Yu Zhe, Tsay Candice, Lacour Stéphanie P, Wagner Sigurd, Morrison Barclay
Department of Biomedical Engineering, Columbia University, New York, New York, USA.
Conf Proc IEEE Eng Med Biol Soc. 2006;Suppl:6732-5. doi: 10.1109/IEMBS.2006.260933.
Traumatic brain injury (TBI) can be caused by motor vehicle accidents, falls and firearms. TBI can result in major neurological dysfunction such as chronic seizures and memory disturbances. To discover mechanisms of functional deficits underlying TBI, we developed a stretchable microelectrode array (SMEA),which can be used for continuous recording of neuronal function, pre-, during, and post-stretch injury. TheSMEA was fabricated on a polydimethylsiloxane (PDMS)substrate with stretchable, 100 pm wide, 25 nm thick gold electrodes patterned there on [1]. The electrodes were encapsulated with a 10-20 microm thick, photo-patternable PDMS insulation layer. Previous biocompatibility tests showed no overt necrosis or cell death caused by the SMEAs after 2 weeks in culture [2]. The electrical performance of the SMEAs was tested in electrophysiological saline solution before, during and after biaxial stretching. The results showed that the electrode impedance increased with the strain to reach 800 kL at 8.5% strain and then recovered to 10 kil after relaxation. The working noise level remained below 20 pV pp during the whole process. New methodologiesf or improving the patterning of the encapsulation layer were tested on gold electrode arrays supported on glass. With these prototype arrays, robust population spikes were recorded from organotypic hippocampal slice cultures of brain tissue. Additionally, seizure-like activity induced with 1 mM bicuculline was also recorded. Our results demonstrate that the prototype arrays have good electrical performance compatible with existing multielectrode array systems. They also indicate the ability to record neuronal activity from hippocampal slices. This novel technology will enable new studies to understand injury mechanisms leading to post-traumatic neuronal dysfunction.
创伤性脑损伤(TBI)可由机动车事故、跌倒和火器伤引起。TBI可导致严重的神经功能障碍,如慢性癫痫发作和记忆障碍。为了发现TBI潜在功能缺陷的机制,我们开发了一种可拉伸微电极阵列(SMEA),它可用于在拉伸损伤前、损伤期间和损伤后连续记录神经元功能。SMEA是在聚二甲基硅氧烷(PDMS)基板上制造的,上面有可拉伸的、宽100 pm、厚25 nm的金电极图案[1]。电极用10 - 20微米厚的可光图案化PDMS绝缘层封装。先前的生物相容性测试表明,在培养2周后,SMEA没有引起明显的坏死或细胞死亡[2]。在双轴拉伸前、拉伸期间和拉伸后,在电生理盐溶液中测试了SMEA的电性能。结果表明,电极阻抗随应变增加,在8.5%应变时达到800 kΩ,然后在松弛后恢复到10 kΩ。在整个过程中,工作噪声水平保持在20 pV pp以下。在玻璃支撑的金电极阵列上测试了改进封装层图案化的新方法。使用这些原型阵列,从脑组织的器官型海马切片培养物中记录到了强烈的群体峰电位。此外,还记录了用1 mM荷包牡丹碱诱导的癫痫样活动。我们的结果表明,原型阵列具有与现有多电极阵列系统兼容的良好电性能。它们还表明有能力记录海马切片中的神经元活动。这项新技术将使新的研究能够了解导致创伤后神经元功能障碍的损伤机制。