Roles of Integrins and Intracellular Molecules in the Migration and Neuritogenesis of Fetal Cortical Neurons: MEK Regulates Only the Neuritogenesis
Figure 6
Effects of antibodies, calcium modulators, and pharmacological inhibitors on neuritogenesis. (a) Representative images showing neuritogenesis in the absence (control) or presence of control IgG (50 nMole), antibodies against β1 (50 or 100 nMole) or α3 (50 or 100 nMole) integrin subunits on laminin. BAPTA-AM at low concentration (2.5 μM) inhibited neuritogenesis and at higher concentration (10 μM) totally abolished neuritogenesis. Bar150 microns. (b) Mean + standard error of mean values of neurite lengths/image in untreated neurons (1) and those treated with control IgG, monoclonal antibody against β1 or α3 integrin subunit at 50 nMole or 100 nMole concentration. Neurite lengths reduced significantly () in neurons treated with antibody against β1 integrin subunit at both 50 nMole (2) and 100 nMole (3) concentrations compared to control (1). Neurons treated with monoclonal antibody against α3 integrin subunit at 50 nMole (4) were lower than the control (1) but was not statistically significant (). Neurons treated with monoclonal antibody against α3 integrin subunit at 100 nMole (5) significantly inhibited the neuritogenesis (). Neuritogenesis was not altered in presence of 50 (6) or 100 nMole (7) control IgG (). (c) Mean + standard error of mean values of neurite lengths/image of neurons treated with PP2, PP3, U2, U3, 2-APB, activated Calphostin, BAPTA-AM (2.5 μM), and PD for 22 h in culture (filled bars) were significantly different () from untreated neurons (blank bar) and negative controls (PP3 or U3) (filled bars). No significant changes in neurite lengths () per image were recorded in neurons treated with RR.
