Developmental regulation of the serotonergic transmitter phenotype in rostral and caudal raphe neurons by transforming growth factor-βs

Author(s):  
Dagmar Galter ◽  
Martina Böttner ◽  
Klaus Unsicker
2005 ◽  
Vol 93 (3) ◽  
pp. 1174-1182 ◽  
Author(s):  
Kwon-Seok Chae ◽  
Miguel Martin-Caraballo ◽  
Marc Anderson ◽  
Stuart E. Dryer

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 KCa channels in ciliary ganglion (CG) neurons evoked by β-neuregulin-1 (NRG1) and transforming growth factor-β1 (TGFβ1). Application of NRG1 to embryonic day 9 (E9) CG neurons increased Akt phosphorylation, as observed previously for TGFβ1. NRG1- and TGFβ1-evoked stimulation of KCa 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 KCa channels. NRG1 and TGFβ1 evoked an Akt-dependent increase in cell-surface SLO α-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.


2005 ◽  
Vol 173 (4S) ◽  
pp. 159-159
Author(s):  
Wun-Jae Kim ◽  
ChangYi Quan ◽  
Pil-Du Jeoung ◽  
Eun-Jung Kim ◽  
Ji-Yeon Kim ◽  
...  

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