Figure 5

Disruption of electrical excitability with the Kir2.1 inward rectifying K⁺ channel causes a significant reduction in dendritic morphology of E10 lumbar motoneurons. To study how disruption of electrical excitability alters the maturation of the dendritic morphology of the motoneurons, chicken embryos were infected with the RCASBP(B)-GFP or RCASBP(B)-Kir2.1 viral constructs at E2. Embryos were isolated at E10 and prepared for tracing of the dendritic tree of the motoneurons. (A) Typical Neurolucida drawing of motoneurons, traced from control (non-infected) or RCASBP(B)-GFP or RCASBP(B)-Kir2.1 infected chicken embryos. (B-E) Inhibition of electrical excitability in RCASBP(B)-Kir2.1 infected embryos causes a significant reduction in the dendritic complexity of E10 motoneurons as indicated by the changes in the overall length of the dendritic arbor/cell, the number of branch points and the numbers of ends when compared with control or RCASBP(B)-GFP infected embryos. (F, G) Infection of chicken embryos with RCASBP(B)-GFP or RCASBP(B)-Kir2.1 has no effect on the cell body morphology of E10 motoneurons. (H) Comparison of E10 dendritic morphology as a function of dendritic order in embryos infected with RCASBP(B)-GFP or RCASBP(B)-Kir2. Infection of chicken embryos with RCASBP(B)-Kir2 causes a significant reduction in the number of dendrites between the second and fifth dendritic orders when compared to control or RCASBP(B)-GFP infected embryos. *P < 0.01 versus control (non-infected embryos); **P < 0.05 versus RCASBP(B)-GFP infected embryos. NS denotes no significant differences between the groups as indicated by one-way ANOVA.