Spatiotemporal Imaging of Glutamate-Induced Biophotonic Activities and Transmission in Neural Circuits

Abstract

The processing of neural information in neural circuits plays key roles in neural functions. Biophotons, also called ultra-weak photon emissions (UPE), may play potential roles in neural signal transmission, contributing to the understanding of the high functions of nervous system such as vision, learning and memory, cognition and consciousness. However, the experimental analysis of biophotonic activities (emissions) in neural circuits has been hampered due to technical limitations. Here by developing and optimizing an in vitro biophoton imaging method, we characterize the spatiotemporal biophotonic activities and transmission in mouse brain slices. We show that the long-lasting application of glutamate to coronal brain slices produces a gradual and significant increase of biophotonic activities and achieves the maximal effect within approximately 90 min, which then lasts for a relatively long time (>200 min). The initiation and/or maintenance of biophotonic activities by glutamate can be significantly blocked by oxygen and glucose deprivation, together with the application of a cytochrome c oxidase inhibitor (sodium azide), but only partly by an action potential inhibitor (TTX), an anesthetic (procaine), or the removal of intracellular and extracellular Ca2+. We also show that the detected biophotonic activities in the corpus callosum and thalamus in sagittal brain slices mostly originate from axons or axonal terminals of cortical projection neurons, and that the hyperphosphorylation of microtubule-associated protein tau leads to a significant decrease of biophotonic activities in these two areas. Furthermore, the application of glutamate in the hippocampal dentate gyrus results in increased biophotonic activities in its intrahippocampal projection areas. These results suggest that the glutamate-induced biophotonic activities reflect biophotonic transmission along the axons and in neural circuits, which may be a new mechanism for the processing of neural information.

Phosphene perception is due to the ultra-weak photon emission produced in various parts of the visual system: glutamate in the focus

“…Although the mentioned experiments by Tang and Dai (2014b) as well as by Kobayashi et al (1999a,b) revealed that UPE increased under unphysiologically concentrations of glutamate (i.e. > 25 and 10 mm, respectively), such elevated concentrations of glutamate are still within the range of the glutamate concentration stored in the presynaptic vesicles (60-200 mm; Clements et al, 1992).…”

“…According to Tang and Dai (2014b), 'the glutamateinduced biophotonic activities reflect biophotonic transmission along the axons and in neural circuits, which may be a new mechanism for the processing of neural information.' However, for the real interpretation of many visualrelated phenomena, future research should consider the role of redox-related UPE in neural information processes, as it makes possible to design better prosthetic devices, to reduce phosphenes that perturb normal astronauts' sleep during space travel, to use phosphenes as early markers for various visual-related diseases (as we pointed out previously; Ashtari et al, 2014), and to reduce drug-induced side effects, among others.…”

“…In addition, UPE, free radical production, and lipid peroxidation are Ca 2+ concentration-dependent mechanisms (Pandya et al, 2013;Tang and Dai, 2014b).…”

Are there optical communication channels in the brain

“…(12) in which the number of biophotons emitted per minute by a slice of mouse brain is counted while the neurons are excited with the neurotransmitter glutamate. Ref.…”

“…Although there is already some experimental evidence of biophoton propagation in the brain and axons (12,43,44), it would nevertheless be very interesting to test the light guidance of axons directly in-vitro and in-vivo. For testing in-vitro, one way is to light up one end of a thin brain slice (with proper homogeneous myelinated axons) and look for the bright spots related to the open ends of the myelinated axons at the other end.…”