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Development/Plasticity/Repair Sodium Channel Activation Augments NMDA Receptor
 

Summary: Development/Plasticity/Repair
Sodium Channel Activation Augments NMDA Receptor
Function and Promotes Neurite Outgrowth in Immature
Cerebrocortical Neurons
Joju George,1 Shashank M. Dravid,1 Anand Prakash,1 Jun Xie,1,2 Jennifer Peterson,3 Sairam V. Jabba,1 Daniel G. Baden,4
and Thomas F. Murray1
1Department of Pharmacology, Creighton University School of Medicine, Omaha, Nebraska 68178, 2Department of Biochemistry and Molecular Biology,
Shanxi Medical University, Taiyuan 030001, China, 3College of Veterinary Medicine, University of Georgia, Athens, Georgia 30602, and 4Center for Marine
Science, University of North Carolina at Wilmington, Wilmington, North Carolina 28409
A range of extrinsic signals, including afferent activity, affect neuronal growth and plasticity. Neuronal activity regulates intracellular
Ca2
, and activity-dependent calcium signaling has been shown to regulate dendritic growth and branching (Konur and Ghosh, 2005).
NMDA receptor (NMDAR) stimulation of Ca2
/calmodulin-dependent protein kinase signaling cascades has, moreover, been demon-
stratedtoregulateneurite/axonaloutgrowth(Waymanetal.,2004).Weusedasodiumchannelactivator,brevetoxin(PbTx-2),toexplore
the relationship between intracellular [Na ] and NMDAR-dependent development. PbTx-2 alone, at a concentration of 30 nM, did not
affect Ca2
dynamics in 2 d in vitro cerebrocortical neurons; however, this treatment robustly potentiated NMDA-induced Ca2
influx.
The 30 nM PbTx-2 treatment produced a maximum [Na ]i of 16.9 1.5 mM, representing an increment of 8.8 1.8 mM over basal. The

  

Source: Alford, Simon - Department of Biological Sciences, University of Illinois at Chicago

 

Collections: Biology and Medicine