Adhesion molecules promote chronic neural interfaces following neurotrophin withdrawal

Neural prostheses and recording devices have been successfully interfaced with the nervous system; however, substantial integration issues exist at the biomaterial-tissue interface. In particular, the loss of neurons at the implantation site and the formation of a gliotic scar capsule diminish device performance. We have investigated the potential of a tissue-engineered coating, consisting of adhesion molecule-modified surfaces (i.e., polylysine and collagen) in combination with neurotrophin application (i.e., brain derived neurotrophic factor, BDNF), to enhance the electrode-host interface. Neurite length and density were examined in a retinal explant model. In the presence of BDNF for 7 days, we found no synergistic effect of BDNF and adhesion molecule-modified surfaces on neurite length, although there was a possible increase in neurite density for collagen-coated surfaces. After BDNF withdrawal (7 days BDNF+/7 days BDNF- medium), we found that both polylysine and collagen treated surfaces displayed increases in neurite length and density over negative, untreated control surfaces. These results suggest that adhesion molecules may be used to support chronic neuron-electrode interfaces induced by neurotrophin exposure.