ABSTRACT
The beneficial effect of low-level light therapy (LLLT) via light-
emitting diodes (LEDs) in the far-red to near-infrared (NIR) range
has been tested and substantiated in cultured primary neurons
exposed to various types of toxins, including the voltage-dependent
sodium channel blocker, tetrodotoxin, and toxins known to inhibit
complex I of the mitochondrial electron transport chain, MPP+
and rotenone. The major biological photoacceptors in the NIR are
hemoglobin, myoglobin, and mitochondrial cytochrome c oxidase
(Cox). Since cultured primary neurons do not contain blood or
muscles, one can study the effects of NIR mainly on Cox in neurons.
This has been verified by the positive correlation between effective
wavelengths for activating Cox and ATP production (i.e., 670, 770,
830, and 880 nm) in neurons exposed to toxins and the absorption
spectrum of Cox, and the lack of an effect at 728 nm, which does
not match the absorption spectrum of Cox. The role of Cox is
further strengthened by the fact that increasing concentrations of
KCN, a known irreversible inhibitor of Cox, result in decreasing
effectiveness of NIR. The neuroprotective benefit of LLLT has been
confirmed in vivo when deprived visual cortices of monocularly enucleated rats up-regulated their Cox activity in response to
NIR treatment. NIR also induces changes in gene expression by
up-regulating neuronal activity-related genes and down-regulating
tumor-associated and stress-induced genes.
