, overexpression of a constitutively-active form of Akt was sufficient by itself to increase mobilization of functional K_Ca channels. NRG1 and TGF1 evoked an Akt-dependent increase in cell-surface SLO -subunits. These procedures have no effect on voltage-activated Ca²⁺ currents. Thus Akt plays an essential role in the developmental regulation of excitability in CG neurons.

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