Conclusion
The expression of delayed rectifier VG Kv 1.6 channels in RGCs may determine membrane excitability and responsiveness to trophic factors, this plays a key role in the refinement of developing retinal circuits.
Methods
Neonatal retinal cultures were supplemented with trophic factors of interest, namely BDNF and SCE, at 0 DIV (days in vitro), 6 DIV and both 0 and 6 DIV. The expression of VG Kv 1.6 channels was evaluated by immunostaining with anti Kv 1.6 and immunofluorescence was measured by confocal scanning laser microscopy on 4, 6, 8, 10 and 12 DIV. The immunofluorescence indirectly measured the quantity of ion channels being expressed.
Purpose
To evaluate the role of brain derived neurotrophic factor (BDNF) and superior collicular extract (SCE) on the expression of the 1.6 subfamily of voltage-gated potassium channels (VG Kv 1.6 channels) in retinal ganglion cells (RGCs) of rats in an in vitro model.
Results
RGCs were identified by their soma size. BDNF and SCE enhanced RGC survival by enhancing extensive neurite outgrowth, and increased the expression of VG Kv 1.6 channels; the effect of SCE was more significant than BDNF. Trophic factors also enhanced the survival of RGCs by increasing the expression of ion channels thereby contributing to spontaneous bursts of action potentials in the early stages of RGC development.