In parallel, neurons were pretreated with WM or an Akt inh. for 45 min before treatment with B2-ECD or B4-ECD for an additional hour. Neurons were labeled for surface α7* nAChRs with αBgTx-488 (green), fixed, permeabilized, and costained for NF protein (blue). (A) Representative micrographs of αBgTx-488 staining along NF-positive axons. B4-ECD treatment increased surface αBgTx-488 clusters (b), which did not occur in the presence of WM (d). Linescans of fluorescence intensity profiles of αBgTx-488 along representative axons (see Materials and methods) are shown. Bar, 5 μm. (B) Quantification of surface αBgTx-488 clusters along sensory neuron axons represented in A. B4-ECD treatment induced an ∼1.9-fold increase of surface αBgTx-488 clusters but not in the presence of WM or Akt inh. Data were pooled from three independent experiments. The graph shows means ± SEM. Statistical significance was determined by ANOVA with post-hoc Fisher's PLSD test. *, P < 0.0001 (Statview). (C) Quantification of surface αBgTx-488 cluster area. B4-ECD treatment induced an increase in αBgTx-488 cluster area but not in the presence of WM or Akt inh. Data pooled from three independent experiments were analyzed using nonparametric statistics and presented as box plots (see Materials and methods). Statistical significance determined by the Kolmogorov-Smirnov Test. *, P = 0.0001 (Statview).<p><b>Copyright information:</b></p><p>Taken from "Presynaptic Type III Neuregulin1-ErbB signaling targets α7 nicotinic acetylcholine receptors to axons"</p><p></p><p>The Journal of Cell Biology 2008;181(3):511-521.</p><p>Published online 5 May 2008</p><p>PMCID:PMC2364689.</p><p></p
