Effects of a Peptide Analogue of the Amphiphilic Domain of the Common Neurotrophin Receptor on Nerve Growth Factor‐Mediated Motility of Human Neuroblastoma Cells

: Exposure of human neuroblastoma cells (IMR‐32) to a peptide mimic of the cytoplasmic amphiphilic domain of the common neurotrophin receptor (p75NTR 367–379) resulted in enhanced nerve growth factor (NGF)‐mediated inhibition of cell invasion in vitro. The peptide also enhanced NGF‐mediated neurite extension and GAP‐43 gene expression but had no effect on NGF‐mediated cell survival. These latter functional effects mimicked influences on NGF‐mediated neurite growth in other trkA‐positive cells as reported previously. NGF‐dependent trkA phosphorylation was significantly enhanced by the presence of the peptide, whereas high‐affinity binding of 125I‐NGF, both NGF receptors mRNA and protein expression, and trkA dimer/monomer ratios were not influenced. The studies suggest that ligand‐mediated trkA activation has differential effects on cell motility phenomena and that the amphiphilic domain of p75NTR has a role in this differential signaling.