Intracellular calcium transients evoked by pulsed infrared radiation in neonatal cardiomyocytes

Abstract

Non-technical summary We have investigated the mechanisms underlying the response of cells to pulsed infrared radiation (IR, ∼1862 nm) using the neonatal rat ventricular cardiomyocyte as a model. n = 12), an inhibitor of the mitochondrial Na + /Ca 2+ exchanger (mNCX), (2) Ruthenium Red (40 μM, n = 13), an inhibitor of the mitochondrial Ca 2+ uniporter (mCU), and (3) 2-aminoethoxydiphenylborane (10 μM, n = 6), an IP 3 channel antagonist. Ryanodine blocked the spontaneous [Ca 2+ ] i transients but did not alter the IR-evoked events in the same cells. This pharmacological array implicates mitochondria as the major intracellular store of Ca 2+ involved in IR-evoked responses reported here. Results support the hypothesis that 1862 nm pulsed IR modulates mitochondrial Ca 2+ transport primarily through actions on mCU and mNCX.

Thermal Transients Excite Neurons through Universal Intramembrane Mechanoelectrical Effects

“…This study explored the effects of temperature changes on membrane capacitance and its associated currents in a joint attempt to clarify the experimental results of a key recent study [16] and to pave the way towards predictive modeling of INS [2][3][4][5][6][7][8][9][10][11][12][13][14][15] and other thermal neurostimulation techniques [18][19][20], which could potentially facilitate the development of more advanced and multimodal methods for neural circuit control. Another key motivation to pursue this problem came from our noting the very similar temperature-related capacitance rates of change observed in very different model systems [ Fig.…”

“…Both approaches also offer the long-term prospect of remotely affecting aberrant localized neural circuits that underlie many neurological diseases. A multitude of INS-related studies explored the ability of short-wave infrared (IR) pulses to stimulate neural structures including peripheral [3,4] and cranial nerves [5][6][7][8][9][10], retinal and cortical neurons [10][11][12], as well as cardiomyocytes [13,14]. It is stipulated that the INS phenomenon is mediated by temperature transients induced by IR absorption [15][16][17]; such transients can alternatively be induced using other forms of photoabsorption [18][19][20], or potentially by any other physical form of thermal neurostimulation that can be driven rapidly enough [21,22].…”

Gold Nanorod-assisted Optical Stimulation of Neuronal Cells

“…Recently, Ca 2+ transients have also been observed as a consequence of IR laser exposure in cardiomyocytes. In that work, the Ca 2+ responses evoked after IR exposure exhibited lower amplitudes and faster recovery times than the spontaneous Ca 2+ transients 2 . Figure 3 shows an example of NG108-15 neuronal cells loaded with Fluo-4 AM and imaged with a confocal microscope.…”

“…As previously indicated, NRs were expected to be located intracellularly (Figure 4A-C) and was observed not to be consistently triggered by the laser pulses (Figure 4C) 13 . The most likely explanations were the transient depletion of intracellular Ca 2+ stores attributed to incomplete Ca 2+ loading 2 or the different efficiency of NR internalization in the neuronal cells. When NRs were not used in culture (control experiments, Figure 4D), a stimulatory effect of the 780 nm light was also observed.…”

“…Recent studies have demonstrated that the transient heating associated with the absorption of infrared light by water (wavelength >1,400 nm) can be used to induce action potentials in nerve tissue 1 and intracellular calcium transients in cardiomyocytes 2 . The use of infrared light has raised great interest for applications in neural prostheses, due to the potential finer spatial resolution, lack of direct contact with the tissue, minimization of stimulation artifacts, and removal of the need to genetically modify the cells prior to stimulation (as required in optogenetics) 1 .…”