Department of Electrical and Computer Engineering, Neural Engineering Laboratory, George Mason University, Fairfax, VA 22030, USA.
J Neural Eng. 2010 Feb;7(1):16002. doi: 10.1088/1741-2560/7/1/016002. Epub 2010 Jan 6.
Stimulating neural electrodes are required to deliver charge to an environment that presents itself as hostile. The electrodes need to maintain their electrical characteristics (charge and impedance) in vivo for a proper functioning of neural prostheses. Here we design implantable multi-walled carbon nanotubes coating for stainless steel substrate electrodes, targeted at wide frequency stimulation of deep brain structures. In well-controlled, low-frequency stimulation acute experiments, we show that multi-walled carbon nanotube electrodes maintain their charge storage capacity (CSC) and impedance in vivo. The difference in average CSCs (n = 4) between the in vivo (1.111 mC cm(-2)) and in vitro (1.008 mC cm(-2)) model was statistically insignificant (p > 0.05 or P-value = 0.715, two tailed). We also report on the transcription levels of the pro-inflammatory cytokine IL-1beta and TLR2 receptor as an immediate response to low-frequency stimulation using RT-PCR. We show here that the IL-1beta is part of the inflammatory response to low-frequency stimulation, but TLR2 is not significantly increased in stimulated tissue when compared to controls. The early stages of neuroinflammation due to mechanical and electrical trauma induced by implants can be better understood by detection of pro-inflammatory molecules rather than by histological studies. Tracking of such quantitative response profits from better analysis methods over several temporal and spatial scales. Our results concerning the evaluation of such inflammatory molecules revealed that transcripts for the cytokine IL-1beta are upregulated in response to low-frequency stimulation, whereas no modulation was observed for TLR2. This result indicates that the early response of the brain to mechanical trauma and low-frequency stimulation activates the IL-1beta signaling cascade but not that of TLR2.
刺激神经的电极需要向呈现出敌对环境的部位传递电荷。为了使神经假体正常运作,电极需要在体内保持其电学特性(电荷和阻抗)。在这里,我们设计了用于不锈钢基底电极的可植入多壁碳纳米管涂层,旨在对深部脑结构进行宽频刺激。在经过良好控制的低频刺激急性实验中,我们证明多壁碳纳米管电极在体内保持其电荷存储能力(CSC)和阻抗。体内(1.111 mC cm(-2)) 和体外(1.008 mC cm(-2)) 模型之间的平均 CSC 差异(n = 4)在统计学上无显著差异(p > 0.05 或 P 值 = 0.715,双侧)。我们还报告了使用 RT-PCR 作为对低频刺激的即时反应的促炎细胞因子 IL-1beta 和 TLR2 受体的转录水平。我们在这里表明,IL-1beta 是低频刺激引起的炎症反应的一部分,但与对照相比,刺激组织中的 TLR2 没有显著增加。通过植入物引起的机械和电损伤导致的神经炎症的早期阶段可以通过检测促炎分子而不是通过组织学研究来更好地理解。通过更好的分析方法在几个时间和空间尺度上对这种定量反应进行跟踪。我们关于评估这些炎症分子的结果表明,细胞因子 IL-1beta 的转录物在低频刺激下上调,而 TLR2 没有观察到调节。这一结果表明,大脑对机械创伤和低频刺激的早期反应激活了 IL-1beta 信号级联,但 TLR2 没有被激活。