Ryanodine and IP3 receptor-mediated calcium signaling play a pivotal role in neurological infrared laser modulation

Pulsed infrared (IR) laser energy has been shown to modulate neurological activity through both stimulation and inhibition of action potentials. While the mechanism(s) behind this phenomenon is (are) not completely understood, certain hypotheses suggest that the rise in temperature from IR exposure could activate temperature-or pressure-sensitive ion channels or create pores in the cellular outer membrane, allowing an influx of typically plasma-membrane-impermeant ions. Studies using fluorescent intensity-based calcium ion (Ca2+) sensitive dyes show changes in Ca2+ levels after various IR stimulation parameters, which suggests that Ca2+ may originate from the external solution. However, activation of intracellular signaling pathways has also been demonstrated, indicating a more complex mechanism of increasing intracellular Ca2+ concentration. We quantified the Ca2+ mobilization in terms of influx from the external solution and efflux from intracellular organelles using Fura-2 and a high-speed ratiometric imaging system that rapidly alternates the dye excitation wavelengths. Using nonexcitable Chinese hamster ovarian (CHO-hM(1)) cells and neuroblastomaglioma (NG108) cells, we demonstrate that intracellular IP3 receptors play an important role in the IR-induced Ca2+, with the Ca2+ response augmented by ryanodine receptors in excitable cells. (C) 2017 Society of Photo-Optical Instrumentation Engineers (SPIE)