Cell adhesion molecule immobilized gold surfaces for enhanced neuron-electrode interfaces.

To provide a long-term solution for increasing the biocompatibility of neuroprosthetics, approaches to reduce the side effects of invasive neuro-implantable devices are still in need of improvement. Physical, chemical, and bioactive design aspects of the biomaterials are proven to be important for providing proper cell-to-cell, cell-to-material interactions. Particularly, modification of implant surfaces with bioactive cues, especially cell adhesion molecules (CAMs) that capitalize on native neural adhesion mechanisms, are promising candidates in favor of providing efficient interfaces. Within this concept, this study utilized specific CAMs, namely N-Cadherin (Neural cadherin, N-Cad) and neural cell adhesion molecule (NCAM), to enhance neuron-electrode contact by mimicking the cell-to-ECM interactions for improving the survival of cells and promoting neurite outgrowth. For this purpose, representative gold electrode surfaces were modified with N-Cadherin, NCAM, and the mixture (1:1) of these molecules. Modifications were characterized, and the effect of surface modification on both differentiated and undifferentiated neuroblastoma SH-SY5Y cell lines were compared. The findings demonstrated the successful modification of these molecules which subsequently exhibited biocompatible properties as evidenced by the cell viability results. In cell culture experiments, the CAMs displayed promising results in promoting neurite outgrowth compared to conventional poly-l-lysine coated surfaces, especially NCAM and N-Cad/NCAM modified surfaces clearly showed significant improvement. Overall, this optimized approach is expected to provide an insight into the action mechanisms of cells against the local environment and advance processes for the fabrication of alternative neural interfaces.

Distribution and mRNA Expression of nAChRs in the Rat S1 and M1 Cortices After Electrical Stimulation of the Basal Forebrain.

AIM: To study the changes in the distribution of and the transcriptional levels associated with α4- and α7-subtype nicotinic acetylcholine receptors (nAChRs) in the primary somatosensory (S1) and motor (M1) cortices of rats after electrical stimulation of the basal forebrain (BF). MATERIAL AND METHODS: Immunofluorescence (IF) analyses were performed on brain sections from 20 rats (experimental groups: controls, contralateral, and ipsilateral to BF stimulation). The nAChR receptor complexes were labeled with antibodies and counted (N) in the cortical layers of the hindlimb representation (S1HL), barrel field (S1BF), and M1. To determine the relative transcriptional mRNA levels, qRT-PCR was performed with tissue from the associated brain regions of 14 different animals in two groups, controls and BF stimulation. RESULTS: For all three tested brain regions, N and D (density) of the α7-subtype nAChR increased in both ipsilateral and contralateral hemispheres after BF stimulation. There was no change in N and D of the α4 subtype. Regardless of BF stimulation, N of both subtypes was lower in M1 compared to S1HL and S1BF, and D was highest in layers II-IV. BF stimulation had no significant effect on the relative mRNA levels of both receptor subtypes. CONCLUSION: The results show an upregulation of the α7-subtype nAChR as a result of BF stimulation, based on receptor-complex counts on IF images. However, this change was not reflected in mRNA levels, which suggest post-translational modifications. Overall, this study suggests structural changes from the effects of cholinergic projections to the somatosensory and motor cortices.