Figure 8

GFL-induced enhancement in the stimulated-release of iCGRP is mediated by SFK pathway. A) This representative Western blot demonstrated changes in levels of p-SFKs, SFK, and α-tubulin in DRG in response to a 10 minute incubation with 10 ng/mL GDNF, NRTN, and ARTN and the subsequent prevention of these changes by an inhibitor of the SFK pathway (10 μM PP2). The inactive control compound for this pathway was added as well (10 μM PP3). B) Densitometric analysis of three separate Western blots like that in A probing for SFKs. C) Peptide release elicited by a 10 minute exposure to Hepes buffer alone (open bar) or Hepes buffer containing 50 nM capsaicin (Cap; dark bars) is expressed as mean percent total peptide content of cells in each well ± SEM (n = 12-18 wells per condition). Asterisks (*) indicate statistically significant differences in band density and iCGRP release between treatment groups and the no GFL condition using an ANOVA with Dunnett's post-hoc test (p < 0.05). Ampersands (@) indicate statistically significant differences between the GFL treatment and the PP2 treated condition using a t-test (p < 0.05). In all cases, release stimulated by capsaicin was significantly higher than basal release.