Abstract
Overgrowth of connective tissue and scar formation induced by the electrode array insertion increase the impedance and, thus, diminish the interactions between neural probes as like cochlear implants (CI) and the target tissue. Therefore, it is of great clinical interest to modify the carrier material of the electrodes to improve the electrode nerve interface for selective cell adhesion. On one side connective tissue growth needs to be reduced to avoid electrode array encapsulation, on the other side the carrier material should not compromise the interaction with neuronal cells. The present in vitro-study qualitatively and quantitatively characterises the interaction of fibroblasts, glial cells and spiral ganglion neurons (SGN) with ultrathin poly(N,N-dimethylacrylamide) (PDMAA), poly(2-ethyloxazoline) (PEtOx) and poly([2-methacryloyloxy)ethyl]trimethylammoniumchlorid) (PMTA) films immobilised onto glass surfaces using a photoreactive anchor layer. The layer thickness and hydrophilicity of the polymer films were characterised by ellipsometric and water contact angle measurement. Moreover the topography of the surfaces was investigated using atomic force microscopy (AFM). The neuronal and non-neuronal cells were dissociated from spiral ganglions of postnatal rats and cultivated for 48 h on top of the polymer coatings. Immunocytochemical staining of neuronal and intermediary filaments revealed that glial cells predominantly attached on PMTA films, but not on PDMAA and PEtOx monolayers. Hereby, strong survival rates and neurite outgrowth were only found on PMTA, whereas PDMAA and PEtOx coatings significantly reduced the SG neuron survival and neuritogenesis. As also shown by scanning electron microscopy (SEM) SGN strongly survived and retained their differentiated phenotype only on PMTA. In conclusion, survival and neuritogenesis of SGN may be associated with the extent of the glial cell growth. Since PMTA was the only of the polar polymers used in this study bearing a cationic charge, it can be assumed that this charge favours adhesion of both glial cells and SG neurons glial cells and SGN.
Highlights
The only therapeutic intervention for patients with profound sensory neural hearing loss is the chronic electrical stimulation of the residual auditory neurons via a cochlea implant (CI) [1,2,3]
The successful immobilization of the silane anchor was confirmed by static contact angle (WCA) measurements and ellipsometric analysis of the layer thickness for silicon plates treated under the same conditions
The growth of intracochlear tissue following the insertion of the electrode array is thought to be the result of an inflammatory foreign body reaction, the contamination of perilymph with blood or bone dust, or a local infection following surgery [54,55,56]
Summary
The only therapeutic intervention for patients with profound sensory neural hearing loss is the chronic electrical stimulation of the residual auditory neurons via a cochlea implant (CI) [1,2,3]. Fibrosis and new bone formation inside the scala tympani [8,9,10,11] and most adversely, growth of fibrous tissue on the implant surface [11,12] were found. It is of great clinical interest to modify the surface of carrier material of auditory implants and for other stimulating neural probes to inhibit connective tissue formation. Hereby, engineering and modification of the surface of artificial materials, which are used as medical implants, give great impact on cell and tissue interactions by the physical, biochemical and topographical properties of their surface [22,23,24,25,26,27,28,29]
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