Detection of K Efflux from Stimulated Cortical Neurons by an Aptamer-Modified Silicon Nanowire Field-Effect Transistor.

The concentration gradient of K across the cell membrane of a neuron determines its resting potential and cell excitability. During neurotransmission, the efflux of K from the cell via various channels will not only decrease the intracellular K content but also elevate the extracellular K concentration. However, it is not clear to what extent this change could be. In this study, we developed a multiple-parallel-connected silicon nanowire field-effect transistor (SiNW-FET) modified with K-specific DNA-aptamers (aptamer/SiNW-FET) for the real-time detection of the K efflux from cultured cortical neurons. The aptamer/SiNW-FET showed an association constant of (2.18 ± 0.44) × 10 M against K and an either less or negligible response to other alkali metal ions. The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) stimulation induced an outward current and hyperpolarized the membrane potential in a whole-cell patched neuron under a Na/K-free buffer. When neurons were placed atop the aptamer/SiNW-FET in a Na/K-free buffer, AMPA (13 μM) stimulation elevated the extracellular K concentration to ∼800 nM, which is greatly reduced by 6,7-dinitroquinoxaline-2,3-dione, an AMPA receptor antagonist. The EC of AMPA in elevating the extracellular K concentration was 10.3 μM. By stimulating the neurons with AMPA under a normal physiological buffer, the K concentration in the isolated cytosolic fraction was decreased by 75%. These experiments demonstrate that the aptamer/SiNW-FET is sensitive for detecting cations and the K concentrations inside and outside the neurons could be greatly changed to modulate the neuron excitability.